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Fernández, E. Fieira, D. González, M. Delgado, L. Méndez, J.M. Borro" "autores" => array:7 [ 0 => array:2 [ "Iniciales" => "M." "apellidos" => "de la Torre" ] 1 => array:2 [ "Iniciales" => "R." "apellidos" => "Fernández" ] 2 => array:2 [ "Iniciales" => "E." "apellidos" => "Fieira" ] 3 => array:2 [ "Iniciales" => "D." "apellidos" => "González" ] 4 => array:2 [ "Iniciales" => "M." "apellidos" => "Delgado" ] 5 => array:2 [ "Iniciales" => "L." "apellidos" => "Méndez" ] 6 => array:2 [ "Iniciales" => "J.M." "apellidos" => "Borro" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X0873215915856142?idApp=UINPBA00004E" "url" => "/08732159/0000002100000001/v0_201604141151/X0873215915856142/v0_201604141151/en/main.assets" ] "itemAnterior" => array:16 [ "pii" => "X0873215915856126" "issn" => "08732159" "doi" => "10.1016/j.rppnen.2014.05.004" "estado" => "S300" "fechaPublicacion" => "2015-01-01" "documento" => "article" "licencia" => "http://www.elsevier.com/open-access/userlicense/1.0/" "subdocumento" => "fla" "cita" => "Rev Port Pneumol. 2015;21:22-9" "abierto" => array:3 [ "ES" => true "ES2" => true "LATM" => true ] "gratuito" => true "lecturas" => array:2 [ "total" => 5067 "formatos" => array:3 [ "EPUB" => 244 "HTML" => 3897 "PDF" => 926 ] ] "en" => array:11 [ "idiomaDefecto" => true "titulo" => "Exploratory study comparing dysautonomia between asthmatic and non-asthmatic elite swimmers" "tienePdf" => "en" "tieneTextoCompleto" => "en" "tieneResumen" => "en" "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "22" "paginaFinal" => "29" ] ] "contieneResumen" => array:1 [ "en" => true ] "contieneTextoCompleto" => array:1 [ "en" => true ] "contienePdf" => array:1 [ "en" => true ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig1" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "420v21n01-90385612fig1.jpg" "Alto" => 3882 "Ancho" => 2808 "Tamanyo" => 1126594 ] ] "descripcion" => array:1 [ "en" => "Procedure for measurement of pupillary light reflexes and pupil sizes and pupillometer displaying results. (A) The sequence of figures represent the adequate position to perform the scan: at the right angle to the patient's axis of vision, in a good alignment, closely adapted to the face and the pupil in the center of LCD screen. (B) The sequence of figures presents the pupil measurement phases: targeting phase (1), ready phase (2) and measurement phase. (C) Pupillometer display of one measurement results." ] ] ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "M. Couto, D. Silva, P. Santos, S. Queirós, L. Delgado, A. Moreira" "autores" => array:6 [ 0 => array:2 [ "Iniciales" => "M." "apellidos" => "Couto" ] 1 => array:2 [ "Iniciales" => "D." "apellidos" => "Silva" ] 2 => array:2 [ "Iniciales" => "P." "apellidos" => "Santos" ] 3 => array:2 [ "Iniciales" => "S." "apellidos" => "Queirós" ] 4 => array:2 [ "Iniciales" => "L." "apellidos" => "Delgado" ] 5 => array:2 [ "Iniciales" => "A." "apellidos" => "Moreira" ] ] ] ] ] "idiomaDefecto" => "en" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/X0873215915856126?idApp=UINPBA00004E" "url" => "/08732159/0000002100000001/v0_201604141151/X0873215915856126/v0_201604141151/en/main.assets" ] "en" => array:14 [ "idiomaDefecto" => true "titulo" => "Melatonin attenuates lung injury in a hind limb ischemia–reperfusion rat model" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:2 [ "paginaInicial" => "30" "paginaFinal" => "35" ] ] "autores" => array:1 [ 0 => array:4 [ "autoresLista" => "Hamed Takhtfooladi, Mohammad Takhtfooladi, Fariborz Moayer, Sayed Mobarakeh" "autores" => array:4 [ 0 => array:3 [ "nombre" => "Hamed" "apellidos" => "Takhtfooladi" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] 1 => array:4 [ "nombre" => "Mohammad" "apellidos" => "Takhtfooladi" "email" => array:1 [ 0 => "dr_ashrafzadeh@yahoo.com" ] "referencia" => array:2 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] 1 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">*</span>" "identificador" => "cor1" ] ] ] 2 => array:3 [ "nombre" => "Fariborz" "apellidos" => "Moayer" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "affc" ] ] ] 3 => array:3 [ "nombre" => "Sayed" "apellidos" => "Mobarakeh" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">d</span>" "identificador" => "affd" ] ] ] ] "afiliaciones" => array:4 [ 0 => array:3 [ "entidad" => "Faculty of Veterinary Science, Karaj Branch, Islamic Azad University, Karaj, Iran" "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] 1 => array:3 [ "entidad" => "Department of Surgery, Faculty of Specialized Veterinary Sciences, Science and Research Branch, Islamic Azad University, Tehran, Iran" "etiqueta" => "<span class="elsevierStyleSup">b</span>" "identificador" => "affb" ] 2 => array:3 [ "entidad" => "Department of Pathobiology, Faculty of Veterinary Medicine, Karaj Branch, Islamic Azad University, Karaj, Iran" "etiqueta" => "<span class="elsevierStyleSup">c</span>" "identificador" => "affc" ] 3 => array:3 [ "entidad" => "Faculty of Medical Sciences, Shahid Sadughi University, Yazd, Iran" "etiqueta" => "<span class="elsevierStyleSup">d</span>" "identificador" => "affd" ] ] "correspondencia" => array:1 [ 0 => array:3 [ "identificador" => "cor1" "etiqueta" => "<span class="elsevierStyleSup">*</span>" "correspondencia" => "Corresponding author. dr_ashrafzadeh@yahoo.com" ] ] ] ] "resumenGrafico" => array:2 [ "original" => 0 "multimedia" => array:8 [ "identificador" => "fig1" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "420v21n01-90385613fig1.jpg" "Alto" => 800 "Ancho" => 995 "Tamanyo" => 623285 ] ] "descripcion" => array:1 [ "en" => "Light microscopic view of lung tissues from ischemia¿reperfusion group. Extensive histological changes with inflammatory cell infiltration and partial destruction of lung architecture (magnification of 10 × 10, H&E staining)." ] ] ] "textoCompleto" => "<a name="sec0005" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Introduction</span><p class="elsevierStylePara">The pathophysiology of ischemia–reperfusion injury has been previously described. Polymorphonuclear leukocytes and free radical species have been shown to have pivotal roles in the etiology.<a href="#bib45" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">1</span></a> Skeletal muscle ischemia–reperfusion resulting from trauma, limb revascularization, orthopedic surgery and free-flap reconstruction or any other condition not only leads to local damage, but also causes severe injury involving destruction of remote organs.<a href="#bib46" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">2</span></a><span class="elsevierStyleSup">, </span><a href="#bib47" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">3</span></a><span class="elsevierStyleSup">, </span><a href="#bib48" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">4</span></a>Many studies have shown that several agents such as caffeic acid phenethyl ester or erdosteine,<a href="#bib49" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">5</span></a><span class="elsevierStyleSup">, </span><a href="#bib50" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">6</span></a> N-acetylcysteine,<a href="#bib48" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">4</span></a> zinc aspartate,<a href="#bib51" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">7</span></a> trapidil<a href="#bib52" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">8</span></a> and tramadol<a href="#bib53" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">9</span></a> are useful against lung injury induced by oxidative stress damage in ischemia–reperfusion.</p><p class="elsevierStylePara">Melatonin, the chief hormone of the pineal gland, is a well-known potent antioxidant and free radical scavenger<a href="#bib54" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">10</span></a><span class="elsevierStyleSup">, </span><a href="#bib55" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">11</span></a> that can counteract the damaging effects of free radicals.<a href="#bib56" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">12</span></a><span class="elsevierStyleSup">, </span><a href="#bib57" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">13</span></a> Melatonin also shows a protective effect on lung injuries induced by ischemia–reperfusion.<a href="#bib58" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">14</span></a> There have been no studies to test the effect of melatonin on lung histological changes induced by skeletal muscle ischemia–reperfusion. The aim of this study was to examine the effects of melatonin on acute lung injury in a rat model of skeletal muscle ischemia–reperfusion by transient femoral artery occlusion.</p><a name="sec0010" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Materials and methods</span><p class="elsevierStylePara">All experimental procedures were performed according to the guidelines for the ethical treatment of experimental animals and approved by Islamic Azad University School of Veterinary Science, Animal Care and Use Local Ethics Committee.</p><a name="sec0015" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Experimental groups</span><p class="elsevierStylePara">Thirty male Wistar rats weighing 300 ± 35 g were used in this study. They were maintained under constant room temperature of 25 ± 2 °C, relative humidity of 75 ± 5%, 12 h/12 h light/dark cycle, with <span class="elsevierStyleItalic">ad libitum</span> access to water and commercial food and were placed in individual cages. Animals were randomly allocated into three experimental groups of ten rats each:</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Group I</span> – Sham group with no ischemia–reperfusion. The animals were subjected to all operative procedures, except arterial occlusion and reperfusion. After isolation and exposure of the femoral artery for 2 h, the animals received 2 ml of 0.9% saline via the external jugular vein.</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Group II (ischemia–reperfusion group)</span> – The animals were subjected to 2 h of ischemia followed by 24 h of reperfusion. Two milliliters of 0.9% saline was administered intravenously prior to reperfusion.</p><p class="elsevierStylePara"><span class="elsevierStyleItalic">Group III (ischemia–reperfusion</span> + <span class="elsevierStyleItalic">melatonin group)</span> – All animals underwent 2 hours of ischemia by occlusion of the femoral artery followed by 24 h of reperfusion. A solution of 10 mg/kg melatonin was administered immediately via the external jugular vein, with a total volume of 2 ml.</p><a name="sec0020" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Surgery</span><p class="elsevierStylePara">Anesthesia was induced using ketamine plus xylazine (10 mg/kg and 50 mg/kg i.m., respectively). After induction of anesthesia, the left hind limb was prepared for sterile surgery. A skin incision was made on the medial surface of the left hind limb and the femoral artery was isolated and clamped with a vascular forceps for 2 h. Following the ischemic period, the vascular forceps was removed and then the surgical site was routinely closed. Rats were returned to their cages with a commercial balanced diet and water <span class="elsevierStyleItalic">ad libitum</span>.</p><a name="sec0025" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Specimen collection</span><p class="elsevierStylePara">At the end of the trial, the rats were euthanized with an overdose of intraperitoneal pentobarbital injection (300 mg/kg) and the lungs were removed <span class="elsevierStyleItalic">en bloc</span>. The right lungs were used for water content determination and histopathological analysis under light microscope and the left lungs were stored at −20 °C till the biochemical analysis. The lung tissue homogenate and supernatant samples were prepared as described by Yildirim et al.<a href="#bib59" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">15</span></a></p><a name="sec0030" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Biochemical assay</span><p class="elsevierStylePara">Myeloperoxidase (MPO) activity and nitric oxide (NO) levels were studied in lung tissues. The activity of MPO was analyzed spectrophotometrically as described by Wei et al.<a href="#bib60" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">16</span></a> NO level in lung tissue was measured by Griess reaction.<a href="#bib61" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">17</span></a></p><a name="sec0035" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Lung wet/dry weight ratio</span><p class="elsevierStylePara">Lung wet/dry weight ratio was used as an indicator of pulmonary edema. The lower lobe of the right lung from each animal was weighed and placed in a vacuum oven (at 54 °C) until a stable,<a href="#bib62" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">18</span></a> dry weight was achieved. The ratio of lung wet weight to dry weight was then calculated.</p><a name="sec0040" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Histopathological examination</span><p class="elsevierStylePara">The anterior lobe of the right lung (tissue) was placed in a 10% formalin solution and processed routinely by embedding in paraffin and then tissues were sectioned into 5 μm pieces and stained with hematoxylin & eosin stain. Pulmonary injury was graded into four grades as follows: grade 0, no diagnostic change; grade 1, mild neutrophil leukocyte infiltration and mild to moderate interstitial congestion; grade 2, moderate neutrophil leukocyte infiltration, perivascular edema formation, and partial destruction of pulmonary architecture; and grade 3, dense neutrophil leukocyte infiltration and complete destruction of pulmonary structure.<a href="#bib63" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">19</span></a> A total of five slides from each lung sample were randomly screened, and the mean was accepted as the representative value of the sample.</p><p class="elsevierStylePara">The Statistical Package for the Social Sciences for Windows 11.5 was used for statistical analysis. All values were given as mean ± standard deviation. Differences between groups were statistically analyzed by Kruskal–Wallis test (ANOVA) and chi-square test. Statistical significance was accepted as <span class="elsevierStyleItalic">P</span> < 0.05.</p><a name="sec0045" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Results</span><p class="elsevierStylePara">All of the rats survived until the end of the study period. Data belonging to histological changes from lung samples after reperfusion are represented in <a href="#t0005" class="elsevierStyleCrossRefs">Table 1</a>. In the ischemia–reperfusion group, tissues showed histological changes with partial destruction of pulmonary architecture, neutrophilic infiltration, intra-alveolar hemorrhage and edema (<a href="#f0005" class="elsevierStyleCrossRefs">Figure 1</a>). Grades 1, 2 and 3 of lesions were obtained in the ischemia–reperfusion group, with an average of 2.3. These pathological changes in the ischemia–reperfusion + melatonin group, particularly neutrophilic infiltration and edema, were much less than in the ischemia–reperfusion group (<a href="#f0010" class="elsevierStyleCrossRefs">Figure 2</a>). Four animals in the ischemia–reperfusion + melatonin group presented no injury and the others had lesions grades 1 and 2, averaging 0.7. Histopathologically, there was a significant difference (<span class="elsevierStyleItalic">P</span> = 0.001) between the two groups. The average of histological changes in the sham group (0.2) was lower than the ischemia–reperfusion + melatonin group, but with no statistical significance (<a href="#f0015" class="elsevierStyleCrossRefs">Figure 3</a>).</p><p class="elsevierStylePara">Table 1. Histopathologic evaluation, myeloperoxidase (MPO) activity and level of nitric oxide (NO) in lung tissue for each group.</p><a name="t0005" class="elsevierStyleCrossRefs"></a><p class="elsevierStylePara"></p><table><tr align="left"><td>Groups</td><td>Histological score</td><td>MPO (U/g protein)</td><td>NO (μmol/g protein)</td><td>Lung wet/dry weight</td></tr><tr align="left"><td>Sham</td><td>0.2 ± 0.46</td><td>0.06 ± 0.04</td><td>20.18 ± 1.06</td><td>4.10 ± 0.21</td></tr><tr align="left"><td>Ischemia–reperfusion</td><td>2.3 ± 0.51 <span class="elsevierStyleSup">*</span></td><td>0.47 ± 0.11 <span class="elsevierStyleSup">*</span></td><td>58.07 ± 11.45 <span class="elsevierStyleSup">*</span></td><td>8.12 ± 1.37 <span class="elsevierStyleSup">*</span></td></tr><tr align="left"><td>Ischemia–reperfusion + melatonin</td><td>0.7 ± 0.17 <span class="elsevierStyleSup">+</span></td><td>0.17 ± 0.03 <span class="elsevierStyleSup">+</span></td><td>25.68 ± 4.30 <span class="elsevierStyleSup">+</span></td><td>5.01 ± 0.39 <span class="elsevierStyleSup">+</span></td></tr></table><p class="elsevierStylePara">+ <span class="elsevierStyleItalic">P</span> > 0.05 versus sham group, <span class="elsevierStyleItalic">P</span> < 0.05 versus ischemia–reperfusion group.<br></br>* <span class="elsevierStyleItalic">P</span> < 0.05 versus sham group, <span class="elsevierStyleItalic">P</span> < 0.05 versus ischemia–reperfusion + melatonin group.<br></br></p><a name="f0005" class="elsevierStyleCrossRefs"></a><p class="elsevierStylePara"><img src="420v21n01-90385613fig1.jpg" alt="Light microscopic view of lung tissues from ischemia–reperfusion group. Extensive histological changes with inflammatory cell infiltration and partial destruction of lung architecture (magnification of 10 × 10, H&E staining)."></img></p><p class="elsevierStylePara">Figure 1. Light microscopic view of lung tissues from ischemia–reperfusion group. Extensive histological changes with inflammatory cell infiltration and partial destruction of lung architecture (magnification of 10 × 10, H&E staining).</p><a name="f0010" class="elsevierStyleCrossRefs"></a><p class="elsevierStylePara"><img src="420v21n01-90385613fig2.jpg" alt="Light microscopic view of lung tissues from ischemia–reperfusion + melatonin group. More preservation of nearly normal structure (magnification of 10 × 10, H&E staining)."></img></p><p class="elsevierStylePara">Figure 2. Light microscopic view of lung tissues from ischemia–reperfusion + melatonin group. More preservation of nearly normal structure (magnification of 10 × 10, H&E staining).</p><a name="f0015" class="elsevierStyleCrossRefs"></a><p class="elsevierStylePara"><img src="420v21n01-90385613fig3.jpg" alt="Representative photomicrograph of lung tissues in the sham group showing normal structure (magnification of 10 × 10, H&E staining)."></img></p><p class="elsevierStylePara">Figure 3. Representative photomicrograph of lung tissues in the sham group showing normal structure (magnification of 10 × 10, H&E staining).</p><p class="elsevierStylePara">Measurement of lung water content was used to estimate pulmonary edema. Compared with the ischemia–reperfusion group, the lung water content in the ischemia–reperfusion + melatonin and sham groups was decreased significantly (<span class="elsevierStyleItalic">P</span> = 0.000). No significant difference in lung wet/dry weight ratio was found between the ischemia–reperfusion + melatonin and sham groups (<span class="elsevierStyleItalic">P</span> > 0.05).</p><p class="elsevierStylePara">The NO level of lung tissue was increased in the ischemia–reperfusion group (<a href="#t0005" class="elsevierStyleCrossRefs">Table 1</a>). The treatment with melatonin recovered this increase and caused a reduction in comparison with the ischemia–reperfusion group (<span class="elsevierStyleItalic">P</span> = 0.000). No significant difference in NO level was found between the ischemia–reperfusion + melatonin and sham groups (<span class="elsevierStyleItalic">P</span> > 0.05).</p><p class="elsevierStylePara">The novel indicator for neutrophil function, MPO activity, in the ischemia–reperfusion group was found to be increased dramatically compared to the ischemia–reperfusion + melatonin and sham groups (<span class="elsevierStyleItalic">P</span> = 0.000) (<a href="#t0005" class="elsevierStyleCrossRefs">Table 1</a>). MPO activity comparison between the ischemia–reperfusion + melatonin and sham groups did not show significant results (<span class="elsevierStyleItalic">P</span> > 0.05).</p><a name="sec0050" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Discussion</span><p class="elsevierStylePara">Peripheral arterial clamping, as a surgical procedure, is routinely used for orthopedic surgery or trauma in elective and emergency cases. Lung damage has been shown to occur following transient arterial occlusion. The ischemic damage resulted from a decrease in the blood flow to an organ. When restoring blood flow a more pronounced damage, so called reperfusion injury, occurs. In the development of ischemia–reperfusion injury, the enhanced generation of oxygen radicals has been suggested.<a href="#bib64" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">20</span></a> Free radicals have been previously demonstrated to play a significant role in the etiology of remote lung injury in animal models.<a href="#bib48" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">4</span></a><span class="elsevierStyleSup">, </span><a href="#bib65" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">21</span></a> It has been widely described that lung injury often occurs after skeletal muscle ischemia due to release of free radicals of reperfusing tissues.<a href="#bib48" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">4</span></a></p><p class="elsevierStylePara">Melatonin and its metabolites have been shown to have antioxidant properties in <span class="elsevierStyleItalic">in vitro</span> and <span class="elsevierStyleItalic">in vivo</span> systems, both in cells and body fluids.<a href="#bib66" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">22</span></a><span class="elsevierStyleSup">, </span><a href="#bib67" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">23</span></a><span class="elsevierStyleSup">, </span><a href="#bib68" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">24</span></a> Furthermore, melatonin plays an important role in activating antioxidant defences,<a href="#bib69" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">25</span></a><span class="elsevierStyleSup">, </span><a href="#bib70" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">26</span></a> and protects cells from oxidative loads and apoptosis induced by mitochondrial DNA deletion.<a href="#bib71" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">27</span></a> Both effects allow melatonin to reduce the extent of reactive oxygen species, improving the outcomes of oxidative related pathologies such as ischemia<a href="#bib79" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">35</span></a> and prevention of aging.<a href="#bib72" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">28</span></a><span class="elsevierStyleSup">, </span><a href="#bib73" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">29</span></a><span class="elsevierStyleSup">, </span><a href="#bib74" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">30</span></a>It has been demonstrated that melatonin can prevent ischemia–reperfusion injury in cerebral artery occlusion induced stroke, in traumatic brain and spinal cord injuries, in animal models.<a href="#bib75" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">31</span></a><span class="elsevierStyleSup">, </span><a href="#bib76" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">32</span></a><span class="elsevierStyleSup">, </span><a href="#bib77" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">33</span></a> Besides the generation of free radicals, the ischemia–reperfusion injury is associated with exaggerated inflammatory response.<a href="#bib78" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">34</span></a> Activated polymorphonuclear leukocytes aggregate and adhere to endothelium, and impair blood flow and development of endothelial cell edema.<a href="#bib79" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">35</span></a> Recently, melatonin reduced morphological injury due to inhibition of neutrophils infiltration into the reperfused intestine with abolished P-selectin expression and intercellular adhesion molecule-1 up-regulation on endothelial cells.<a href="#bib76" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">32</span></a></p><p class="elsevierStylePara">Several methods have been used to define the role of neutrophils in reperfusion tissue injury. MPO plays a fundamental role in oxidant production by neutrophils. Neutrophils are a main potential source of oxygen-free radicals.<a href="#bib80" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">36</span></a> A previous study clearly demonstrated that skeletal muscle ischemia–reperfusion led to remote lung inflammation, which was characterized by increased MPO activity and significant neutrophil infiltration in the lung.<a href="#bib81" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">37</span></a> NO level is a significant determinant of the lung injury process which is caused by lower extremity ischemia–reperfusion.<a href="#bib82" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">38</span></a></p><p class="elsevierStylePara">The effects of melatonin on ischemia–reperfusion injury in an <span class="elsevierStyleItalic">ex vivo</span> rat heart model was studied by Lagneux et al.<a href="#bib83" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">39</span></a> The authors explained that the melatonin significantly reduced infarct size and the incidence of reperfusion arrhythmias.<a href="#bib83" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">39</span></a> In an experimental study Erkanlı et al.<a href="#bib84" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">40</span></a> reported that melatonin has a protective effect against skeletal muscle ischemia–reperfusion injury and can reduce the incidence of compartment syndrome after chronic or acute peripheral arterial occlusions. Other studies have shown that melatonin protects kidney,<a href="#bib85" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">41</span></a> liver,<a href="#bib86" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">42</span></a> testis<a href="#bib87" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">43</span></a> and intestine<a href="#bib88" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">44</span></a> against ischemia–reperfusion injury.</p><p class="elsevierStylePara">In the last few years, Okutan et al.<a href="#bib58" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">14</span></a> investigated the protective role of melatonin in lung remote organ injury. For that purpose, they induced lung injury by the occlusion of infrarenal abdominal aorta for 30 min and reperfusion for 12 h. These authors administered melatonin intraperitoneally at 20 mg/kg, 1 h prior to trial. They found that pre-treating rats with melatonin significantly decreases malondialdehyde (MDA) levels as well as MPO activity. Based on this finding, they believed that their study indicated the potential of attenuating lung injury, and require further studies to show improvement in the morphology of the injured lungs. In the current research, we tested the hypothesis that 10 mg/kg i.v. of melatonin could protect the lungs after 2 h femoral artery occlusion and 24 h reperfusion. In this study melatonin inhibited MPO activity and decreased NO level which was increased by ischemia–reperfusion. Pulmonary architecture, neutrophilic infiltration, intra-alveolar hemorrhage and edema were much reduced in the treated group. However, there are further studies to be conducted to test the effects of various doses of melatonin treatment against ischemia–reperfusion injury in lung.</p><p class="elsevierStylePara">Sharma et al.<a href="#bib62" class="elsevierStyleCrossRefs"><span class="elsevierStyleSup">18</span></a> showed that lungs undergoing ischemia–reperfusion displayed increased vascular permeability and pulmonary edema. The conclusion of increased vascular permeability is an assumption based on the lung wet\dry weight ratio. Significant lung edema occurred after ischemia–reperfusion in rat which was attenuated by melatonin treatment.</p><p class="elsevierStylePara">Data acquired demonstrates that melatonin can significantly decrease the severity of pulmonary edema, decrease vascular permeability, decrease leukocytes infiltration and inhibits cellular apoptosis, after skeletal muscle ischemia–reperfusion. Our findings support the potential use of melatonin as a therapeutic agent in the prevention of acute lung injury associated with skeletal muscle ischemia–reperfusion.</p><a name="sec0055" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Ethical disclosures</span><a name="sec0060" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Protection of human and animal subjects</span><p class="elsevierStylePara">The authors declare that the procedures followed were in accordance with the regulations of the relevant clinical research ethics committee and with those of the Code of Ethics of the World Medical Association (Declaration of Helsinki).</p><a name="sec0065" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Confidentiality of data</span><p class="elsevierStylePara">The authors declare that no patient data appear in this article.</p><a name="sec0070" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Right to privacy and informed consent</span><p class="elsevierStylePara">The authors declare that no patient data appear in this article.</p><a name="sec0075" class="elsevierStyleCrossRefs"></a><span class="elsevierStyleSectionTitle">Conflicts of interest</span><p class="elsevierStylePara">The authors have no conflicts of interest to declare.</p><p class="elsevierStylePara">Received 10 September 2013 <br></br>Accepted 8 January 2014 </p><p class="elsevierStylePara">Corresponding author. dr_ashrafzadeh@yahoo.com</p>" "pdfFichero" => "320v21n01a90385614pdf001.pdf" "tienePdf" => true "PalabrasClave" => array:1 [ "en" => array:1 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec641001" "palabras" => array:6 [ 0 => "Melatonin" 1 => "Ischemia–reperfusion" 2 => "Lung remote injury" 3 => "Histopathology" 4 => "Myeloperoxidase" 5 => "Nitric oxide" ] ] ] ] "tieneResumen" => true "resumen" => array:1 [ "en" => array:1 [ "resumen" => "<span class="elsevierStyleSectionTitle">Objective</span><br/><p class="elsevierStylePara">This study evaluated the protective antioxidant effect of melatonin on lung injury as a remote organ after skeletal muscle ischemia–reperfusion in rats.</p><span class="elsevierStyleSectionTitle">Methods</span><br/><p class="elsevierStylePara">Thirty male Wistar rats were allocated randomly into three experimental groups: operated with no ischemia (Sham) group, ischemia–reperfusion group and ischemia–reperfusion + melatonin group. Hind limb ischemia was induced by clamping the femoral artery. After 2 h ischemia, the clamp was removed and the animal underwent 24 h reperfusion. Rats in the ischemia–reperfusion + melatonin group received melatonin (10 mg/kg i.v.), immediately before the clamp was removed. At the end of the trial, animals were euthanized and the lungs were removed for water content determination, histopathological and biochemical studies.</p><span class="elsevierStyleSectionTitle">Results</span><br/><p class="elsevierStylePara">In the ischemia–reperfusion + melatonin group, tissues showed less intense histological abnormalities such as neutrophilic infiltration, intra-alveolar hemorrhage and edema compared with the ischemia–reperfusion group. Histopathologically, there was a significant difference (<span class="elsevierStyleItalic">P</span> < 0.05) between the two groups. The lung water content in the ischemia–reperfusion + melatonin group was significantly lower than the ischemia–reperfusion group (<span class="elsevierStyleItalic">P</span> < 0.05). Lung tissue myeloperoxidase (MPO) activity and nitric oxide (NO) level were significantly (<span class="elsevierStyleItalic">P</span> < 0.05) increased by ischemia–reperfusion. The increase in these parameters was reduced by melatonin.</p><p class="elsevierStylePara">Comparing the ischemia–reperfusion + melatonin group with the sham group, no significant increase in all analyzed aspects of the research was observed.</p><span class="elsevierStyleSectionTitle">Conclusions</span><br/><p class="elsevierStylePara">These findings suggest that melatonin has preventive effects in lung tissue injury after transient femoral artery occlusion.</p>" ] ] "multimedia" => array:6 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Figure 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "420v21n01-90385613fig1.jpg" "Alto" => 800 "Ancho" => 995 "Tamanyo" => 623285 ] ] "descripcion" => array:1 [ "en" => "Light microscopic view of lung tissues from ischemia¿reperfusion group. Extensive histological changes with inflammatory cell infiltration and partial destruction of lung architecture (magnification of 10 × 10, H&E staining)." ] ] 1 => array:8 [ "identificador" => "fig2" "etiqueta" => "Figure 2" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "420v21n01-90385613fig2.jpg" "Alto" => 742 "Ancho" => 995 "Tamanyo" => 822057 ] ] "descripcion" => array:1 [ "en" => "Light microscopic view of lung tissues from ischemia¿reperfusion + melatonin group. More preservation of nearly normal structure (magnification of 10 × 10, H&E staining)." ] ] 2 => array:8 [ "identificador" => "fig3" "etiqueta" => "Figure 3" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "420v21n01-90385613fig3.jpg" "Alto" => 767 "Ancho" => 995 "Tamanyo" => 480139 ] ] "descripcion" => array:1 [ "en" => "Representative photomicrograph of lung tissues in the sham group showing normal structure (magnification of 10 × 10, H&E staining)." ] ] 3 => array:6 [ "identificador" => "fig4" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "descripcion" => array:1 [ "en" => "Light microscopic view of lung tissues from ischemia–reperfusion group. Extensive histological changes with inflammatory cell infiltration and partial destruction of lung architecture (magnification of 10 × 10, H&E staining)." ] ] 4 => array:6 [ "identificador" => "fig5" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "descripcion" => array:1 [ "en" => "Light microscopic view of lung tissues from ischemia–reperfusion + melatonin group. More preservation of nearly normal structure (magnification of 10 × 10, H&E staining)." ] ] 5 => array:6 [ "identificador" => "fig6" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "descripcion" => array:1 [ "en" => "Representative photomicrograph of lung tissues in the sham group showing normal structure (magnification of 10 × 10, H&E staining)." ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:44 [ 0 => array:3 [ "identificador" => "bib45" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review. Cardiovasc Surg. 2002; 10:620-30." "contribucion" => array:1 [ 0 => array:3 [ "titulo" => "The pathophysiology of skeletal muscle ischemia and the reperfusion syndrome: a review." 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Year/Month | Html | Total | |
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2024 November | 9 | 4 | 13 |
2024 October | 45 | 28 | 73 |
2024 September | 53 | 46 | 99 |
2024 August | 56 | 51 | 107 |
2024 July | 63 | 39 | 102 |
2024 June | 54 | 14 | 68 |
2024 May | 56 | 37 | 93 |
2024 April | 51 | 27 | 78 |
2024 March | 47 | 30 | 77 |
2024 February | 88 | 25 | 113 |
2024 January | 63 | 26 | 89 |
2023 December | 40 | 32 | 72 |
2023 November | 45 | 31 | 76 |
2023 October | 53 | 32 | 85 |
2023 September | 43 | 36 | 79 |
2023 August | 37 | 16 | 53 |
2023 July | 35 | 26 | 61 |
2023 June | 33 | 17 | 50 |
2023 May | 59 | 24 | 83 |
2023 April | 53 | 18 | 71 |
2023 March | 132 | 23 | 155 |
2023 February | 81 | 29 | 110 |
2023 January | 35 | 23 | 58 |
2022 December | 74 | 22 | 96 |
2022 November | 102 | 43 | 145 |
2022 October | 57 | 31 | 88 |
2022 September | 32 | 22 | 54 |
2022 August | 56 | 43 | 99 |
2022 July | 58 | 45 | 103 |
2022 June | 38 | 58 | 96 |
2022 May | 57 | 49 | 106 |
2022 April | 56 | 27 | 83 |
2022 March | 54 | 46 | 100 |
2022 February | 42 | 42 | 84 |
2022 January | 47 | 45 | 92 |
2021 December | 43 | 37 | 80 |
2021 November | 40 | 43 | 83 |
2021 October | 31 | 44 | 75 |
2021 September | 35 | 37 | 72 |
2021 August | 39 | 33 | 72 |
2021 July | 36 | 29 | 65 |
2021 June | 44 | 33 | 77 |
2021 May | 32 | 32 | 64 |
2021 April | 101 | 65 | 166 |
2021 March | 75 | 22 | 97 |
2021 February | 49 | 21 | 70 |
2021 January | 52 | 17 | 69 |
2020 December | 52 | 17 | 69 |
2020 November | 49 | 20 | 69 |
2020 October | 61 | 24 | 85 |
2020 September | 53 | 16 | 69 |
2020 August | 60 | 29 | 89 |
2020 July | 98 | 27 | 125 |
2020 June | 97 | 28 | 125 |
2020 May | 98 | 26 | 124 |
2020 April | 94 | 13 | 107 |
2020 March | 101 | 19 | 120 |
2020 February | 78 | 26 | 104 |
2020 January | 93 | 25 | 118 |
2019 December | 97 | 16 | 113 |
2019 November | 96 | 18 | 114 |
2019 October | 84 | 22 | 106 |
2019 September | 97 | 21 | 118 |
2019 August | 252 | 29 | 281 |
2019 July | 266 | 18 | 284 |
2019 June | 328 | 11 | 339 |
2019 May | 268 | 14 | 282 |
2019 April | 274 | 28 | 302 |
2019 March | 375 | 12 | 387 |
2019 February | 301 | 10 | 311 |
2019 January | 351 | 39 | 390 |
2018 December | 177 | 4 | 181 |
2018 November | 76 | 1 | 77 |
2018 October | 83 | 13 | 96 |
2018 September | 47 | 8 | 55 |
2018 August | 42 | 16 | 58 |
2018 July | 55 | 22 | 77 |
2018 June | 73 | 12 | 85 |
2018 May | 76 | 20 | 96 |
2018 April | 126 | 19 | 145 |
2018 March | 144 | 23 | 167 |
2018 February | 125 | 9 | 134 |
2018 January | 17 | 10 | 27 |
2017 December | 184 | 19 | 203 |
2017 November | 28 | 9 | 37 |
2017 October | 15 | 11 | 26 |
2017 September | 33 | 18 | 51 |
2017 August | 46 | 12 | 58 |
2017 July | 34 | 17 | 51 |
2017 June | 34 | 16 | 50 |
2017 May | 48 | 19 | 67 |
2017 April | 28 | 4 | 32 |
2017 March | 33 | 4 | 37 |
2017 February | 22 | 2 | 24 |
2017 January | 15 | 6 | 21 |
2016 December | 13 | 10 | 23 |
2016 November | 20 | 4 | 24 |
2016 October | 13 | 2 | 15 |
2016 September | 13 | 4 | 17 |
2016 August | 7 | 5 | 12 |
2016 July | 4 | 12 | 16 |
2016 June | 15 | 6 | 21 |
2016 May | 17 | 3 | 20 |
2016 April | 35 | 21 | 56 |
2016 March | 64 | 37 | 101 |
2016 February | 80 | 32 | 112 |
2016 January | 150 | 58 | 208 |
2015 December | 54 | 28 | 82 |
2015 November | 53 | 18 | 71 |
2015 October | 65 | 30 | 95 |
2015 September | 58 | 21 | 79 |
2015 August | 36 | 13 | 49 |
2015 July | 50 | 11 | 61 |
2015 June | 29 | 15 | 44 |
2015 May | 53 | 9 | 62 |
2015 April | 62 | 36 | 98 |
2015 March | 80 | 42 | 122 |
2015 February | 75 | 43 | 118 |