Methimazole protects lungs during hepatic ischemia-reperfusion injury in rats: an effect not induced by hypothyroidism.
BACKGROUND
Hepatic ischemia-reperfusion injury may lead to remote organ failure with mortal respiratory dysfunction. The aim of the present study was to analyze the possible protective effects of methimazole on lungs after hepatic ischemia-reperfusion injury.


METHODS
Forty male Wistar albino rats were randomized into five groups: a control group, in which bilateral pulmonary lobectomy was done; a hepatic ischemia-reperfusion group, in which bilateral pulmonary lobectomy was done after hepatic ischemia-reperfusion; a thyroidectomy-ischemia-reperfusion group (total thyroidectomy followed by, 7 days later, bilateral pulmonary lobectomy after hepatic ischemia-reperfusion); a methimazole-ischemia-reperfusion group (following methimazole administration for 7 days, bilateral pulmonary lobectomy was done after hepatic ischemia-reperfusion); and a methimazole +L-thyroxine-ischemia-reperfusion group (following methimazole and L-thyroxine administration for 7 days, bilateral pulmonary lobectomy was performed after hepatic ischemia-reperfusion). Pulmonary tissue specimens were evaluated histopathologically and for myeloperoxidase and malondialdehyde levels.


RESULTS
All of the ischemia-reperfusion intervention groups had higher pulmonary injury scoring indices than the control group (P < 0.001). Pulmonary injury index of the ischemia-reperfusion group was higher than that of both the methimazole-supplemented hypothyroid and euthyroid groups (P = 0028; P = 0,038, respectively) and was similar to that of the thyroidectomized group. Pulmonary tissue myeloperoxidase and malondialdehyde levels in the ischemia-reperfusion group were similar with that in the thyroidectomized rats but were significantly higher than that in the control, and both the methimazole-supplemented hypothyroid and euthyroid groups.


CONCLUSIONS
Methimazole exerts a protective role on lungs during hepatic ischemia-reperfusion injury, which can be attributed to its anti-inflammatory and anti-oxidant effects rather than hypothyroidism alone.
Tütüncü
Tanju
T
Fourth Department of Surgery, Ankara Numune Education and Research Hospital, Sihhiye, Turkey.
Demirci
Cagatay
C
Gözalan
Ugur
U
Yüksek
Yunus Nadi
YN
Bilgihan
Ayse
A
Kama
Nuri Aydin
NA
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D000975:Antioxidants / Q000494:pharmacology* / Q000627:therapeutic use; D013956:Antithyroid Agents / Q000494:pharmacology; D004195:Disease Models, Animal; D006499:Hepatic Artery / Q000601:surgery; D008099:Liver / Q000098:blood supply*; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D008171:Lung Diseases / Q000209:etiology / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008713:Methimazole / Q000494:pharmacology* / Q000627:therapeutic use; D009195:Peroxidase / Q000378:metabolism; D011013:Pneumonectomy; D011169:Portal Vein / Q000601:surgery; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D013965:Thyroidectomy; D013974:Thyroxine / Q000494:pharmacology
D000893:Anti-Inflammatory Agents; D000975:Antioxidants; D013956:Antithyroid Agents; D008315:Malondialdehyde; D008713:Methimazole; D009195:Peroxidase; D013974:Thyroxine