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Methimazole protects lungs during hepatic ischemia-reperfusion injury in rats: an effect not induced by
Tanju Tütüncü1, Cagatay Demirci, Ugur Gözalan
1Fourth Department of Surgery, Ankara Numune Education and Research Hospital, Sihhiye, Turkey.
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.
Conclusion:
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.
Insights
Methimazole protects lungs from hepatic ischemia-reperfusion injury by reducing inflammation and oxidative stress. This study shows methimazole’s benefits extend beyond its effects on thyroid hormones.
Area of Science:
- Medical research
- Toxicology
- Organ injury
Background:
- Hepatic ischemia-reperfusion injury (HIRI) can cause remote organ damage, notably respiratory dysfunction.
- Understanding protective mechanisms against HIRI-induced lung injury is crucial for patient outcomes.
Purpose of the Study:
- To investigate the potential protective effects of methimazole on lung tissue following HIRI.
- To differentiate the effects of methimazole from hypothyroidism-induced changes.
Main Methods:
- Male Wistar rats underwent HIRI and pulmonary lobectomy, with interventions including thyroidectomy, methimazole, and L-thyroxine administration.
- Pulmonary tissue was analyzed histopathologically and biochemically for myeloperoxidase and malondialdehyde levels.
Main Results:
- All HIRI groups exhibited increased pulmonary injury indices compared to controls.
- Methimazole administration significantly reduced pulmonary injury and biochemical markers of damage compared to the HIRI-only group.
- Pulmonary damage in the HIRI group was comparable to the thyroidectomized group, suggesting effects beyond hypothyroidism.
Conclusions:
- Methimazole demonstrates a protective effect on lung tissue during HIRI.
- These protective effects are likely due to methimazole's anti-inflammatory and antioxidant properties.
- The benefits of methimazole are not solely attributable to the induction of hypothyroidism.
