Role of mitochondrial permeability transition pore in TNF?-induced cardio protection in isolated rat hearts subjected to hypoxia and reoxygenation
- VernacularTitle:线粒体渗透转换孔在肿瘤坏死因子?诱导的抗心肌缺氧/复氧损伤中的作用
- Author:
Qin GAO
;
Qiang XIA
;
Chunmei CAO
;
Shizhong ZHANG
- Publication Type:Journal Article
- Keywords:
Tumor necrosis factor;
Heart;
Anoxia;
Mitochondrial permeability transition pore
- From:
Chinese Journal of Pathophysiology
1986;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate whether tumor necrosis factor ? (TNF?) pretreatment can inhibit mitochondrial permeability transition pore opening in isolated rat hearts subjected to hypoxia and reoxygenation. METHODS: Isolated perfused rat hearts were subjected to 30 min regional hypoxia (occlusion of left anterior descending artery) and 120 min reoxygenation. The infarct size, lactate dehydrogenase (LDH) release during reoxygenation and ventricular hemodynamic parameters were measured. RESULTS: Pretreatment with TNF? at concentration of 1?104 U/L for 7 min followed by 10 min washout reduced the infarct size and LDH release, and improved the left ventricular performance (left ventricular developed pressure and rate-pressure product) and left ventricular end-diastolic pressure during hypoxia and reoxygenation. Administration of atractyloside (Atr, an opener of mitochondrial permeability transition pore, 20 ?mol/L) for 20 min (last 5 min of hypoxia and first 15 min of reoxygenation) and paxilline (Pax, a calcium activated potassium channel antagonist, 1 ?mol/L) for 5 min before hypoxia attenuated the reduction of infarct size and LDH release and improved the left ventricular performance induced by TNF?. CONCLUSION: The findings indicate that in the isolated rat heart model, TNF? protects myocardium against hypoxia and reoxygenation injury via inhibiting mitochondrial permeability transition pore opening as well as activating calcium, activated potassium channel.
