Yokoyama S, Korthuis R J, Benoit J N
Department of Physiology and Biophysics, Louisiana State University Medical Center, Shreveport 71130, USA.
Am J Physiol. 1996 May;270(5 Pt 2):R1126-31. doi: 10.1152/ajpregu.1996.270.5.R1126.
The effects of hypoxia followed by reoxygenation on endothelium-dependent relaxation in isolated rat aorta were investigated. Acetylcholine (ACh, 3 nM-10 microM) and calcium ionophore A-23187 (3 nM-300 nM)-induced endothelium-dependent vasorelaxation of isolated rate aortic vessel rings was impaired after 15 min of hypoxia followed by 30 min of reoxygenation. Impairment of ACh-induced relaxation was prevented by pretreatment with the combination of superoxide dismutase (200 U/ml) and catalase (1,000 U/ml). Hypoxia-reoxygenation did not affect sodium nitroprusside (0.1 nM-1 microM)-induced endothelium-independent relaxation nor the dissociation constant of ACh to endothelial M3 muscarinic receptors. Propidium iodide staining of the vascular endothelium revealed a significant increase in the number of dead endothelial cells on the aortic vessel rings following hypoxia-reoxygenation, but not on those pretreated with superoxide dismutase and catalase. These results suggest that hypoxia-reoxygenation impairs endothelium-dependent relaxation of rat aorta by a mechanism that involves oxidant-mediated endothelial cell death.
研究了缺氧后再给氧对离体大鼠主动脉内皮依赖性舒张的影响。乙酰胆碱（ACh，3 nM - 10 μM）和钙离子载体A - 23187（3 nM - 300 nM）诱导的离体大鼠主动脉血管环内皮依赖性血管舒张在缺氧15分钟后再给氧30分钟受到损害。超氧化物歧化酶（200 U/ml）和过氧化氢酶（1000 U/ml）联合预处理可防止ACh诱导的舒张功能受损。缺氧-再给氧不影响硝普钠（0.1 nM - 1 μM）诱导的非内皮依赖性舒张，也不影响ACh与内皮M3毒蕈碱受体的解离常数。血管内皮的碘化丙啶染色显示，缺氧-再给氧后主动脉血管环上死亡内皮细胞数量显著增加，但用超氧化物歧化酶和过氧化氢酶预处理的血管环上则没有。这些结果表明，缺氧-再给氧通过涉及氧化剂介导的内皮细胞死亡的机制损害大鼠主动脉的内皮依赖性舒张。
