Dhaliwal H, Kirshenbaum L A, Randhawa A K, Singal P K
Cardiovascular Sciences Division, St. Boniface General Hospital Research Center, Winnipeg, Manitoba, Canada.
Am J Physiol. 1991 Sep;261(3 Pt 2):H632-8. doi: 10.1152/ajpheart.1991.261.3.H632.
Changes in myocardial antioxidants due to different durations of hypoxia at normal or lower temperatures were correlated with the recovery of structure and function on reoxygenation. Hearts perfused with substrate-free hypoxic buffer at 37 degrees C for 5 or 10 min and at 22 degrees C for 10 min showed a significant depression in the contractile function and rise in resting tension. Reoxygenation of these hearts at 37 degrees C for 20 min resulted in a recovery of these functions. On reoxygenation, hearts made hypoxic for 10 min at 37 degrees C showed poor recovery of the contractile function, increase in malondialdehyde content and a dramatic increase in the creatine phosphokinase activity in the coronary effluent. Addition of catalase to the perfusion medium markedly improved function recovery of these hearts. Hypoxia at 37 degrees C for 5 min or at 22 degrees C for 10 min with or without reoxygenation had no effect on superoxide dismutase (SOD) or glutathione peroxidase (GSHPx) activities. These antioxidants were depressed in hearts made hypoxic for 10 min at 37 degrees C with no further change on reoxygenation. Neither SOD nor GSHPx was detected in the coronary effluent during hypoxia or reoxygenation. Hypoxia at 37 or 22 degrees C for 10 min caused significant ultrastructural changes, and on reoxygenation 37 degrees C hypoxic hearts showed exacerbation, whereas the 22 degrees C hypoxic hearts showed recovery. These data support the hypothesis that reduced antioxidant reserve during hypoxia may contribute to the oxidative injury on reoxygenation, suggesting that maintenance of endogenous antioxidant levels during hypoxia may be important for recovery.
在正常或较低温度下，不同时长的缺氧导致的心肌抗氧化剂变化与复氧时结构和功能的恢复相关。在37℃用无底物缺氧缓冲液灌注心脏5或10分钟以及在22℃灌注10分钟，会导致收缩功能显著降低和静息张力升高。这些心脏在37℃复氧20分钟后，这些功能得以恢复。复氧时，在37℃缺氧10分钟的心脏收缩功能恢复较差，丙二醛含量增加，冠状动脉流出液中肌酸磷酸激酶活性急剧升高。向灌注培养基中添加过氧化氢酶可显著改善这些心脏的功能恢复。在37℃缺氧5分钟或在22℃缺氧10分钟，无论是否复氧，对超氧化物歧化酶（SOD）或谷胱甘肽过氧化物酶（GSHPx）活性均无影响。在37℃缺氧10分钟的心脏中，这些抗氧化剂水平降低，复氧时无进一步变化。在缺氧或复氧期间，冠状动脉流出液中均未检测到SOD和GSHPx。在37℃或22℃缺氧10分钟会导致显著的超微结构变化，复氧时，37℃缺氧的心脏变化加剧，而22℃缺氧的心脏则显示恢复。这些数据支持以下假设：缺氧期间抗氧化储备减少可能导致复氧时的氧化损伤，这表明在缺氧期间维持内源性抗氧化剂水平可能对恢复很重要。
