Shizukuda Y, Iwamoto T, Mallet R T, Downey H F
Department of Physiology, Texas College of Osteopathic Medicine, Fort Worth 76107-2699.
Cardiovasc Res. 1993 Apr;27(4):559-64. doi: 10.1093/cvr/27.4.559.
The aim was to test whether a brief period of non-ischaemic hypoxia can attenuate cardiac contractile dysfunction, ie, "stunning", due to repeated coronary artery occlusions.
20 anaesthetised dogs underwent six 5 min occlusions of the left anterior descending coronary artery with intervening 10 min reperfusions, prior to 90 min reperfusion. In the treated group (n = 9), hearts were preconditioned by 5 min extracorporeal left anterior perfusion with severely hypoxic blood [O2 content 14(SEM 3) ml.litre-1] followed by 10 min reperfusion, prior to the repeated coronary occlusions. Controls (n = 9) were sham preconditioned by 5 min extracorporeal perfusion with normoxic blood [O2 content 179(7) ml.litre-1]. Regional contractile function was assessed by systolic segmental shortening measured by microsonometry. Regional myocardial oxygen consumption, an index of ATP utilisation, was measured in these protocols to evaluate the hypothesis that reduction of myocardial energy demand could be a mechanism of hypoxic preconditioning.
Hypoxic preconditioning slightly decreased systolic segmental shortening [64.1(9.5)% of baseline at 10 min reoxygenation v 85.5(6.5)% for control, p < 0.05]. In contrast, 5 min coronary occlusion in controls produced more marked cardiodepression [segmental shortening 33.5(10.1)% of baseline at 10 min reperfusion; p < 0.05 v 10 min reoxygenation in the hypoxic-preconditioned group]. Systolic shortening was preserved in hypoxic-preconditioned hearts as compared to controls during each 10 min reperfusion period. Furthermore, functional recovery at 90 min reperfusion after the last occlusion in hypoxic preconditioned hearts was more complete than in control hearts, at 40.8(13.1)% v -16.1(14.4)%; p < 0.05. However, myocardial oxygen consumption was not suppressed by hypoxic preconditioning.
Five minutes of hypoxic preconditioning attenuated contractile dysfunction due to repeated brief ischaemia/reperfusion stress. This protective effect was not due to the suppression of myocardial energy demand.
旨在测试短时间的非缺血性缺氧是否能减轻因反复冠状动脉闭塞导致的心脏收缩功能障碍，即“心肌顿抑”。
20只麻醉犬在90分钟再灌注前，左前降支冠状动脉经历6次5分钟闭塞及中间间隔10分钟的再灌注。在治疗组（n = 9）中，心脏在反复冠状动脉闭塞前，先通过体外左前向灌注5分钟严重缺氧血液[氧含量14（标准误3）ml·升⁻¹]，随后再灌注10分钟进行预处理。对照组（n = 9）通过体外灌注5分钟常氧血液[氧含量179（7）ml·升⁻¹]进行假预处理。通过微音器测量收缩期节段缩短来评估局部收缩功能。在这些实验方案中测量局部心肌耗氧量（ATP利用的一个指标），以评估心肌能量需求降低可能是缺氧预处理机制的这一假设。
缺氧预处理使收缩期节段缩短略有减少[复氧10分钟时为基线的64.1（9.5）%，而对照组为85.5（6.5）%，p < 0.05]。相比之下，对照组5分钟冠状动脉闭塞导致更明显的心功能抑制[再灌注10分钟时节段缩短为基线的33.5（10.1）%；与缺氧预处理组复氧10分钟相比，p < 0.05]。在每次10分钟再灌注期间，与对照组相比，缺氧预处理心脏的收缩期缩短得以保留。此外，缺氧预处理心脏在最后一次闭塞后90分钟再灌注时的功能恢复比对照心脏更完全，分别为40.8（13.1）%和 -16.1（14.4）%；p < 0.05。然而，缺氧预处理并未抑制心肌耗氧量。
5分钟的缺氧预处理减轻了因反复短暂缺血/再灌注应激导致的收缩功能障碍。这种保护作用并非由于心肌能量需求的抑制。
