Will-Shahab L, Krause E G, Schulze W, Bartel S
Cor Vasa. 1986;28(2):107-13.
Anoxic stress is accompanied by activation of the central and peripheral sympathetic nervous system resulting in a high local catecholamine concentration. The authors studied how myocardial cells cope with the high level of catecholamines under ischaemic conditions. The beta-adrenoceptor-adenylate cyclase system (AC) was investigated in different models of ischaemia and anoxia (global ischaemia, low-perfused hearts, coronary artery ligation) in rat hearts. It was shown that beta-receptor function is not changed up to 40 min of ischaemia. Myocardial AC function was depressed in the total ischaemic myocardium but not in the low-perfused hearts indicating a non-uniform alteration of AC function. Reduced AC activity was completely reversible by aerobic perfusion as long as the ischaemic period did not exceed 20 min. Depression of AC function during severe ischaemia was avoided by reducing Ca2+ in the extracellular fluid and by pretreatment with Ca2+ channel blockers (verapamil). Depression of AC function during severe ischaemia is caused mainly by increased intracellular Ca2+ which inhibits AC at its catalytic site. Myocardial ischaemia alters the response of myocardial cells to catecholamines and other activators of the AC system. This alteration is time-limited and turns damage to AC function from reversible to irreversible after prolongation of ischaemia to more than 30 min.
缺氧应激伴随着中枢和外周交感神经系统的激活，导致局部儿茶酚胺浓度升高。作者研究了心肌细胞在缺血条件下如何应对高水平的儿茶酚胺。在大鼠心脏的不同缺血和缺氧模型（全心缺血、低灌注心脏、冠状动脉结扎）中研究了β-肾上腺素能受体-腺苷酸环化酶系统（AC）。结果表明，在缺血40分钟内β受体功能未发生改变。全心缺血心肌中的心肌AC功能受到抑制，但低灌注心脏中未受抑制，这表明AC功能存在不均匀改变。只要缺血时间不超过20分钟，有氧灌注可使降低的AC活性完全恢复。通过减少细胞外液中的Ca2+以及用Ca2+通道阻滞剂（维拉帕米）预处理可避免严重缺血期间AC功能的抑制。严重缺血期间AC功能的抑制主要是由细胞内Ca2+增加引起的，细胞内Ca2+在其催化位点抑制AC。心肌缺血改变了心肌细胞对儿茶酚胺和AC系统其他激活剂的反应。这种改变是有时间限制的，缺血延长至超过30分钟后，AC功能的损伤从可逆变为不可逆。
