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“冬眠”与“顿抑”心肌的特征,重点关注钙拮抗剂在“顿抑”心肌中的应用。

Characterization of "hibernating" and "stunned" myocardium with focus on the use of calcium antagonists in "stunned" myocardium.

作者信息

Ehring T, Schulz R, Heusch G

机构信息

Department of Pathophysiology, University of Essen, Germany.

出版信息

J Cardiovasc Pharmacol. 1992;20 Suppl 5:S25-33.

PMID:1282610
Abstract

In the initial seconds after a sudden reduction in coronary blood flow, a temporary mismatch between myocardial energy demand and supply exists. The mechanisms underlying the rapidly ensuing reduction in contractile function in the ischemic myocardium are still unknown. In the presence of some residual blood flow, a state of "perfusion-contraction matching" develops. The metabolic status of such hypoperfused myocardium improves, since myocardial lactate production is attenuated and creatine phosphate (CP), after an initial reduction, returns toward control values. The hypoperfused myocardium responds to inotropic stimulation by dobutamine. The recruitment of an inotropic reserve implies increased energy utilization. During inotropic stimulation, after partial normalization, lactate production is again increased, and CP is decreased again. Thus, a supply-demand imbalance that had been at least partially corrected by the ischemia-induced decrease in regional contractile function is precipitated again. A situation of chronic contractile failure in viable myocardium that normalizes upon reperfusion has been termed myocardial "hibernation." Myocardial "stunning" is characterized by a reversible postischemic contractile dysfunction despite full restoration of blood flow. The details of the underlying mechanisms are not clear. An inadequate energy supply and impaired sympathetic neurotransmission have been excluded. Potential mechanisms, which are not mutually exclusive, may include (a) damage of membranes by free radicals, (b) an increase in free cytosolic calcium during ischemia and reperfusion, and (c) a decrease in the calcium sensitivity of the myofibrils. The equally pronounced increases in regional contractility in normal and "stunned" myocardium during postextrasystolic potentiation and the infusion of calcium or the calcium-sensitizing agent AR-L-57, however, suggest an unchanged calcium sensitivity of reperfused myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在冠状动脉血流突然减少后的最初几秒内,心肌能量需求与供应之间存在暂时的不匹配。缺血心肌收缩功能迅速随之降低的潜在机制仍不清楚。在存在一些残余血流的情况下,会出现“灌注-收缩匹配”状态。这种灌注不足心肌的代谢状态得到改善,因为心肌乳酸生成减少,肌酸磷酸(CP)在最初降低后又恢复至对照值。灌注不足的心肌对多巴酚丁胺的变力刺激有反应。变力储备的启用意味着能量利用增加。在变力刺激期间,部分恢复正常后,乳酸生成再次增加,CP再次降低。因此,之前至少部分由缺血诱导的局部收缩功能降低所纠正的供需失衡再次出现。存活心肌中慢性收缩功能衰竭在再灌注后恢复正常的情况被称为心肌“冬眠”。心肌“顿抑”的特征是尽管血流已完全恢复,但仍存在可逆的缺血后收缩功能障碍。其潜在机制的细节尚不清楚。能量供应不足和交感神经传递受损已被排除。并非相互排斥的潜在机制可能包括:(a)自由基对膜的损伤;(b)缺血和再灌注期间胞浆游离钙增加;(c)肌原纤维对钙的敏感性降低。然而,在早搏后增强以及输注钙或钙敏化剂AR-L-57期间,正常心肌和“顿抑”心肌局部收缩力同样明显增加,这表明再灌注心肌的钙敏感性未改变。(摘要截选至250词)

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