Hellstrom H R
Laboratory Service, Veteran Administration Medical Center, Syracuse, New York 13210.
Med Hypotheses. 1990 Oct;33(2):117-24. doi: 10.1016/0306-9877(90)90189-l.
Myocardial reperfusion injury will be discussed in context to the spasm of resistance vessel concept of ischemic heart disease. This hypothesis attributes symptoms in this disorder directly to primary spasm of resistance vessels, and is based in part on a study of no-reflow which provided evidence that no-reflow is due to ischemia-induced injury-spasm of resistance vessels. Studies of no-reflow and reperfusion injury are rather similar, and the concept asserts that ischemia-induced injury-spasm causing no-reflow is involved in reperfusion injury. It is recognized that oxygen free radicals cause both myocardial and vascular injury during reperfusion injury, and the concept suggests that vascular injury contributes significantly to reperfusion injury by inducing the sequence of injury-spasm, no-reflow, fresh ischemia, and fresh ischemic reperfusion injury. In keeping with this, the possible involvement of spasm and no-reflow in reperfusion injury occasionally is mentioned. However, it seems to be generally accepted that reperfusion injury is due essentially solely to direct myocardial injury by free radicals, and possible reasons will be explored for a relative disinterest in spasm and no-reflow in reperfusion injury.
将结合缺血性心脏病阻力血管痉挛的概念来讨论心肌再灌注损伤。该假说将这种疾病的症状直接归因于阻力血管的原发性痉挛,部分基于一项无再流研究,该研究提供了证据表明无再流是由于缺血诱导的阻力血管损伤性痉挛所致。无再流和再灌注损伤的研究颇为相似,该概念认为导致无再流的缺血诱导损伤性痉挛参与了再灌注损伤。人们认识到,在再灌注损伤期间,氧自由基会导致心肌和血管损伤,该概念表明血管损伤通过引发损伤性痉挛、无再流、新的缺血以及新的缺血再灌注损伤序列,对再灌注损伤有显著影响。与此相符的是,偶尔会提及痉挛和无再流在再灌注损伤中的可能作用。然而,人们似乎普遍认为再灌注损伤本质上完全是由自由基直接导致的心肌损伤引起的,并且将探讨对再灌注损伤中痉挛和无再流相对不感兴趣的可能原因。