Comparison of the effect of ischaemia and anoxia on the sarcolemma of the dog heart.
Comparison of the effect of ischaemia and anoxia on the sarcolemma of the dog heart.
复制标题
缺血和缺氧对狗心脏肌膜的影响比较。
DOI：
10.1093/eurheartj/4.suppl_h.123
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发表时间：
1983
影响因子：
39.3
通讯作者：
Reimer,KA
中科院分区：
文献类型：
--
作者：
Jennings,RB;SteenbergenJr,C;Kinney,RB;Hill,ML;Reimer,KA
收缩带坏死是一种显著的形态学损害，常见于许多类型的心肌损伤，包括钙反常和缺血再灌注损伤。这种病变的特征是爆发性肿胀、大量钙超载和由于收缩带形成而导致的肌原纤维严重破坏。本文综述的研究提供的证据表明，在缺血和再灌注，这些变化之前的肌膜损伤，发生在缺血期间。采用离体培养的心肌薄片，通过电镜观察和测定菊粉扩散间隙（IDS）来评价心肌细胞膜损伤。可逆性损伤的缺血性心肌细胞具有对菊粉不可渗透的超微结构完整的质膜。缺血持续时间更长，足以在再灌注期间产生收缩带坏死。结果在缺血间隔期间质膜破裂，并且在随后的孵育期间IDS显著增加。因此，膜损伤的超微结构证据存在于缺血的早期，并与IDS的增加暂时相关。缺氧的作用，经s.c.在37 ℃下在充氮的晶体培养基中孵育的组织切片中研究了诱导膜损伤的作用。缺氧切片产生乳酸并丢失ATP和腺嘌呤核苷酸，但细胞体积和IDS至少在15小时内没有显著增加（是完全缺血中严重膜损伤所需时间的两倍），并且通过电子显微镜观察质膜保持完整。因此，尽管消耗的高能磷酸盐，膜损伤，检测IDS或超微结构的改变，发生更缓慢地在缺氧单独比缺血。这些结果表明，缺氧，每硒，可能不是缺血膜损伤的原因。
Contraction-band necrosis, a striking morphologic lesion, is common to many types of myocardial injury including the calcium paradox and ischaemic injury with reperfusion. This lesion is characterized by explosive swelling, massive calcium overload, and severe disruption of the myofibrils due to the formation of contraction bands. The studies reviewed in this paper provide evidence that in ischaemia and reperfusion, these changes are preceded by sarcolemmal injury that occurs during the period of ischaemia. Sarcolemmal injury was evaluated by electron microscopy and by measurements of inulin diffusible space (IDS) in thin slices of myocardium incubatedin vitro. Reversibly injured ischaemic myocvtes have ultra-structurally intact plasma membranes which are impermeable to inulin. Longer durations of ischaemia, sufficient to produce contraction-band necrosis during reperfusion. result in fragmentation of plasma membranes during the ischaemic intervals, and the IDS is markedly increased during subsequent incu bation. Thus ultrastructural evidence of membrane damage is present early in ischaemia and is associated temporally with the increased IDS. The role of anoxia, per s.c. in inducing membrane damage was in vestigated in tissue slices incubated at 37ΰC in crystalloidal media gassed with nitrogen. Anoxic slices produced lactate and lost ATP and adenine nucleotides, but cell volume and the IDS were not significantly increased for at least jive hours (twice the time required for severe membrane damage to develop in total ischaemia) and the plasmalemma remained intact by electron microscopy. Thus, despite depletion of high energy phosphates, membrane damage, detectable by alterations in IDS or ultrastructure, occurs much more slowly during anoxia alone than during ischaemia. These results suggest that anoxia, per Se, may not be the cause of membrane damage in ischaemia.