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心肌缺血期间的微血管受压:无复流现象的机制基础。

Microvascular compression during myocardial ischemia: mechanistic basis for no-reflow phenomenon.

作者信息

Manciet L H, Poole D C, McDonagh P F, Copeland J G, Mathieu-Costello O

机构信息

Department of Surgery, University of Arizona Health Sciences Center, Tucson 85724-0001.

出版信息

Am J Physiol. 1994 Apr;266(4 Pt 2):H1541-50. doi: 10.1152/ajpheart.1994.266.4.H1541.

DOI:10.1152/ajpheart.1994.266.4.H1541
PMID:8184932
Abstract

Alterations in fiber size and capillary diameter were highly correlated with perfusion deficits after myocardial ischemia. After 5 (n = 3) and 30 (n = 5) min of global normothermic ischemia, isolated rabbit hearts were perfused with India ink and then with glutaraldehyde. Morphometric techniques were used to determine mean fiber cross-sectional area [a(f)], mean effective capillary diameter [d(c)], total and perfused capillary number per fiber area, and capillary length per fiber volume in subepicardium (Epi) and subendocardium (Endo). Sarcomere length was measured to differentiate between effects of fiber shortening and intracellular edema on a(f). After 30 min of ischemia, a(f) increased 41 (Epi) and 36% (Endo). Of these percentages, fiber shortening accounted for 2 (Epi) and 25% (Endo). Decreased d(c) was correlated with increased a(f) as well as reductions in perfused capillary number and length. Whereas intracellular edema had the greatest overall effect on a(f), fiber shortening accounted for a significant increase of a(f) in Endo, where perfusion deficits were most pronounced. These data support the hypothesis that microvascular compression consequent to increased a(f) contributes to perfusion deficits after myocardial ischemia.

摘要

纤维大小和毛细血管直径的改变与心肌缺血后的灌注不足高度相关。在进行5分钟(n = 3)和30分钟(n = 5)的整体常温缺血后,将离体兔心先用印度墨汁灌注,然后用戊二醛灌注。采用形态计量学技术测定心外膜(Epi)和心内膜(Endo)下的平均纤维横截面积[a(f)]、平均有效毛细血管直径[d(c)]、每纤维面积的总毛细血管数和灌注毛细血管数,以及每纤维体积的毛细血管长度。测量肌节长度以区分纤维缩短和细胞内水肿对a(f)的影响。缺血30分钟后,a(f)在Epi增加了41%,在Endo增加了36%。在这些增加的百分比中,纤维缩短在Epi占2%,在Endo占25%。d(c)的降低与a(f)的增加以及灌注毛细血管数和长度的减少相关。虽然细胞内水肿对a(f)的总体影响最大,但在灌注不足最明显的Endo,纤维缩短导致a(f)显著增加。这些数据支持以下假说:a(f)增加导致的微血管受压是心肌缺血后灌注不足的原因之一。

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