大鼠梗死灶延迟再灌注对存活心肌结构变化的影响。

The effect of delayed reperfusion following infarction in the rat on structural changes in viable myocardium.

作者信息

McDonald K, Chu C, Francis G, Judd D, Carlyle W, Toher C, Hauer K, Hartman M

机构信息

Department of Medicine, University of Minnesota, Minneapolis 55455, USA.

出版信息

Cardiovasc Res. 1997 Dec;36(3):347-53. doi: 10.1016/s0008-6363(97)00201-0.

DOI:10.1016/s0008-6363(97)00201-0

PMID:9534855

Abstract

OBJECTIVE

Evidence indicates that patency of the infarct related artery following the completion of myocardial necrosis can attenuate ventricular remodeling. Data have also demonstrated that inhibition of infarct expansion contributes to the anti-remodeling effect of delayed reperfusion. However, the influence of a patent artery on components of the remodeling process in the viable myocardium is poorly understood.

METHODS

Myocyte morphometrics (isolated cell technique) and collagen content (hydroxyproline analysis) were assessed 28 days following experimental myocardial infarction from rats with permanently ligated left coronary vessels (NRP; n = 10) compared with rats who underwent reperfusion 150 minutes after ligation (RP; n = 11) and a sham-operated group (n = 10).

RESULTS

Analysis of infarct size (planimetry) in a separate group of rats demonstrated that reperfusion at this late time point did not reduce infarct size (NRP: 33 +/- 3 vs. RP: 35 +/- 5%). Myocyte length in RP rats was less than in NRP rats in viable, non-infarcted left ventricular tissue (155 +/- 3 vs. 167 +/- 4 microns, p = 0.02), in the right ventricle (154 +/- 4 vs. 167 +/- 3 microns, p = 0.02) and in the septum (158 +/- 4 vs. 169 +/- 4 microns, p = 0.05). Reperfusion also attenuated the expected increase in cell volume compared with NRP rats (left ventricle 39.4 +/- 1.7 x 10(3) vs. 44.1 +/- 1.6 x 10(3) micron 3, p = 0.06; right ventricle 36.7 +/- 1.6 x 10(3) vs. 42.7 +/- 2.0 x 10(3) micron 3, p = 0.02; septum 41.0 +/- 1.6 x 10(3) vs. 44.2 +/- 1.8 x 10(3) micron 3, p = 0.19). Hydroxyproline content increased in the viable left ventricular tissue in both the reperfused and non-reperfused groups.

CONCLUSION

Reperfusion without myocardial salvage attenuates the increase in myocyte length and volume that occurs in remodeling myocardium following infarction in the rat, with no effect on the increase in collagen content. These data indicate that patency of the infarct vessel, which is known to have an inhibitory effect on infarct expansion, also has an anti-remodeling effect remote from the area perfused by this artery.

摘要

目的

有证据表明，心肌坏死完成后梗死相关动脉的通畅可减轻心室重构。数据还表明，抑制梗死扩展有助于延迟再灌注的抗重构作用。然而，通畅的动脉对存活心肌中重构过程各成分的影响尚不清楚。

方法

与左冠状动脉永久结扎的大鼠（NRP；n = 10）、结扎后150分钟进行再灌注的大鼠（RP；n = 11）以及假手术组（n = 10）相比，在实验性心肌梗死后28天评估大鼠的心肌细胞形态计量学（分离细胞技术）和胶原含量（羟脯氨酸分析）。

结果

在另一组大鼠中对梗死面积（平面测量法）进行分析表明，在此晚期时间点进行再灌注并未减小梗死面积（NRP：33±3% vs. RP：35±5%）。在存活的、未梗死的左心室组织中，RP组大鼠的心肌细胞长度小于NRP组大鼠（155±3 vs. 167±4微米，p = 0.02），右心室中也是如此（154±4 vs. 167±3微米，p = 0.02），在室间隔中同样如此（158±4 vs. 169±4微米，p = 0.05）。与NRP组大鼠相比，再灌注还减弱了预期的细胞体积增加（左心室39.4±1.7×10³ vs. 44.1±1.6×10³微米³，p = 0.06；右心室36.7±1.6×10³ vs. 42.7±2.0×10³微米³，p = 0.02；室间隔41.0±1.6×10³ vs. 44.2±1.8×10³微米³，p = 0.19）。再灌注组和未再灌注组存活的左心室组织中的羟脯氨酸含量均增加。