Ito N, Isoyama S, Takahashi T, Takishima T
First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
J Mol Cell Cardiol. 1993 Jan;25(1):3-14. doi: 10.1006/jmcc.1993.1002.
Using a rat model of short- (4 weeks) and long-term (10 weeks) ascending aortic banding and debanding, we examined the relationship between coronary dilator reserve and morphological vascular changes. After 4 or 10-week banding, in vivo systolic left ventricular pressure and ventricular wt/body wt ratio increased to a similar level, compared with controls. The coronary dilator reserve measured in an isolated heart preparation decreased similarly in the two banded groups, compared with controls. The ratios of medial to luminal area and perivascular collagen to luminal area in coronary microvessels increased in the banded groups. At 4 weeks after debanding, cardiac hypertrophy regressed to the control level, and the duration of banding did not alter the extent of the regression. The coronary dilator reserve normalized in the group debanded after 4-week banding, but did not regress in the group debanded after 10-week banding. In both of the debanded groups, the hypertrophied media regressed completely. The increased perivascular collagen regressed almost completely in the group debanded after 4-week banding, but remained greater in the group debanded after 10-week banding than in the controls. From these results, we conclude that (i) the regression of medial hypertrophy does not always improve the decreased coronary dilator reserve, and (ii) the vascular fibrosis may be the major cause of the irreversibility of decreased coronary dilator reserve in long-term cardiac hypertrophy.
利用短期（4周）和长期（10周）升主动脉缩窄及解除缩窄的大鼠模型，我们研究了冠状动脉扩张储备与血管形态学改变之间的关系。与对照组相比，在4周或10周缩窄后，体内收缩期左心室压力和心室重量/体重比升高至相似水平。与对照组相比，在离体心脏标本中测量的冠状动脉扩张储备在两个缩窄组中同样降低。冠状动脉微血管中中膜与管腔面积之比以及血管周围胶原与管腔面积之比在缩窄组中增加。在解除缩窄4周后，心肌肥大恢复至对照水平，缩窄持续时间未改变恢复程度。在4周缩窄后解除缩窄的组中冠状动脉扩张储备恢复正常，但在10周缩窄后解除缩窄的组中未恢复。在两个解除缩窄的组中，肥厚的中膜完全恢复。在4周缩窄后解除缩窄的组中，增加的血管周围胶原几乎完全恢复，但在10周缩窄后解除缩窄的组中仍高于对照组。从这些结果，我们得出结论：（i）中膜肥厚的恢复并不总是能改善降低的冠状动脉扩张储备，以及（ii）血管纤维化可能是长期心肌肥大中冠状动脉扩张储备降低不可逆性的主要原因。
