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心室收缩、压力及室壁伸展对室壁不同位置血管的影响。

Effect of ventricular contraction, pressure, and wall stretch on vessels at different locations in the wall.

作者信息

Vis M A, Bovendeerd P H, Sipkema P, Westerhof N

机构信息

Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands.

出版信息

Am J Physiol. 1997 Jun;272(6 Pt 2):H2963-75. doi: 10.1152/ajpheart.1997.272.6.H2963.

Abstract

A cylindrical model of the heart was used to calculate the influence of ventricular filling and (isovolumic and isobaric) contraction on the cross-sectional area and resistance of a subendocardial and subepicardial maximally dilated arteriole and venule. Contraction is defined as the difference between static diastole and static systole. Furthermore, a small piece of rectangular myocardium containing the vessel was modeled to distinguish between the individual contributions of contractility (i.e., myocardial elastic properties), ventricular pressure, and local circumferential stretch to the changes in vascular area and resistance during contraction. Calculations were performed assuming the muscle fibers ran in either an apex-to-base or a circumferential direction. The results were similar for the two directions. Assuming constant, physiological arteriolar and venular pressures of 45 and 10 mmHg, respectively, coronary blood vessels were predicted not to collapse during ventricular contraction. Moreover, vascular area reduction was found to be larger for the arteriole (approximately 50%) than for the venule (approximately 30%) during both isovolumic and isobaric contractions. Consequently, arteriolar resistance was found to increase more than venular resistance (approximately 340 and 120%, respectively). Subendocardial area reductions were found to be somewhat smaller than subepicardial area reductions for the venule (by approximately 10%) but not for the arteriole. Contractility was found to be the main contributor to the changes in vascular area and resistance in the subepicardium but to contribute by < 50% to the changes in the subendocardium. Because pressure does, but stretch does not, contribute to the area change during isovolumic contraction and the reverse is true during isobaric contraction, it was concluded that although changes in vascular area and resistance may be similar for different contractions, the causes for these changes are very different.

摘要

使用心脏的圆柱形模型来计算心室充盈以及(等容和等压)收缩对心内膜下和心外膜下最大扩张的小动脉和小静脉的横截面积和阻力的影响。收缩定义为静态舒张期和静态收缩期之间的差异。此外,对包含血管的一小片矩形心肌进行建模,以区分收缩性(即心肌弹性特性)、心室压力和局部圆周拉伸对收缩期间血管面积和阻力变化的各自贡献。计算是在假设肌肉纤维沿心尖到心底方向或圆周方向排列的情况下进行的。两个方向的结果相似。假设小动脉和小静脉的生理压力分别恒定为45 mmHg和10 mmHg,则预计冠状动脉血管在心室收缩期间不会塌陷。此外,发现在等容收缩和等压收缩期间,小动脉的血管面积减少(约50%)比小静脉(约30%)更大。因此,发现小动脉阻力的增加大于小静脉阻力(分别约为340%和120%)。发现小静脉的心内膜下面积减少比心外膜下面积减少略小(约10%),但小动脉并非如此。发现收缩性是心外膜下血管面积和阻力变化的主要因素,但对心内膜下变化的贡献小于50%。由于在等容收缩期间压力对面积变化有贡献而拉伸没有,而在等压收缩期间情况相反,因此得出结论,尽管不同收缩期间血管面积和阻力的变化可能相似,但这些变化的原因却大不相同。

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