Hypertension and Increased Hindlimb Vascular Reactivity in Experimental Coarctation of the Aorta
Hypertension and Increased Hindlimb Vascular Reactivity in Experimental Coarctation of the Aorta
复制标题
实验性主动脉缩窄中的高血压和后肢血管反应性增加
DOI：
--
复制
发表时间：
1963
期刊：
影响因子：
--
通讯作者：
J. Nolla
中科院分区：
文献类型：
--
作者：
J. Nolla
已经在大鼠身上产生了实验性的主动脉缩窄。将夹在双肾动脉上方的动物与夹在双肾动脉以下的动物以及假手术的大鼠进行了比较。测量了前肢和后肢的血压、心脏重量和灌注压，以及去甲肾上腺素的反应。只有肾动脉上方有夹子的动物才会出现高血压和心脏肥大。血压的上升是渐进性的，大约需要10天才能达到高血压水平。与其他两组动物相比，这些动物表现出去甲肾上腺素反应和后肢血管灌流压的增加。这些差异在统计上是显著的。在肾动脉夹闭的大鼠中，后肢去甲肾上腺素反应与后肢灌流压和心脏重量之间存在高度显著的回归线。我们认为：(A)实验性主动脉缩窄时的高血压不是纯粹机械性的，肾脏对这类高血压的发展是必不可少的；及(B)肾动脉以上的主动脉缩窄大鼠的后肢血管床内去甲肾上腺素反应和灌流压力的增加并非高血压本身的继发因素，但在某种程度上与实验性主动脉缩窄时高血压的产生机制有关。
Experimental coarctation of the aorta has been produced in rats. Animals with the clip above both renal arteries have been compared with animals with the clip below both renal arteries and with dummy operated rats. The fore- and hindlimb blood pressures, heart weights and perfusion pressure, and norepinephrine responses of the isolated perfused hindquarters have been measured. Only the animals with a clip above the renal arteries developed hypertension and hypertrophy of the heart. The increase in blood pressure was progressive, requiring about 10 days to reach hypertensive levels. Such animals showed an increase in the norepinephrine responses and in the perfusion pressure of hindlimb blood vessels when compared with either of the other two groups. The differences are statistically significant. In rats with clips above the renal arteries, there is a highly significant regression line of hindlimb norepinephrine responses on hindlimb perfusion pressure and of either of these values on heart weight. It is considered: (a) that the hypertension in experimental coarctation of the aorta is not purely mechanical and the kidneys are essential for the development of this type of hypertension; and (b) that the increase in the norepinephrine responses and in the perfusion pressure found in the hindquarter vascular bed of rats with coarctation of the aorta above the renal arteries is not secondary to the hypertension as such, but in some way is related to the mechanism that produces the hypertension in experimental coarctation of the aorta.