Reflex vascular responses to left ventricular outflow obstruction and activation of ventricular baroreceptors in dogs.
Reflex vascular responses to left ventricular outflow obstruction and activation of ventricular baroreceptors in dogs.
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狗对左心室流出道阻塞和心室压力感受器激活的反射性血管反应。
DOI：
10.1172/jci107281
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发表时间：
1973
期刊：
影响因子：
--
通讯作者：
D. Heistad
中科院分区：
文献类型：
--
作者：
A. Mark;F. Abboud;P. Schmid;D. Heistad
研究了麻醉狗对急性左心室流出道梗阻的反射性血管反应。这些研究的目的是比较心室压力感受器激活对骨骼肌（股薄肌）和皮肤（后爪）血管阻力的影响；识别介导反射性血管舒张的传入和传出通路；并评估心室压力感受器以及左心房和肺血管压力感受器对左心室流出道阻塞反应的相对贡献。股薄动脉和通向爪子的胫骨动脉分别以恒定流量进行灌注。每张床的灌注压的变化反映了血管阻力的变化。通过将左心室流出道中的气球充气 15 秒来产生流出阻塞，同时测量左心室和主动脉弓的压力。球囊的膨胀增加了左心室压力并降低了主动脉弓的压力。低水平和高水平的阻塞产生的扩张器反应在肌肉中平均为-5+/-3 (SE)和-42+/-11 mm Hg，在爪子中产生平均为-1+/-1和-3+/-2 mm Hg。去神经支配、酚妥拉明和三硝酸甘油引起的爪扩张程度比左心室流出道阻塞更大。这表明爪子中的扩张器反应不受低水平的静息神经源性收缩张力或这些血管的可忽略不计的扩张器能力的限制。左心室流入受阻会增加左心房压力，但不会引起反射性血管舒张。这表明心房或肺血管中的低压压力感受器不会导致血管扩张剂对左心室流出道阻塞的反应。双侧迷走神经切断术、切断坐骨神经和闭孔神经以及给予酚妥拉明可阻断血管舒张剂对流出道阻塞的反应，但阿托品或三苯拉明不会降低血管扩张剂的反应。结果表明，左心室压力感受器的激活在骨骼肌中产生显着的血管舒张，但在皮肤中仅产生轻微的血管舒张。数据表明，两个床中扩张器反应的差异是由于骨骼肌的肾上腺素能收缩张力比皮肤的肾上腺素收缩张力更大。交感胆碱能或组胺能扩张通路的激活不会导致扩张。
Reflex vascular responses to acute left ventricular outflow obstruction were studied in anesthetized dogs. The studies were done to compare the effects of activation of ventricular baroreceptors on vascular resistance in skeletal muscle (gracilis muscle) and skin (hindpaw); to identify afferent and efferent pathways which mediate the reflex vasodilatation; and to assess the relative contribution of ventricular baroreceptors and baroreceptors in left atrium and pulmonary vessels in responses to left ventricular outflow obstruction. The gracilis artery and the cranial tibial artery to the paw were perfused separately at constant flow. Changes in perfusion pressure to each bed reflected changes in vascular resistance. Outflow obstruction was produced by inflating a balloon in the left ventricular outflow tract for 15 s while pressures in the left ventricle and aortic arch were measured. Inflation of the balloon increased left ventricular pressure and decreased pressure in the aortic arch. Low and high levels of obstruction produced dilator responses averaging -5+/-3 (SE) and -42+/-11 mm Hg in muscle and -1+/-1 and -3+/-2 mm Hg in paw. Denervation, phentolamine, and glyceryltrinitrate caused greater dilatation in paw than did left ventricular outflow obstruction. This indicates that dilator responses in the paw were not limited by a low level of resting neurogenic constrictor tone or by a negligible dilator capacity of these vessels. Obstruction to left ventricular inflow increased left atrial pressure, but did not cause reflex vasodilatation. This suggests that low pressure baroreceptors in atria or pulmonary vessels did not contribute to vasodilator responses to left ventricular outflow obstruction. Vasodilator responses to outflow obstruction were blocked by bilateral vagotomy, sectioning the sciatic and obturator nerves, and administration of phentolamine, but were not decreased by atropine or tripelennamine. The results indicate that activation of left ventricular baroreceptors produces striking vasodilatation in skeletal muscle, but only slight vasodilatation in skin. The data suggest that the difference in dilator responses in the two beds results from greater withdrawal of adrenergic constrictor tone to skeletal muscle than to skin. Activation of sympathetic cholinergic or histaminergic dilator pathways does not contribute to the dilatation.