Vacca G, Battaglia A, Grossini E, Mary D A, Molinari C, Surico N
Dipartimento di Scienze Mediche, Facoltà di Medicina e Chirurgia di Novara, Università di Torino, Italy.
J Auton Nerv Syst. 1997 Mar 19;63(1-2):1-11. doi: 10.1016/s0165-1838(96)00124-5.
The present study was undertaken in anaesthetized pigs to determine whether distension of the uterus reflexly affects the aortic blood pressure, heart rate, left ventricular inotropic state and the coronary circulation. Experiments were performed in 17 pigs anaesthetized with alpha-chloralose and artificially ventilated. Coronary blood flow was measured with an electromagnetic flowmeter positioned around the origin of the left circumflex coronary artery. The uterus was distended by injecting 20 ml warm Ringer solution into a balloon positioned within the uterus (mean transmural pressure of about 17 mmHg). Distension of the uterus without controlling any haemodynamic variable caused an increase in aortic blood pressure. When this response was prevented, an increase in heart rate was obtained in each animal. When the heart rate and blood pressure responses were prevented, the distension did not cause significant changes in the maximum rate of change of left ventricular pressure, but always caused a decrease in mean coronary blood flow. In five pigs, the increase in heart rate and the decrease in mean coronary blood flow were graded by step increments of distension. In six pigs, the haemodynamic responses to distension of the uterus were not affected by the administration of atropine. In 12 pigs, which included the six given atropine, the increase in heart rate was abolished by the administration of propranolol and the increase in aortic blood pressure and the decrease in mean coronary blood flow were abolished by the subsequent administration of phentolamine. In the remaining five pigs, the haemodynamic responses caused by uterine distension were abolished by the administration of bretylium tosylate. The present study showed that distension of the uterus in anaesthetized pigs primarily caused reflex increases in heart rate and aortic blood pressure and coronary vasoconstriction. These reflex responses were mediated by efferent sympathetic mechanisms.
本研究在麻醉猪身上进行，以确定子宫扩张是否会反射性地影响主动脉血压、心率、左心室收缩状态和冠状动脉循环。实验在17只用α-氯醛糖麻醉并人工通气的猪身上进行。用电磁流量计测量环绕左旋冠状动脉起始处的冠状动脉血流量。通过向置于子宫内的气囊注入20ml温林格溶液（平均跨壁压力约为17mmHg）使子宫扩张。在不控制任何血流动力学变量的情况下子宫扩张会导致主动脉血压升高。当这种反应被阻止时，每只动物的心率都会升高。当心率和血压反应被阻止时，扩张不会引起左心室压力最大变化率的显著改变，但总会导致平均冠状动脉血流量减少。在5只猪中，通过逐步增加扩张程度来分级心率升高和平均冠状动脉血流量减少。在6只猪中，子宫扩张的血流动力学反应不受阿托品给药的影响。在12只猪（包括给予阿托品的6只）中，普萘洛尔给药可消除心率升高，随后酚妥拉明给药可消除主动脉血压升高和平均冠状动脉血流量减少。在其余5只猪中，子宫扩张引起的血流动力学反应可被溴苄铵给药消除。本研究表明，麻醉猪的子宫扩张主要引起心率和主动脉血压反射性升高以及冠状动脉血管收缩。这些反射反应是由传出交感神经机制介导的。
