SOME DIRECT AND REFLEX CARDIOVASCULAR ACTIONS OF PROSTACYCLIN (PGI2) AND PROSTAGLANDIN-E2 IN ANESTHETIZED DOGS
SOME DIRECT AND REFLEX CARDIOVASCULAR ACTIONS OF PROSTACYCLIN (PGI2) AND PROSTAGLANDIN-E2 IN ANESTHETIZED DOGS
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DOI：
10.1111/j.1476-5381.1980.tb14557.x
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发表时间：
1980-01-01
影响因子：
7.3
通讯作者：
VANE, JR
中科院分区：
文献类型：
--
作者：
CHAPPLE, DJ;DUSTING, GJ;VANE, JR
1探讨前列环素（PGI 2）引起低血压和心动过缓的机制。2在19只开胸比格犬中进行了氯醛糖麻醉的血液动力学研究。PGI 2经静脉或左心房输注。3静脉或左心房输注PGI 2均能降低动脉压和总外周阻力，但左心房输注后心动过缓程度更大。4.比较前列腺素E2（PGE 2）和前列腺素I2的作用，发现虽然左房灌注能降低主动脉压和总外周阻力，但PGE 2总是增加心率、心输出量和最大加速度。5硝普钠也有类似的作用，只是它总是引起心动过速和每搏输出量减少。6阿托品（0.05或1 mg/kg i. v.）减少或逆转PGI_2引起的心动过缓，但仅在阿托品1 mg/kg后才能减少其抑制作用。迷走神经切断后心输出量、每搏输出量和最大加速度增加，PGI 2的扩张作用减弱，心动过缓逆转，而PGE 2的作用无明显改变。前列环素引起的低血压有两个原因，一是血管平滑肌的直接舒张，二是反射性的非胆碱能血管舒张。心动过缓本质上是反射性的，部分由迷走神经通路介导。
1 The aim of the study was to determine the mechanism of the hypotension and bradycardia produced by prostacyclin (PGI2). 2 Haemodynamic studies were carried out in nineteen open-chest beagle dogs anaesthetized with chloralose. PGI2 was infused intravenously or into the left atrium. 3 Infusions of PGI2 either intravenously or into the left atrium equally reduced arterial pressure and total peripheral resistance but bradycardia was greater after infusion into the left atrium. 4 Comparison of effects of PGI2 with those of prostaglandin E2 (PGE2) showed that although left atrial infusions both reduced aortic pressure and total peripheral resistance, PGE2 always increased heart rate, cardiac output and maximum acceleration. 5 Similar effects were observed with sodium nitroprusside except that it always caused tachycardia and reduced stroke volume. 6 Atropine (0.05 or 1 mg/kg i.v.) reduced or reversed the bradycardia induced by PGI2 but its hypotensive effects were reduced only after 1 mg/kg atropine. After vagotomy changes in cardiac output, stroke volume and maximum acceleration were increased, the hypotensive effects of PGI2 were reduced and the bradycardia was reversed; effects induced by PGE2 were not significantly altered. 7 The hypotension induced by prostacyclin is due to two components, a direct relaxation of vascular smooth muscle and a reflex, non-cholinergic vasodilatation. The bradycardia is reflex in nature and is partially mediated by the vagus pathway.