Cicardo V H
Acta Physiol Lat Am. 1981;31(2):85-91.
In anesthetized dogs the intravenous injection of prostaglandins (PGs) A2 and E2 (5-200 micrograms/kg) produced a dose-dependent fall (P less than 0.001) of the blood pressure with blockade of the baroreceptor reflex. The hypotension can increase the heart rate and decrease myocardial contractile force, which is neither prevented by atropine, phentolamine, diphenhydramine, verapamil nor by inhibitors of prostaglandin synthesis. Intravenous, intraaortic or intraventricular (left) injections evoked an equipotent fall of the arterial pressure. Less decrement is elicited by the intramuscular injection. The gastric route is ineffective. The intracisternal injection of high doses (20-130 micrograms/kg) of prostaglandins A2 or E2 decreases the blood pressure slightly after 5-10 minutes, probably because of prostaglandins transport across the blood-brain barrier. The blood pressure increases by stimulation of the sympathetic nerves of the spleen and of the liver, or by exogenous noradrenaline are equally significative before and after the injections of prostaglandins A2 or E2. Indomethacin and aspirin failed to affect the pressor increase produced by stimulation of the sympathetic nerves, or that of the exogenous noradrenaline in the normal dogs or in animals injected previously with PGs. It is concluded that the hypotensive action of the PGs is due to peripheric vasodilatation apparently without inactivation by the lung.
在麻醉犬中，静脉注射前列腺素（PGs）A2和E2（5 - 200微克/千克）会导致血压呈剂量依赖性下降（P < 0.001），同时压力感受器反射被阻断。低血压可使心率增加并降低心肌收缩力，阿托品、酚妥拉明、苯海拉明、维拉帕米以及前列腺素合成抑制剂均不能预防这种情况。静脉、主动脉内或心室内（左）注射均可引起动脉压同等程度的下降。肌肉注射引起的血压下降较小。经胃途径无效。脑池内注射高剂量（20 - 130微克/千克）的前列腺素A2或E2在5 - 10分钟后可使血压略有下降，这可能是由于前列腺素透过血脑屏障所致。在注射前列腺素A2或E2之前和之后，刺激脾脏和肝脏的交感神经或注射外源性去甲肾上腺素引起的血压升高同样显著。吲哚美辛和阿司匹林在正常犬或预先注射过PGs的动物中，均不能影响刺激交感神经或注射外源性去甲肾上腺素所产生的升压作用。结论是，PGs的降压作用是由于外周血管扩张，显然不受肺的灭活作用影响。
