Lautt W W, Legare D J
Department of Pharmacology and Therapeutics, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Am J Physiol. 1992 Mar;262(3 Pt 1):G510-6. doi: 10.1152/ajpgi.1992.262.3.G510.
Hepatic vascular responses to 1.25 micrograms.kg-1.min-1 norepinephrine, infused into the hepatic artery, and 8-Hz nerve stimulation were monitored in anesthetized cats using a recently introduced index of contractility (IC). IC was validated in that it did not change passively in response to passive changes in portal flow or distending blood pressure, whereas the distensible venous resistance sites showed dramatic changes in resistance. Resistance is altered by both active contractile responses and passive distensibility; IC is not altered passively but is affected by changes in vascular tone. Resistance was a less sensitive index of vasoconstriction because, although the constriction increased resistance, the subsequent elevation in portal and intrahepatic pressure counteracted the constriction; the extent of active neurogenic response using resistance as the index was grossly underestimated due to venous distensibility. IC showed that pre- and postsinusoidal constriction occurred to both norepinephrine and nerves; extensive vascular escape from neurogenic constriction occurred for the portal vein so that by 5 min almost all the rise in portal pressure was due to hepatic venous constriction.
在麻醉猫中,使用最近引入的收缩性指数(IC)监测肝动脉输注1.25微克·千克⁻¹·分钟⁻¹去甲肾上腺素以及8赫兹神经刺激时的肝血管反应。IC经过验证,即它不会因门静脉血流或扩张血压的被动变化而被动改变,而可扩张的静脉阻力部位的阻力则有显著变化。阻力会因主动收缩反应和被动扩张性而改变;IC不会被动改变,但会受到血管张力变化的影响。阻力作为血管收缩的指标不太敏感,因为尽管收缩会增加阻力,但随后门静脉和肝内压力的升高会抵消这种收缩;由于静脉扩张性,以阻力为指标的主动神经源性反应程度被严重低估。IC表明,去甲肾上腺素和神经均可引起窦前和窦后收缩;门静脉发生了广泛的神经源性收缩逃逸,以至于到5分钟时,门静脉压力的几乎所有升高都归因于肝静脉收缩。