Imms F J, Neame R L, Powis D A
Br J Pharmacol. 1977 May;60(1):107-14. doi: 10.1111/j.1476-5381.1977.tb16754.x.
1 The effects of intravenously infused phenylephrine and isoprenaline upon the cardiovascular system of the rat anaesthetized with pentobarbitone, have been investigated.2 Phenylephrine produces a dose-dependent rise in mean arterial blood pressure (MABP) that is due mainly to an increase in total peripheral vascular resistance (TPR), though at all doses tested cardiac output was invariably raised.3 The increase in cardiac output was due in each instance to an increase in stroke volume, heart rate being unchanged. This increase in cardiac output is probably brought about by effects of phenylephrine on the capacitance vessels rather than by an effect on the heart.4 Evidence is presented to show that the effects of phenylephrine are mediated largely by alpha-adrenoceptors, but that beta-adrenoceptors which affect TPR are also stimulated by the amine.5 Isoprenaline produces a dose-dependent fall in MABP that is due entirely to a fall in TPR since the cardiac output increases.6 Unlike phenylephrine, the increase in cardiac output obtained with isoprenaline was achieved by an increase in heart rate while stroke volume remained close to control values. It is contended that the augmented venous return required for the elevated cardiac output results in this case mainly from the isoprenaline-induced fall in TPR which enhances transfer of blood from arteries to the veins.7 Evidence is presented to show that the effects of isoprenaline are mediated mainly by beta-adrenoceptors.8 Under the present experimental conditions the adrenoceptor-mediated cardiovascular changes are little modified reflexly by the arterial baroreceptors.
研究了静脉注射去氧肾上腺素和异丙肾上腺素对戊巴比妥麻醉大鼠心血管系统的影响。
去氧肾上腺素可使平均动脉血压(MABP)呈剂量依赖性升高,这主要归因于总外周血管阻力(TPR)增加,不过在所有测试剂量下,心输出量均始终升高。
每次心输出量增加均是由于每搏输出量增加,心率未变。心输出量的这种增加可能是去氧肾上腺素对容量血管的作用所致,而非对心脏的作用。
有证据表明,去氧肾上腺素的作用主要由α - 肾上腺素能受体介导,但影响TPR的β - 肾上腺素能受体也受到该胺类物质的刺激。
异丙肾上腺素可使MABP呈剂量依赖性下降,这完全是由于TPR下降,因为心输出量增加。
与去氧肾上腺素不同,异丙肾上腺素所致的心输出量增加是通过心率增加实现的,而每搏输出量仍接近对照值。有人认为,在此情况下,心输出量升高所需的静脉回流量增加主要源于异丙肾上腺素引起的TPR下降,这增强了血液从动脉向静脉的转移。
有证据表明,异丙肾上腺素的作用主要由β - 肾上腺素能受体介导。
在当前实验条件下,肾上腺素能受体介导的心血管变化很少受到动脉压力感受器的反射性调节。