Hiley C R, Thomas G R
Br J Pharmacol. 1987 Jan;90(1):61-70. doi: 10.1111/j.1476-5381.1987.tb16825.x.
Cardiac output, its distribution and tissue blood flows were determined with tracer microspheres in pithed rats during pressor responses elicited by either alpha 1-adrenoceptor agonists (cirazoline, phenylephrine) or alpha 2-adrenoceptor agonists (xylaxine, B-HT 933). Two doses were used for each of cirazoline and B-HT 933 and phenylephrine was investigated in the presence of propranolol (3 mg kg-1). The rats were pithed under halothane anaesthesia. Cardiac output was increased by xylazine, the higher dose of B-HT 933 and phenylephrine. Heart rate was increased by phenylephrine and the higher doses of both cirazoline and B-HT 933. Stroke volume was greater in those groups given xylazine, phenylephrine and the higher dose of B-HT 933 but was decreased in those animals given the higher dose of cirazoline. Both alpha 2-adrenoceptor agonists increased the number of microspheres trapped in the lungs and the proportion of the cardiac output passing through the hepatic artery but decreased that flowing through the spleen and gastrointestinal tract. The higher dose of B-HT 933 also decreased the fraction of cardiac output flowing to the kidneys but kidney blood flow was maintained as a result of the increased cardiac output. Also, this treatment reduced blood flow in the epididimal fat pads. Both alpha 1-adrenoceptor agonists increased the fraction of cardiac output received by the coronary vasculature but the only other effect on distribution common to these agents was an increase in the percentage of the cardiac output passing to the hepatic artery. Cirazoline decreased the proportion of cardiac output distributed to the gastrointestinal tract and spleen but the total fraction of cardiac output passing to the hepatosplanchnic region was maintained as a result of the increase to the hepatic artery. Cirazoline markedly reduced the proportion of the cardiac output received by the kidneys and absolute flow in these organs was only 1.4% of control after the higher dose of this agonist but flow at the lower dose was maintained by the higher cardiac output. It is concluded that there is a significant contribution to the pressor responses elicited by alpha-agonists resulting from an alpha-adrenoceptor-mediated increase in cardiac output that may result from greater heart rates or stroke volumes. Also, there is a differential distribution of alpha-receptor subtypes throughout the vasculature which is especially noticeable in the kidneys.
在深度麻醉的大鼠中，使用示踪微球测定了由α1肾上腺素能受体激动剂（可乐唑啉、去氧肾上腺素）或α2肾上腺素能受体激动剂（赛拉嗪、B-HT 933）引起的升压反应期间的心输出量、其分布以及组织血流量。可乐唑啉和B-HT 933各使用了两种剂量，去氧肾上腺素是在普萘洛尔（3mg/kg）存在的情况下进行研究的。大鼠在氟烷麻醉下深度麻醉。赛拉嗪、较高剂量的B-HT 933和去氧肾上腺素使心输出量增加。去氧肾上腺素以及较高剂量的可乐唑啉和B-HT 933使心率增加。给予赛拉嗪、去氧肾上腺素和较高剂量B-HT 933的组中风量较大，但给予较高剂量可乐唑啉的动物中风量减少。两种α2肾上腺素能受体激动剂均增加了滞留在肺中的微球数量以及流经肝动脉的心输出量比例，但减少了流经脾脏和胃肠道的血流量。较高剂量的B-HT 933也降低了流向肾脏的心输出量比例，但由于心输出量增加，肾血流量得以维持。此外，这种处理减少了附睾脂肪垫中的血流量。两种α1肾上腺素能受体激动剂均增加了冠状动脉血管系统接受的心输出量比例，但这些药物对分布的唯一其他共同影响是流经肝动脉的心输出量百分比增加。可乐唑啉降低了分配到胃肠道和脾脏的心输出量比例，但由于肝动脉血流量增加，流经肝脾区域的心输出量总比例得以维持。可乐唑啉显著降低了肾脏接受的心输出量比例，在给予该激动剂较高剂量后，这些器官的绝对血流量仅为对照的1.4%，但较低剂量时的血流量因较高的心输出量而得以维持。结论是，α肾上腺素能受体介导的心输出量增加对α激动剂引起的升压反应有显著贡献，这可能是由于心率或 stroke 量增加所致。此外，α受体亚型在整个血管系统中的分布存在差异，在肾脏中尤为明显。
