Vidrio H, García-Márquez F
Arch Int Pharmacodyn Ther. 1986 Sep;283(1):94-104.
The role of the sympatho-adrenal system in the production of tachycardia accompanying the hypotensive response to hydralazine was studied in urethane-anesthetized rats subjected to previous bilateral adrenal demedullation or to pretreatment with 6-hydroxydopamine and compared with intact control animals. The prolonged hypotension induced by the vasodilator was not affected by these maneuvers, but the slowly developing tachycardia was reversed to bradycardia, which in the demedullated group was followed after 60 min by a moderate increase in heart rate. In the chemically sympathectomized rats, the cardiac depressant response was completely blocked by pretreatment with atropine. In additional experiments, previous administration of methylatropine enhanced hydralazine tachycardia, but atropine partially inhibited this response and changed its time course to mirror that of the hypotension. These results indicate that in urethane-anesthetized rats, hydralazine tachycardia is mediated by sympatho-adrenal activation and that it is accompanied by a simultaneous heart rate-lowering parasympathetic discharge normally masked by the predominant tachycardia. They further suggest that the tachycardia is facilitated by a muscarinic mechanism which modulates central sympathetic influences on cardiovascular function.
在乌拉坦麻醉的大鼠中,研究了交感 - 肾上腺系统在伴随肼屈嗪降压反应的心动过速产生中的作用。这些大鼠事先进行了双侧肾上腺髓质切除术或用6 - 羟基多巴胺预处理,并与完整的对照动物进行比较。血管扩张剂诱导的长时间低血压不受这些操作的影响,但缓慢发展的心动过速转变为心动过缓,在去髓质组中,60分钟后心率适度增加。在化学性交感神经切除的大鼠中,心脏抑制反应被阿托品预处理完全阻断。在另外的实验中,事先给予甲基阿托品可增强肼屈嗪引起的心动过速,但阿托品部分抑制了这种反应,并改变了其时间进程,使其与低血压的时间进程相似。这些结果表明,在乌拉坦麻醉的大鼠中,肼屈嗪引起的心动过速是由交感 - 肾上腺激活介导的,并且同时伴有通常被占主导地位的心动过速掩盖的心率降低的副交感神经放电。它们进一步表明,心动过速由一种毒蕈碱机制促进,该机制调节中枢交感神经对心血管功能的影响。