Farber N E, Samso E, Kampine J P, Schmeling W T
Department of Anesthesiology, Medical College of Wisconsin, Milwaukee 53226.
Anesthesiology. 1995 Jan;82(1):153-65. doi: 10.1097/00000542-199501000-00020.
This study examined the effects of halothane on arterial pressure after central nervous system (CNS) pressor site stimulation in anesthetized cats, cats rendered unconscious by midcollicular transection, and conscious cats.
Two anesthetized groups and two nonanesthetized groups were used. Cats were anesthetized with either alpha-chloralose and urethane or pentobarbital. Nonanesthetized groups were cats with midcollicular transections or conscious cats with chronically implanted electrodes. Stimulating electrodes were placed into vasomotor areas of the hypothalamus (HYP), reticular formation (RF), and medulla, and arterial pressure responses to increasing stimulus currents were examined during different halothane concentrations. Two groups of cats were also anesthetized with either pentobarbital or urethane and underwent bilateral carotid artery occlusion.
Stimulation at each CNS site produced increases in arterial pressure and heart rate. Halothane attenuated pressor responses evoked by stimulation of all loci in all groups of cats. The inhibition by halothane on these cardiovascular responses was greatest at HYP and RF sites, while the medulla was more resistant to the effects of halothane in the anesthetized animals. Midcollicular transection decreased this medullary resistance. The inhibition of pressor responses by halothane was also greater in pentobarbital-than chloralose urethane-anesthetized animals. In contrast, pressor responses elicited by bilateral carotid occlusion were attenuated by halothane similarly in both anesthetic groups. Reticular formation stimulation in conscious animals resulted in "altering responses" in addition to pressor effects, both of which were attenuated by halothane.
Modulation of CNS cardiovascular control centers contribute to halothane-induced hemodynamic alterations. Baseline anesthesia, CNS stimulation site, and the suprabulbar system influence the effects of halothane.
本研究考察了氟烷对麻醉猫、经中脑横断致无意识的猫以及清醒猫在中枢神经系统(CNS)升压位点受到刺激后动脉血压的影响。
使用了两个麻醉组和两个非麻醉组。猫分别用α - 氯醛糖和乌拉坦或戊巴比妥麻醉。非麻醉组为经中脑横断的猫或长期植入电极的清醒猫。将刺激电极置于下丘脑(HYP)、网状结构(RF)和延髓的血管运动区,在不同氟烷浓度下检测动脉血压对递增刺激电流的反应。两组猫还用戊巴比妥或乌拉坦麻醉并进行双侧颈动脉闭塞。
在每个CNS位点进行刺激均会使动脉血压和心率升高。氟烷减弱了所有组猫在刺激所有位点时诱发的升压反应。氟烷对这些心血管反应的抑制在HYP和RF位点最为明显,而在麻醉动物中,延髓对氟烷的作用更具抗性。中脑横断降低了这种延髓抗性。在戊巴比妥麻醉的动物中,氟烷对升压反应的抑制也比对氯醛糖乌拉坦麻醉的动物更大。相比之下,在两个麻醉组中,氟烷对双侧颈动脉闭塞引起的升压反应的减弱作用相似。在清醒动物中,网状结构刺激除了产生升压作用外还导致“反应改变”,这两种作用均被氟烷减弱。
中枢神经系统心血管控制中心的调节作用导致了氟烷引起的血流动力学改变。基础麻醉、中枢神经系统刺激位点和延髓上系统影响氟烷的作用。