Turner D M, Kassell N F, Sasaki T, Comair Y G, Beck D O, Klein S L
Neurosurgery. 1984 Mar;14(3):276-82. doi: 10.1227/00006123-198403000-00003.
In this study, 10 mongrel dogs were anesthetized with sodium pentobarbital and nitrous oxide. Blood flow was determined using the radioactive microsphere technique before and after the bolus intravenous injection of naloxone (10 mg/kg). Naloxone significantly increased cerebral blood flow to cerebral cortex and the total cerebral hemisphere without an associated change in the cerebral metabolic rate of oxygen. The increase in cerebral blood flow was proportional to the elevation in mean arterial pressure. There were no consistent changes in electrical activity as measured by electroencephalography (EEG) and Fourier analysis of EEG. Systemically, naloxone induced a proportional rise in mean arterial pressure and peripheral vascular resistance and also stimulated the myocardium, as evidenced by an improved cardiac index and stroke volume. These data suggest that naloxone may interfere with cerebral autoregulation or have direct vasodilatory effects on cerebral blood vessels that are not associated with opiate receptor blockade or changes in cerebral metabolism. In addition, naloxone did not appear to reverse the cerebral depressive effects of pentobarbital. Systemically, naloxone seemed to potentiate pentobarbital-induced vasoconstriction and reverse myocardial depression.
在本研究中,10只杂种犬用戊巴比妥钠和氧化亚氮麻醉。在静脉推注纳洛酮(10mg/kg)前后,使用放射性微球技术测定血流量。纳洛酮显著增加了大脑皮质和整个大脑半球的脑血流量,而脑氧代谢率没有相关变化。脑血流量的增加与平均动脉压的升高成正比。通过脑电图(EEG)和EEG的傅里叶分析测量,电活动没有一致的变化。在全身方面,纳洛酮使平均动脉压和外周血管阻力成比例升高,并且还刺激了心肌,这由改善的心指数和每搏量证明。这些数据表明,纳洛酮可能会干扰脑自动调节,或对脑血管具有直接的血管舒张作用,这与阿片受体阻断或脑代谢变化无关。此外,纳洛酮似乎并未逆转戊巴比妥的脑抑制作用。在全身方面,纳洛酮似乎增强了戊巴比妥诱导的血管收缩并逆转了心肌抑制。