Covert R F, Schreiber M D, Torgerson L J
Department of Pediatrics, Pritzker School of Medicine, University of Chicago, IL.
J Cardiovasc Pharmacol. 1992 Dec;20(6):990-6. doi: 10.1097/00005344-199212000-00021.
alpha-Chloralose is an anesthetic commonly used in cardiovascular research. Using a chronically instrumented neonatal lamb model, we previously determined that chloralose has important effects on basal hemodynamics and arterial oxygen tension as compared with those of paired conscious control lambs. We wished to determine whether beta-adrenergic receptor stimulation accounted for chloralose-induced hemodynamic effects and to investigate the influence of chloralose and beta-adrenergic receptor antagonism on oxygen metabolism. In paired studies, five lambs were given chloralose intravenously (30 mg/kg i.v.) after propranolol (1 mg/kg i.v.) or saline control. The group pretreated with propranolol had reduced heart rate (HR 206 +/- 12 vs. 244 +/- 10 beats/min, p = 0.04) and cardiac output (CO 253 +/- 29 vs. 302 +/- 40 ml/min/kg, p = 0.005) 30 min after chloralose as compared with control; pretreatment with propranolol also attenuated the systemic hypertensive response to chloralose (77 +/- 8 vs. 89 +/- 5 mm Hg, p = 0.055). No difference in the response of stroke volume (SV), atrial or pulmonary arterial pressures, or pulmonary and systemic vascular resistances (PVR, SVR) were observed between treatment groups. No differences between propranolol and saline treatment groups were observed in arterial and mixed venous oxygen contents, arteriovenous (A-V) oxygen difference, oxygen extraction, or oxygen consumption; a reduction in oxygen delivery observed after propranolol as compared with saline was not altered by chloralose. We conclude that tachycardia and increase in CO induced by chloralose in lambs probably are mediated by beta-adrenergic receptor stimulation, which may be direct or indirect.(ABSTRACT TRUNCATED AT 250 WORDS)
α-氯醛糖是心血管研究中常用的一种麻醉剂。利用长期植入仪器的新生羔羊模型,我们之前确定,与配对的清醒对照羔羊相比,氯醛糖对基础血流动力学和动脉血氧张力有重要影响。我们希望确定β-肾上腺素能受体刺激是否是氯醛糖诱导的血流动力学效应的原因,并研究氯醛糖和β-肾上腺素能受体拮抗作用对氧代谢的影响。在配对研究中,五只羔羊在给予普萘洛尔(1mg/kg静脉注射)或生理盐水对照后静脉注射氯醛糖(30mg/kg静脉注射)。与对照组相比,普萘洛尔预处理组在注射氯醛糖30分钟后心率降低(心率206±12次/分钟对244±10次/分钟,p=0.04),心输出量降低(心输出量253±29对302±40ml/分钟/千克,p=0.005);普萘洛尔预处理也减弱了对氯醛糖的全身高血压反应(77±8对89±5mmHg,p=0.055)。治疗组之间在每搏输出量(SV)、心房或肺动脉压以及肺和全身血管阻力(PVR、SVR)的反应上没有差异。在动脉和混合静脉血氧含量、动静脉(A-V)氧差、氧摄取或氧消耗方面,普萘洛尔和生理盐水治疗组之间没有差异;与生理盐水相比,普萘洛尔后观察到的氧输送减少并未因氯醛糖而改变。我们得出结论,氯醛糖在羔羊中诱导的心动过速和心输出量增加可能是由β-肾上腺素能受体刺激介导的,这可能是直接的或间接的。(摘要截断于250字)