收缩性
普萘洛尔
戊巴比妥
体内
医学
麻醉
丸(消化)
心室压
内科学
等容收缩
血流动力学
心脏病学
血压
舒张期
生物
生物技术
作者
Helmut Unruh,R. Wang,D. Böse,Steven N. Mink
出处
期刊:American Journal of Physiology-heart and Circulatory Physiology
[American Physical Society]
日期:1991-09-01
卷期号:261 (3): H700-H706
被引量:18
标识
DOI:10.1152/ajpheart.1991.261.3.h700
摘要
Although pentobarbital sodium (NP) anesthesia has been shown to depress left ventricular (LV) contractility in dogs, measurements of LV contractility in previous studies have been made soon after a bolus of NP was given when serum concentrations would be extremely high. In this study, we compared indexes of LV contractility during awake and anesthetized conditions. During anesthesia, measurements were obtained 1 h after an intravenous bolus of NP was given when serum concentrations were approximately 25 mg/l and above that reported to abolish pain. In 13 dogs, subendocardial ultrasonic crystal transducers and a high-fidelity pressure transducer were implanted into the LV. Measurements were obtained with and without prior treatment with propranolol to produce beta-adrenergic blockade. LV contractility was assessed by ejection fraction and the end-systolic pressure-volume relationship. The effect of NP on ventricular myocardium was also examined in an in vitro canine right trabecular preparation to compare in vivo and in vitro effects. In the in vivo study, the results showed no decrease in LV contractility during anesthesia regardless of whether propranolol was administered. The in vitro preparation showed only a minimal decrease in isometric tension at the concentrations used in the in vivo study. We conclude that NP anesthesia does not depress LV contractility when concentrations are maintained at approximately 25 mg/l.
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