title: A time-course study of the effects of pentobarbital, fentanyl, and morphine chloralose on myocardial mechanics.
abstract: Cardiovascular physiological studies in anesthetized animals may be confounded by the hemodynamic actions of the anesthetic agents themselves. To identify an anesthetic regimen that does not significantly influence cardiovascular physiology, the hemodynamic responses of 28 dogs were studied. Animals were equally divided among groups with 1) no anesthesia (i.e., trained conscious preparation), 2) pentobarbital sodium, 3) fentanyl citrate, and 4) a combination of morphine sulfate and alpha-chloralose. Anesthesia was maintained for 3 h. Data were acquired with the use of ultrasound imaging of the heart in conjunction with invasive pressure measurements. Left ventricular ejection phase indexes and end-systolic force-velocity relations were used to evaluate the effects of each anesthetic agent on overall systolic performance and myocardial contractility. Compared with the conscious animals, pentobarbital profoundly depressed systolic performance (P less than 0.05 vs. control) because of a reduction in myocardial contractility (P less than 0.01) and an increase in left ventricular afterload (end-systolic wall stress, P less than 0.05). Fentanyl increased myocardial contractility (P less than 0.05) but also tended to increase afterload with the net result that overall systolic performance remained unchanged. Morphine-chloralose did not affect overall ventricular systolic performance or its individual determinants. Pentobarbital and fentanyl also caused progressive time-dependent deteriorations in all parameters of systolic function during prolonged anesthesia. In contrast, cardiac function was stable for greater than or equal to 3 h after induction of morphine-chloralose anesthesia. The hemodynamic profile of dogs anesthetized with morphine-chloralose most closely resembled that of the conscious animals. Morphine-chloralose is recommended when prolonged anesthesia is required for studies of cardiovascular physiology.
authors.affiliation: Department of Medicine, University of Chicago, Illinois 60637.
authors.forename: R M
authors.initials: RM
authors.lastname: Lang
authors.forename: R H
authors.initials: RH
authors.lastname: Marcus
authors.forename: A
authors.initials: A
authors.lastname: Neumann
authors.forename: D
authors.initials: D
authors.lastname: Janzen
authors.forename: D
authors.initials: D
authors.lastname: Hansen
authors.forename: A M
authors.initials: AM
authors.lastname: Fujii
authors.forename: K M
authors.initials: KM
authors.lastname: Borow
mesh_terms: D000777:Anesthetics / Q000494:pharmacology*; D000818:Animals; D002698:Chloralose / Q000494:pharmacology; D004285:Dogs; D005283:Fentanyl / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D007442:Intubation, Intratracheal; D009020:Morphine / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D010424:Pentobarbital / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects
chemical_list: D000777:Anesthetics; D002698:Chloralose; D009020:Morphine; D010424:Pentobarbital; D005283:Fentanyl