Study on the effects of six intravenous anesthetic agents on regional ventricular function in dogs (thiopental, etomidate, propofol, fentanyl, sufentanil, alfentanil).
This study evaluates the effects of 30 min increasing doses infusions of six intravenous anesthetic agents (thiopental, etomidate, propofol, fentanyl, sufentanil and alfentanil) on regional ventricular function in a normal and an acute ischemic heart segment in dogs. Part 1 discusses the methodology used in this experimental design with emphasis on the sensitivity and the limitations of the parameters used to assess ventricular performance and contractility. Part 2 reports the effects on regional and global ventricular function, which occur when one segment is made acutely ischemic. Part 3 reports and discusses the effects of increasing infusions of the three induction agents thiopental, etomidate and propofol on systemic and regional ventricular function. These agents induced a dose-dependent decrease in left ventricular end-systolic pressure. End-diastolic length also decreased in the normal and the acute ischemic segment for the three agents, indicating a decrease in left ventricular loading. This effect was most pronounced for propofol. At the doses tested, etomidate did not alter regional myocardial function significantly in any of the two segments. Thiopental, on the other hand was associated with a dose-dependent decrease in systolic shortening, that was significantly greater in the ischemic segment. This suggested that thiopental depresses myocardial function more in the acute ischemic heart than in the normal heart. Propofol decreased systolic shortening similarly in both segments. In part 4 the effects of the three narcotics fentanyl, sufentanil and alfentanil are reported. Fentanyl and sufentanil induced a dose-dependent decrease in heart rate. Left ventricular end-systolic pressure remained unchanged despite the increasing infusion rate. Fentanyl increased regional end-diastolic length and systolic shortening at the highest infusion rate. This phenomenon is not apparent for sufentanil, suggesting that different mechanisms are involved to compensate for the expected bradycardia-induced hypotension. Alfentanil did not alter systemic and regional hemodynamics significantly in this study design.
De Hert
S G
SG
Department of Anesthesiology, University Hospital Antwerp.
D015760:Alfentanil / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D003327:Coronary Disease / Q000503:physiopathology; D004285:Dogs; D005045:Etomidate / Q000008:administration & dosage / Q000494:pharmacology*; D005260:Female; D005283:Fentanyl / Q000008:administration & dosage / Q000031:analogs & derivatives* / Q000494:pharmacology*; D006439:Hemodynamics / Q000187:drug effects / Q000502:physiology; D007262:Infusions, Intravenous; D008297:Male; D015742:Propofol / Q000008:administration & dosage / Q000494:pharmacology*; D017409:Sufentanil; D013874:Thiopental / Q000008:administration & dosage / Q000494:pharmacology*; D016276:Ventricular Function / Q000187:drug effects* / Q000502:physiology
D015760:Alfentanil; D017409:Sufentanil; D013874:Thiopental; D005283:Fentanyl; D015742:Propofol; D005045:Etomidate