JPET Introducing ALZET?ew Model 2006 Pump

Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Schwartz, D. A.
Right arrow Articles by Horwitz, L. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Schwartz, D. A.
Right arrow Articles by Horwitz, L. D.

Effects of ketamine on left ventricular performance

DA Schwartz and LD Horwitz

The cariac response to anesthetic doses of ketamine hydrochloride was studied in dogs, initially in the absence of other drugs and subsequently during beta adrenergic block with propranolol and combined beta adrenergic and cholinergic blockade with propranolol and atropine. Ketamine (4 mg/kg) was injected into the left atrium or the jugular vein. Administration of ketamine alone resulted in increases in heart rate (61 beats/min, P smaller than .001), cardiac output and left ventricular systolic pressure, but left ventricular end-diastolic pressure and dP/dt max (maximum rate of change of left ventricular isovolumic pressure development) were unchanged. After propranolol, the increase in heart rate produced by ketamine was attenuated, and a transient fall in dP/dt max occurred. After propranolol and atropine, heart rate was not changed by ketamine, but dP/dt max fell and left ventricular end-diastolic pressure rose. Systemic vascular resistance was not altered by ketamine. It is concluded that administration of ketamine increases sympathetic discharge and reduces vagal discharge to the heart. In the absence of sympathetic and vegal control over the heart, the drug depresses myocardial contractility.

Volume 194, Issue 2, pp. 410-414, 08/01/1975
Copyright © 1975 by American Society for Pharmacology and Experimental Therapeutics




This article has been cited by other articles:


Home page
Anesth. Analg.Home page
T. Ikeda, T. Kazama, D. I. Sessler, S. Toriyama, K. Niwa, C. Shimada, and S. Sato
Induction of Anesthesia with Ketamine Reduces the Magnitude of Redistribution Hypothermia
Anesth. Analg., October 1, 2001; 93(4): 934 - 938.
[Abstract] [Full Text] [PDF]


Home page
J. Pharmacol. Exp. Ther.Home page
G. J. Locker, R. M. Mader, B. Rizovski, S. Knapp, H. Domanovits, M. Muellner, C. Hoeller, G. G. Steger, F. Sterz, M. Freissmuth, et al.
Negative Chronotropic Effects of Fentanyl Attenuate Beneficial Effects of Dobutamine on Oxygen Metabolism: Hemodynamic and Pharmacokinetic Interactions
J. Pharmacol. Exp. Ther., July 1, 1999; 290(1): 43 - 50.
[Abstract] [Full Text]




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
All ASPET Journals Molecular Pharmacology Pharmacological Reviews
 Molecular Interventions Drug Metabolism and Disposition

Copyright © 1975 by the American Society for Pharmacology and Experimental Therapeutics.