Abstract
Summary
E. coli endotoxin exerts a direct vasoconstrictor effect on the coronary vessels. E. coli endotoxin also causes an initial increase in aortic blood flow, myocardial contractile force, and left ventricular work done. These initial cardiac responses can be attenuated by depleting catecholamines or by blocking beta-adrenergic receptor sites. The initial responses are somewhat modified by depletion of histamine indicating that catecholamines are not the sole mediators for the initial effects of endotoxin.
The author gratefully acknowledges the advice of Professor Shoji Saito (Nihon University School of Medicine, Department of Pharmacology, Tokyo, Japan) and the technical assistance of Mr. M. H. Hayman and Miss L. A. Anderson (both senior Medical Students at LSU Medical School in New Orleans). This study was partially supported by the Institutional Research Grant from Louisiana State University School of Medicine in New Orleans (No. 456-99-8602).
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