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1 From the Cardiovascular Laboratory, General Medical Research Service, Veterans Administration Center, and the Department of Medicine, School of Medicine, University of California, Los Angeles, California
Hemodynamic measurements were made in dogs following coronary artery embolization with plastic microspheres. The data obtained in nine dogs which remained normotensive were compared with those obtained in 12 dogs in which severe hypotension was produced comparable to human coronary shock. The amount of myocardial injury and the reduction in cardiac output were approximately equal in the two groups. Total peripheral resistance rose markedly in the normotensive animals and failed to rise in the shocked animals. The production of experimental coronary shock was not dependent on the presence of heart failure. The levarterenol responses showed that the shocked animal was able to elevate its cardiac output as well as its total peripheral resistance. It is concluded that heart injury is not the sole and perhaps not even the major cause of experimental coronary shock but that some extracardiac mechanism exists. It is conjectured that a reflex arises in the injured area which in some manner interferes with normal homeostasis. The production of coronary shock after bilateral cervical vagotomy indicates that this proposed reflex is not that described by Jarisch and Bezold.
Note:
with the technical assistance of F. J. KOTICHAS.
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P. R. ELLIS JR., N. J. BAILAS, J. D. VISKOS, S. H. WONG, and J. W. HYLAND Experimental Heart Failure In Dogs Arch Surg, August 1, 1964; 89(2): 299 - 306. [Abstract] [PDF] |
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