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Effects as a Complication of Shock

WENDELL B. THROWER, M.D.; THOMAS D. DARBY, Ph.D.; EARL E. ALDINGER, M.S.

AMA Arch Surg. 1961;82(1):56-65.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

Introduction

Shock provokes marked sympathetic activity through hypotensive reflexes and subsequent hypoxia.^1-3 Both hypoxia and elevated levels of endogenously released sympathetic hormones lead to a severe acidosis characterized by an increase in lactic acid production.^4-7 In previous animal experiments from this laboratory acidosis has been produced by lactic acid infusion, by hypercapnea, by limiting venous return to that supplied by the azygos and coronary veins, or by rapid intravenous infusions of epinephrine or levarterenol.^7,8 In all cases acidosis was accompanied by a decrease in ventricular contractile force (VCF) and arterial blood pressure (BP). There was a decrease in the response of the myocardium to injections of test doses of levarterenol. Cardiac output has been observed by others to be significantly decreased during such an addition acidosis.⁹ Conditions which impose a decrease in circulating blood volume have been reported to increase endogenous releases of catechol amines.^1,2,5,7 . . . [Full Text PDF of this Article]

Author Affiliations
CHARLESTON, S.C.

From the Departments of Surgery and Pharmacology, Medical College of South Carolina.; Assistant Professor of Surgery (Dr. Thrower); Assistant Professor of Pharmacology (Dr. Darby); Graduate Student in Pharmacology (Mr. Aldinger).

Footnotes
Submitted for publication June 16, 1960.

This study was supported in part by grants from the National Heart Institute and the South Carolina Heart Association.

Read before the Eighth Scientific Meeting of the International Cardiovascular Society, North American Chapter, Miami Beach, June 11, 1960.

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