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Pathogenesis of the low cardiac output syndrome in postresuscitation states

  • I. E. Trubina
  • A. V. Volkov
Pathological Physiology and General Pathology

Abstract

Acute hypervolemia induced in experiments on dogs by infusion of dextran, did not produce decompensation of the circulation in animals whose cardiac output was sharply depressed in the postresuscitation period after circulatory arrest lasting 15 min. The increase in the venous return and change in the conditions of the peripheral circulation as a result of dextran administration temporarily increased the central venous pressure, caused a lasting increase in the arterial pressure, cardiac output, stroke volume, work of the left ventricle, and total oxygen consumption by the body, and lowered the peripheral vascular resistance. In model experiments on dogs subjected to isolated compression ischemia of the brain for 20 min, a low cardiac output syndrome also developed.

Key Words

hypoxia postresuscitation period cardiac output hemodynamics 

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Copyright information

© Plenum Publishing Corporation 1976

Authors and Affiliations

  • I. E. Trubina
    • 1
  • A. V. Volkov
    • 1
  1. 1.Laboratory of Experimental Physiology of ResuscitationAcademy of Medical Sciences of the USSRMoscow

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