AJP - Heart and Circulatory Physiology, Vol 257, Issue 1 198-H208, Copyright © 1989 by American Physiological Society
Hemorrhagic shock complicated by chronic ethanolism
J. W. Horton
Department of Surgery, University of Texas, Southwestern Medical Center, Dallas 75235.
To evaluate the effects of chronic ethanolism on responses to hemorrhagic
shock (HS), 24 dogs were fed a diet mixed with 3 g/kg ethanol (ETOH) for 3
mo (group 1, n = 12) and 9 mo (group 2, n = 12); 12 dogs were fed a regular
diet with no alcohol. Blood alcohol level 2-3 h after food consumption was
116 +/- 10 mg/100 ml. On the experimental day, both ETOH-treated and
ETOH-free dogs were divided into two subgroups, one for HS [mean arterial
pressure (MAP) of 30 mmHg for 2 h] and one for observation during
anesthesia. Chronic ethanolism altered cardiocirculatory function
(increased MAP, arterial lactate, and hematocrit and decreased cardiac
output, stroke work, and pancreatic blood flow) regardless of the length of
time ETOH was consumed. HS impaired cardiovascular performance regardless
of ETOH consumption. However, coronary blood flow, myocardial oxygen
delivery, extraction, and consumption were significantly higher in the
ETOH-treated compared with ETOH-free dogs after 2 h of shock.
Cardiocirculatory dysfunction after fluid resuscitation from shock in the
ETOH group was not related to inadequate coronary perfusion, metabolic
acidosis, or cardiac hypertrophy. An increased total myocardial tissue
calcium content in the ETOH group suggests that ETOH-mediated changes in
calcium homeostasis contribute to cardiac contractile dysfunction in the
trauma subject who chronically consumes alcohol.
