Hemorrhagic shock complicated by chronic ethanolism
Horton, J.W.
American Journal of Physiology 257(1 Pt 2): H198-H208
1989
ISSN/ISBN: 0002-9513 PMID: 2750937 Document Number: 346289
To evaluate the effects of chronicethanolism 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 anaesthesia. 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 hmoeostasis contribute to cardiac contractile dysfunction in the trauma subject who chronically consumes alcohol.