Haemorrhagic shock in a canine model leads to a persistent myocardial metabolic defect and the production of a circulating myocardial depressant factor.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for a myocardial depressant factor in haemorrhagic shock; does not yet inform clinical practice.
Using selective cardiac catheterization and a 133Xe wash-out technique, myocardial blood-flow and oxygen utilization were studied in greyhounds during and following brief and prolonged haemorrhagic hypotension. The progressive fall in myocardial oxygen extraction as the shock period was prolonged and the subsequent failure of myocardial oxygen consumption to rise during re-infusion suggested the presence of a metabolic defect in the myocardial cell. The use of a special ‘elemental’ diet was shown to eliminate the intestinal blood-loss typical of canine haemorrhagic shock models; despite this the apparent myocardial cellular metabolic defect persisted. In addition, a myocardial depressant factor which depressed myocardial function in vitro was isolated from ultrafiltrates of post-shock plasma.
No takes yet. Share an insight, caveat, or question.
McArdle et al. (1973) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: