The role of myocardial deterioration in the pathogenesis of endotoxin (septic) shock is under serious consideration in both basic and clinical reports. The present collaborative study was devised to join together the expertise of several laboratories in the evaluation and correlation of cardiac performance, myocardial mitochondrial activity, and ultrastructural morphology in response of canine heart to lethal endotoxin administration. Studies were conducted on adult animals in which both intact and isolated hearts were studied 4 to 7 hr postendotoxin. Results demonstrated cardiac failure as evidenced by markedly elevated left ventricular end diastolic pressure, whereas mitochondrial oxidative metabolism and energy production capacities, as measured in isolated mitochondria, were within normal ranges. Ultrastructural studies carried out on separate animals during the same time period after endotoxin revealed minimal mitochondrial edema formation together with moderate swelling of T tubular structures. Results show that irreversible mitochondrial oxidative dysfunction is not a precipitory event in the elicitation of myocardial failure after endotoxin, although depression of mitochondrial activity in in vivo mitochondria cannot be excluded as an etiologic factor. Myocardial edema formation is hypothesized to be an early critical stimulus in the precipitation of heart dysfunction in endotoxin shock.
|Original language||English (US)|
|Number of pages||8|
|State||Published - Jan 1 1974|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine