The slope of the left ventricular (LV) end-systolic pressure-diameter relationship (E(es)) was analyzed in open-chest, pentobarbital-anesthetized dogs before and after endotoxin administration. A lead II electrocardiogram, systemic arterial pressure, LV pressure, LV dP/dt, and LV minor axis diameter were measured. After control measurements were taken, dogs were given either 1 mg/kg Salmonella entritidis endotoxin (n = 5) or an equivalent volume of saline (n = 4). Control dogs were followed for 240 min. Endotoxic dogs were monitored until death (246 ± 44 min). There were no significant changes in E(es) in control dogs (17 ± 3 mmHg/mm), which were hemodynamically stable for 4 h. E(es) was significantly increased in endotoxic dogs even into the late stages of shock (41 ± 11 mmHg/mm, P<0.01). Only during the terminal phase did E(es) fall significantly below control (11 ± 2 mmHg/mm, P<0.05). End-diastolic diameter decreased following endotoxin administration (P<0.05) but returned toward control by the terminal stage. Peak + LV dP/dt was depressed following endotoxin injection. Myocardial contractility was depressed except as a terminal event. Early depression of cardiovascular performance in endotoxic dogs was therefore due to decreased preload and not cardiac dysfunction.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|State||Published - Jan 1 1985|
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Physiology (medical)