TY - JOUR
T1 - Increased myocardial contractility during endotoxin shock in dogs
AU - Kober, P. M.
AU - Thomas, J. X.
AU - Raymond, R. M.
PY - 1985
Y1 - 1985
N2 - 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.
AB - 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.
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U2 - 10.1152/ajpheart.1985.249.4.h715
DO - 10.1152/ajpheart.1985.249.4.h715
M3 - Article
C2 - 4051010
AN - SCOPUS:0022134358
SN - 0363-6135
VL - 18
SP - H715-H722
JO - American Journal of Physiology - Heart and Circulatory Physiology
JF - American Journal of Physiology - Heart and Circulatory Physiology
IS - 4
ER -