W Tambolini | PubMed Health

PubMed1985

Canine left ventricular function during experimental pancreatitis.

Left ventricular contractility following induction of experimental pancreatitis (EP) was studied. Contractility was evaluated by analyzing the left ventricular end systolic pressure-diameter relationship (sigma ES). Sigma ES is independent of large changes in preload, afterload, and heart rate, but sensitive to changes in ventricular contractility. Following injection of 100,000 IU trypsin in 4% taurocholate into the pancreas to induce EP, seven of eight dogs survived 5 hr. These dogs exhibited an initial significant reduction in mean arterial pressure (MABP) which stabilized at 90% of control at 3-5 hr post-EP. Cardiac output (CO) dropped slowly after EP induction (from 3.08 +/- 0.43 to 2.22 +/- 0.22 liters/min) associated with no significant change in peripheral resistance. Stroke work and stroke volume were markedly depressed reflecting the changes in MABP and CO. No consistent changes in +dP/dt or -dP/dt were observed. The ratio of endo/epicardial blood flow was unchanged as was blood Ca2+ levels throughout the experiment. Ventricular contractility as reflected by sigma ES tended to improve (from 49.7 to 69.6 mm Hg/mm at 4 hr following EP). Therefore, it was concluded that these animals exhibited no loss of ventricular contractility during EP.

Acute Disease↗

PubMed1983

Canine left ventricular performance during LD50 endotoxemia.

Previous reports of the effect of endotoxin shock on cardiac performance have not achieved uniform results. These discrepancies have possibly been caused by the use of indices of cardiac performance that may have been sensitive to altered heart rate or preconditions of cardiac contraction as well as altered cardiac performance. We tested the hypothesis that, following a median lethal dose (LD50) of E. coli endotoxin, cardiac performance would be diminished in nonsurviving animals and maintained in surviving animals. We elected to employ the analysis of the end-systolic pressure-diameter relationship (sigma ES) as well as other measurements of cardiac performance to test this hypothesis. We established that the sigma ES measurement was independent of increased and decreased afterload and relatively insensitive to altered heart rate. In the nonsurviving animals, sigma ES exhibited a marked depression following endotoxin a administration. In the surviving animals, sigma ES exhibited a nonsignificant decrease followed by a return toward preendotoxin values. All other cardiodynamic measurements were uninterpretable due to the marked changes in heart rate, peripheral vascular function, aortic pressure, and cardiac output. We conclude that, following endotoxin administration, those animals that exhibited a diminished myocardial contractility failed to survive more than 2.5 h postendotoxin, whereas the surviving animals were able to restore normal cardiac contractility. Thus survival of endotoxin administration is associated with the maintenance of normal cardiac contractility.

Animals↗