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 ( Σ ES). Σ 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 Ca 2+ levels throughout the experiment. Ventricular contractility as reflected by Σ 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.