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.
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D003326:Coronary Circulation; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D006352:Heart Ventricles; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology; D010195:Pancreatitis / Q000473:pathology / Q000503:physiopathology*; D013318:Stroke Volume; D013599:Systole; D014655:Vascular Resistance