Cardiocirculatory pathophysiological mechanisms in severe acute pancreatitis

Figure 1 Basal and CCK-stimulated cytosolic calcium homeostasis are impaired in two different models of experimental AP. Experimental AP was induced in rats by infusing 5% (wt/vol) sodium taurocholate through the pancreatic duct (Taurocholate) or by subcutaneous injections of caerulein at a dose of 20 μg/kg

Figure 2 Hypotension associated with severe acute pancreatitis (SAP) is prevented with previous infusion of S-nitroso-N-acetylpenicillamine (SNAP). Mean arterial pressure (MAP) values along the experimental time in rats that were infused with 5% taurocholate through the pancreatic duct for 10 min (black horizontal bar) (Pancreatitis) or 5% taurocholate through the pancreatic duct for 10 min and intravenously infused with SNAP (200 μg/kg per hour) for 1 h (gray horizontal bar) (Pancreatitis + SNAP). Results are mean ± SE of changes above or below the basal MAP value (n = 6 for each treatment).

Figure 3 Response of arterial blood pressure to endothelin and angiotensin II is impaired in pancreatitic rats. Taurocholate was retrogradely infused through the pancreatic duct. Once mean arterial pressure in animals with pancreatitis diminished to around 20 mmHg with respect to basal values or at an equivalent time in controls, both endothelin (4 nmol/kg) and angiotensin II (225 ng/kg)