Experimental pancreatitis does not produce pulmonary hypertension.
The onset of experimental hemorrhagic pancreatitis in dogs was rapidly followed by a deterioration of CO, blood pressure, LVSW and RVSW, along with significant elevations of Hct, SVR and PVR. These alterations could all be reversed by the administration of Ringer's lactate. These findings support the concept that the major physiopathologic characteristic of severe acute pancreatitis is a loss of effective plasma and extracellular fluid volumes and that the replacement of fluid losses corrects the hemodynamic alterations. In neither of the experimental groups did pulmonary hypertension develop. We found no evidence in this model of hemorrhagic pancreatitis for a circulating pulmonary vasoactive substance.
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output; D002496:Central Venous Pressure; D004285:Dogs; D006439:Hemodynamics; D006470:Hemorrhage / Q000150:complications; D006976:Hypertension, Pulmonary / Q000209:etiology*; D010195:Pancreatitis / Q000150:complications* / Q000503:physiopathology; D011669:Pulmonary Wedge Pressure