Effect of acute pancreatitis on pulmonary transvascular fluid and protein exchange.
We used the anesthetized sheep lung lymph preparation to examine the effects of acute hemorrhagic pancreatitis on pulmonary transvascular fluid and protein exchange. Induction of acute pancreatitis by injection of trypsin and sodium taurocholate into the pancreatic duct caused significant increases (p less than 0.05) in lung lymph flow, ratio of lymph to plasma protein concentration (L/P ratio), and transvascular protein clearance. Pulmonary arterial and pulmonary arterial wedge pressures did not change significantly, but pulmonary blood flow decreased (p less than 0.05) and pulmonary vascular resistance increased (p less than 0.05). In contrast to the effects of acute pancreatitis, left atrial hypertension caused increases in lung lymph flow that were associated with decreases in the L/P ratio. Extravascular lung water content was increased after acute pancreatitis by 25% from the value obtained in sham-operated animals in which saline was injected into the pancreatic duct. These findings indicate that acute hemorrhagic pancreatitis causes an increase in pulmonary vascular permeability to proteins. Because pulmonary vascular pressures did not change, the increased permeability may be due to the cellular and humoral factors rather than hemodynamic mechanisms.
D000208:Acute Disease; D000818:Animals; D001794:Blood Pressure; D001798:Blood Proteins / Q000502:physiology; D006973:Hypertension / Q000503:physiopathology; D008196:Lymph / Q000502:physiology; D010195:Pancreatitis / Q000150:complications / Q000503:physiopathology*; D011506:Proteins / Q000502:physiology*; D011652:Pulmonary Circulation; D011654:Pulmonary Edema / Q000209:etiology / Q000503:physiopathology*; D012129:Respiratory Function Tests; D012756:Sheep; D013656:Taurocholic Acid; D014357:Trypsin; D014655:Vascular Resistance
D001798:Blood Proteins; D011506:Proteins; D013656:Taurocholic Acid; D014357:Trypsin