Influence of hemorrhagic pancreatitis on the lung. An ultrastructural study

The influence of hemorrhagic pancreatitis on pulmonary ultrastructure was investigated in 21 mongrel dogs. The animals were intubated but not ventilated. Pancreatitis was induced with an autologous bile-trypsin mixture. The degree of pancreatitis was confirmed clinically, chemically, and histologically. The animals were sacrificed at four time frames: zero time, one, three, and five hours after the onset of pancreatitis. There was progression, with time, of distorted pulmonary microarchitecture. Interstitial edema, including dispersion of endoplasmic reticulum, disruption of lamellar bodies, and blunting of the pseudopods in the type II pneumocyte, were noted. There was a decrease in osmiophilic content as well as loss of organization of the lamellar bodies. Since surfactant is produced and stored by the lamellar bodies in the type II pneumocyte, these data add support to the concept of pulmonary congestive atelectasis secondary to pancreatitis--related to absence of or diminished surfactant.