PULMONARY INTERSTITIAL EDEMA IN THE PIG AFTER HEAVY EXERCISE

During exercise (especially in hypoxia), the alveolar-arterial O-2 ten sion difference increases. This impairment of pulmonary gas exchange i s caused partly by diffusion disequilibrium, but it has also been show n that an exercise-induced increase in ventilation-perfusion (VA/Q) in equality develops. Possible explanations of increased VA/Q mismatch in clude nonuniform pulmonary vasoconstriction, reduced gas mixing in the large airways, airway obstruction, and the development of interstitia l pulmonary edema. To directly determine whether the latter develops i n high-intensity short-term exercise, we exercised pigs on a motor-dri ven treadmill at the highest speed that they could sustain for 6-7 min . Heart rate reached 274 +/- 5 min(-1) in the exercised group, confirm ing that the pigs reached a near-maximal level of exercise. While runn ing, the pigs were killed by an intravenous overdose of pentobarbital. Postmortem, the lungs were immediately removed, drained of blood, wei ghed, and then airway fixed with 10% formaldehyde. Four tissue blocks of the right lung of each pig were taken from the ventral and dorsal a reas of the upper and lower lobes, respectively. They were stained wit h hematoxylin and eosin and prepared for histological examination by l ight microscopy. There was no difference in the lung-to-body weight ra tio between exercised pigs (7.72 +/- 0.87 g/kg) and a nonexercised con trol group (7.70 +/- 0.68 g/kg). However, we found a significantly hig her percentage of pulmonary arteries with perivascular edema in exerci sed (33.8 +/- 3.4%) than in nonexercised pigs (20.0 +/- 4.0%; P < 0.02 ). Thus, perivascular edema (and thus possibly also parenchymal inters titial edema) can occur during short-term heavy exercise. Whether this contributes to the increased VA/Q inhomogeneity seen at high levels o f exercise remains to be determined.