Dietary pulmonary hypertension

Abstract

Experiments are mentioned which make it clear that substances released from the gut are capable of eliciting pulmonary vasomotor activity and that the occasional coincidence of severe hepatic injury and pulmonary hypertension can no longer be discounted as happenstance. If damage to the endothelium is truly the initiating event, dietary pulmonary hypertension emerges as a pathophysiological expression of failure of the metabolic and waterproofing function of the pulmonary capillary linings. Clearly this view is consistent with mounting evidence that pulmonary capillary endothelium is an important metabolic machine for coping with the biologically active substances that cross its surface. Also, once endothelial injury allows large circulating macromolecules to penetrate to the pulmonary interstitium, the way is clear for interstitial organization and fibrosis. It is unlikely that the saga of dietary pulmonary hypertension will end with monocrotaline, fulvine, Aminorex, and phenformin. (25 references)