ATRIAL-NATRIURETIC-PEPTIDE AND GLUCAGON-RELEASE IN EXPERIMENTAL INTESTINAL ISCHEMIA AND REPERFUSION

Intestinal ischaemia and reperfusion cause changes in cardiovascular a nd pulmonary function. In a rat model, the plasma concentrations of at rial natriuretic peptide (ANP) and pancreatic glucagon rose on reperfu sion after 20 min of intestinal ischaemia, coinciding with significant arterial hypotension: mean(s.e.m.) ANP 79(13) versus control 36(4) fm ol ml(-1) (P<0.01); and mean(s.e.m.) glucagon 22(2) versus control 10( 1) fmol ml(-1) (P<0.001). Glucagon was also released on reperfusion af ter 5 min of ischaemia: mean(s.e.m.) 18(2)fmol ml(-1) (P<0.001 versus control). In a second experiment, pretreatment of rats with allopurino l did not prevent arterial hypotension but abolished ANP release (mean (s.e.m.) 36(2) fmol ml(-1) versus no pretreatment 70(7) fmol ml(-1), P <0.05), while glucagon release was unaffected. The release of ANP, but not that of glucagon, is therefore mediated by oxygen free radicals a nd may signify cardiac and/or pulmonary injury or dysfunction. The act ions of these peptides may be relevant in the pathophysiological pertu rbation of intestinal ischaemia-reperfusion.