RELEASE OF VASODILATOR, BUT NOT VASOCONSTRICTOR, NEUROPEPTIDES AND OFENTEROGLUCAGON BY INTESTINAL ISCHEMIA-REPERFUSION IN THE RAT

Reperfusion of ischaemic intestine is characterised by an initial hype raemia with ensuing mucosal repair. This study investigated possible r oles for gut vasoactive neuropeptides and trophic peptides in these ph enomena. Groups of rats were monitored during superior mesenteric arte ry occlusion for five or 20 minutes, with or without subsequent reperf usion for five minutes. Peptide concentrations (fmol/ml) in arterial b lood, were measured using specific radioimmunoassays. Intestinal ischa emia alone did not cause haemodynamic disturbance or peptide release. Reperfusion, after five minutes of ischaemia, resulted in arterial hyp otension and a rise in plasma vasoactive intestinal polypeptide (mean (SEM)) (37 (3), control 11 (4), p<0.001). After 20 minutes of ischaemi a, reperfusion resulted in greater hypotension (p<0.05) and release of both vasoactive intestinal polypeptide (31 (3), p<0.05 v control) and the more potent vasodilator beta-calcitonin gene related peptide (49 (3), control 23 (1), p<0.001). By contrast, the vasodilators alpha-cal citonin gene related peptide and substance P and the vasoconstrictors neuropeptide Y, peptide YY, and somatostatin were not released. Bombes in, a stimulatory neuropeptide, was released after 20 minutes of ischa emia/reperfusion (13 (2), control 7 (3), p<0.05). Plasma enteroglucago n rose from control (51 (4)) to 110 (16) (p<0.001) and to 158 (27) (p< 0.005) after five and 20 minutes of ischaemia/ reperfusion. The potent enteric vasodilators vasoactive intestinal polypeptide and beta-calci tonin gene related peptide, unopposed by vasoconstrictors, may promote post-ischaemic intestinal hyperaemia. The rise in plasma enteroglucag on may point to diffuse mucosal injury and is consistent with the puta tive trophic role of this peptide.