BRIEF MESENTERIC ISCHEMIA INCREASES PGE(2), BUT NOT PGI(2), IN INTESTINAL LYMPH OF CATS

Mesenteric ischemia of short duration (5-10 min) can stimulate A delta - and C-fiber afferent nerve endings in the viscera to reflexly activa te the cardiovascular system. The mechanism of activation of abdominal visceral afferents is probably multifactorial and may involve prostag landins (PGs), which have been shown to directly stimulate and/or sens itize visceral afferents when administered exogenously. We hypothesize d that brief visceral ischemia is accompanied by release of PGI(2) and PGE(2) into the interstitium, where these cyclooxygenase products cou ld stimulate or sensitize visceral afferent nerve endings. Accordingly , we measured immunoreactive PGE(2) (iPGE(2)) and 6-keto-PGF(1 alpha) (i6-keto-PGF(1 alpha), the stable metabolite of PGI(2), in lymph drain ing the ischemic viscera as well as in portal venous blood. An intesti nal lymph duct distal to the lymph node was cannulated in pentobarbita l sodium-anesthetized cats. Lymph and plasma iPGE(2) and i6-keto-PGF(1 alpha), concentrations were measured by radioimmunoassay before, duri ng, and immediately after a 5- to 10-min occlusion of the descending a orta. The i6-keto-PGF(1 alpha), concentration increased significantly (P < 0.001) in portal venous plasma (61 +/- 12 to 107 +/- 18 pg/0.1 ml ; n = 14) but not in lymph (148 +/- 30 to 159 +/- 24 pg/0.1 ml; n = 16 ). In contrast, iPGE(2) concentration was significantly (P < 0.01) ele vated in both venous plasma (156 +/- 16 to 207 +/- 26 pg/0.1 ml; n = 1 9) and lymph (520 +/- 48 to 590 ir 52 pg/0.1 mi; n = 20). The increase in PGI(2) concentration in venous plasma but not in lymph suggests th at there is endothelial release of PGI(2) into the circulation during ischemia and that this prostanoid may not play an important role in st imulating nerve endings located in the interstitium. An ischemia-induc ed elevation of interstitial PGE(2) concentration, however, suggests t hat this PG is an important factor in the stimulation of visceral affe rents during brief ischemia.