HYPOXIA DOES NOT DIRECTLY STIMULATE ISCHEMICALLY SENSITIVE ABDOMINAL VISCERAL AFFERENTS DURING ISCHEMIA

Abdominal ischemia activates ischemically sensitive sympathetic viscer al afferents and evokes reflex excitation of the cardiovascular system . These afferents respond to ischemic metabolites, including lactic ac id, bradykinin, prostaglandins, and reactive oxygen species. Severe hy poxemia also has been shown to activate these afferents. It is not kno wn, however, if the regional tissue hypoxia induced by abdominal ische mia directly or indirectly activates ischemically sensitive visceral a fferents. To determine the role of tissue hypoxia in activation of isc hemically sensitive abdominal afferents, continuous single-unit activi ty of ischemically sensitive abdominal sympathetic C-fiber afferents ( conduction velocity = 0.51-1.48 m/s) and regional tissue Po-2, measure d by a polarographic oxygen electrode in the porta hepatis, duodenum, or pancreas, were recorded simultaneously in anesthetized cats before and during 10-15 min of ischemia. Abdominal ischemia rapidly decreased regional tissue PO2 from 161 +/- 10 to 8 +/- 2 mmHg (P < 0.01) within an interval of 136 +/- 12 s. By contrast after longer latency (399 +/ - 24 s, P < 0.01 vs. PO2 interval), the activity of these afferents in creased from 0.06 +/- 0.01 to 0.33 +/- 0.07 imp/s (P < 0.01). Furtherm ore, the activity of ischemically sensitive afferents gradually increa sed throughout ischemia with peak activity (0.68 +/- 0.14 imp/s) occur ring at 600 +/- 39 s, although tissue PO2 remained constant. There was no correlation between the changes of tissue Pot and discharge activi ty of these afferents (r = -0.428, P = 0.144). These data suggest that tissue hypoxia induced by abdominal ischemia is not directly responsi ble for activation of ischemically sensitive sympathetic visceral affe rents but likely acts in an indirect fashion by promoting formation of other metabolic products capable of activating these nerve endings.