Hypoxia does not directly stimulate ischemically sensitive abdominal visceral afferents during ischemia

Abdominal ischemia activates ischemically sensitive sympathetic visceral afferents and evokes reflex excitation of the cardiovascular system. These afferents respond to ischemic metabolites, including lactic acid, bradykinin, prostaglandins, and reactive oxygen species. Severe hypoxemia also has been shown to activate these afferents. It is not known, however, if the regional tissue hypoxia induced by abdominal ischemia directly or indirectly activates ischemically sensitive visceral afferents. To determine the role of tissue hypoxia in activation of ischemically sensitive abdominal afferents, continuous single-unit activity of ischemically sensitive abdominal sympathetic C-fiber afferents (conduction velocity = 0.51-1.48 m/s) and regional tissue PO2, measured 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 increased from 0.06 +/- 0.01 to 0.33 +/- 0.07 imp/s (P < 0.01). Furthermore, the activity of ischemically sensitive afferents gradually increased throughout ischemia with peak activity (0.68 +/- 0.14 imp/s) occurring at 600 +/- 39 s, although tissue PO2 remained constant. There was no correlation between the changes of tissue PO2 and discharge activity of these afferents (r = -0.428, P = 0.144). These data suggest that tissue hypoxia induced by abdominal ischemia is not directly responsible for activation of ischemically sensitive sympathetic visceral afferents but likely acts in an indirect fashion by promoting formation of other metabolic products capable of activating these nerve endings.