Mechanical stimulation is not responsible for activation of gastrointestinal afferents during ischemia.

Abdominal ischemia reflexly excites the cardiovascular system through activation of visceral sympathetic afferents. Although a number of ischemic metabolites are known to stimulate sympathetic afferents, the contribution of mechanical stimulation to activation of afferents during abdominal ischemia remains uncertain. Thus the present study examined the role of changes in motility in activation of gastrointestinal afferents during ischemia. Single-unit activity of C fiber afferents located on the stomach, duodenum, jejunum, or colon was recorded from the right sympathetic chain of anesthetized cats during 15 min of ischemia. Intraluminal pressure, as a reflection of local mechanical activity, was measured by an open catheter placed in the lumen of the gastrointestinal tract. The results show that gastrointestinal motility was mainly inhibited during abdominal ischemia. Changes in intraluminal pressure did not correlate with afferent discharge activity during ischemia (r = -0.32, n = 10). Furthermore, discharge frequency of gastrointestinal afferents during ischemia was not altered significantly by topical application of 100 micrograms/ml of atropine (3.98 +/- 0.62 to 3.83 +/- 0.59 imp/s, n = 12), which profoundly inhibited local gastrointestinal motility. Collectively, these data indicate that gastrointestinal motility changes during abdominal ischemia do not contribute to activation of gastrointestinal sympathetic C fiber afferents.

Role of summation of afferent input in cardiovascular reflexes from splanchnic nerve stimulation.

Stimulation of abdominal sympathetic visceral afferents reflexly excites the cardiovascular system. The present study examined the role of summation of afferent input in this reflex. Single-unit activity of A delta- and C-fiber afferents was recorded from the right thoracic sympathetic chain in anesthetized cats to determine the relationship between intensities of electrical stimulation and the types of nerve fibers within the right greater splanchnic nerve. The differential effect of cooling on A delta- and C-fiber axons in the sympathetic chain also was examined by recording single-unit afferent activity. Reflex cardiovascular responses were induced by electrical stimulation of the central cut end of the right greater splanchnic nerve. We observed that the numbers of A delta and C fibers activated by electrical stimulation were proportional to the intensity of stimulation. However, neither local cooling nor intensity of stimulation provided a means to separate A delta and C fibers contained in the sympathetic chain. The results demonstrate that the magnitude of excitatory cardiovascular reflexes is frequency dependent and is related directly to intensity of electrical stimulation, suggesting that both adequate discharge frequency of the afferent and sufficient numbers of afferents recruited are crucial factors for full expression of reflex cardiovascular responses.

Spatiotemporal aspects of sympathetic C-fiber afferent activity in pressor reflex during abdominal ischemia.

Activation of abdominal sympathetic visceral afferents during ischemia elicits excitatory cardiovascular reflexes. The present study examined the time course and discharge patterns of activation of ischemically sensitive sympathetic C-fiber afferents, and then the relationship between summated afferent activity and the pressor reflex induced by prolonged abdominal ischemia was determined. Single-unit activity of abdominal C-fiber afferents was recorded from the right thoracic sympathetic chain of anesthetized cats during 30 min of ischemia. The reflex pressor response to abdominal ischemia was induced by occlusion of celiac and superior mesenteric arteries. Of 68 C-fiber afferents studied, 36 (approximately 53%) were activated during 30 min of ischemia, whereas the activity of the remaining 32 were not altered. Onset latencies of 36 C-fiber afferents activated by ischemia ranged from 1.0 to 17.4 min with an average of 6.1 +/- 0.8 min. The majority of activated afferents manifested a bursting pattern of discharge activity as ischemia was prolonged beyond 10 min. Summated response of activated afferents, but not individual afferent activity, was related closely to the reflex pressor response during 30 min of ischemia. These results suggest that both recruitment of sufficient numbers of C-fiber afferents and adequate discharge frequency of afferents constitute an encoding mechanism for the pressor reflex during abdominal ischemia.