Endogenous histamine stimulates oschemicauy sensitive abdominal visceral afferents through h, receptors

Abdominal ischemia stimulates sympathetic visceral afférents to reflexly activate the cardiovascular system. Previous studies have shown that topical application of histamine to gastric wall causes reflex cardiovascular responses. Recently, it was found that histamine concentrations are increased in intestinal lymph and portal venous blood during briefly abdominal ischemia and reperfusion. The present study determined the role of endogenously produced histamine in activation of ischemically sensitive visceral afférents. Single-unit activity of abdominal visceral C-fiber afférents was recorded from the right thoracic sympathetic chain of anesthetized cats. Intra-arterial injection of histamine (30g/kg) increased discharge activity of 8 afférents (from 0.10 ±0.06 to 1.41+0.43 imp/s, p<0.01). Intra-arterial injection of 2-(3-Chlorophenyl) histamine (0,25 mg/kg), an H, receptor agonist, also increased discharge activity of these afférents from 0.13 ±0.04 to 0.69 ±0.19 imp/s (p<0.05). However, the H, receptor agonist, dimaprit (0.5 mg/kg, ia) did not alter significantly the impulse activity of these afférents (0.1 ±0.05 vs. 0.09+0.39 imp/s). Furthermore, intravenous injection of pyrilamine (0.2 mg/kg), an H, receptor antagonist, significantly attenuated the peak discharge activity of 6 other afférents during 10 min of abdominal ischemia from 0.73 + 0.30 to 0.24 + 0.05 imp/s, and eliminated the responses of 8 separate afférents to histamine. These data indicate that endogenous histamine contributes to the activation of ischemically sensitive abdominal afférents through stimulation of H₁ receptors.