tetrodotoxin and Dilatation--Pathologic

Noxious stimuli that are applied to different somatic sites interact; often one stimulus diminishes the sensation elicited from another site. By contrast, inhibitory interactions between visceral stimuli are not well documented. We investigated the interaction between the effects of noxious distension of the colorectum and noxious stimuli applied to the jejunum, in the rat. Colorectal distension elicited a visceromotor reflex, which was quantified using electromyographic (EMG) recordings from the external oblique muscle of the upper abdomen. The same motor units were activated when a strong pinch was applied to the flank skin. Distension of the jejunum did not provoke an EMG response at this site, but when it was applied during colorectal distension it blocked the EMG response. Jejunal distension also inhibited the response to noxious skin pinch. The inhibition of the visceromotor response to colorectal distension was prevented by local application of tetrodotoxin to the jejunum, and was markedly reduced when nicardipine was infused into the local jejunal circulation. Chronic sub-diaphragmatic vagotomy had no effect on the colorectal distension-induced EMG activity or its inhibition by jejunal distension. The nicotinic antagonist hexamethonium suppressed phasic contractile activity in the jejunum, had only a small effect on the inhibition of visceromotor response by jejunal distension. It is concluded that signals that arise from skin pinch and colorectal distension converge in the central nervous system with pathways that are activated by jejunal spinal afferents; the jejunal signals strongly inhibit the abdominal motor activity evoked by noxious stimuli.

Topics: Abdominal Muscles; Afferent Pathways; Analgesia; Animals; Calcium Channel Blockers; Calcium Channels, L-Type; Catheterization; Colon; Dilatation, Pathologic; Electromyography; Hexamethonium; Jejunum; Male; Nicardipine; Nicotinic Antagonists; Nociceptors; Pain; Pressure; Rats; Rats, Sprague-Dawley; Rectum; Skin; Sodium Channel Blockers; Spinal Cord; Tetrodotoxin; Transducers, Pressure; Vagotomy

The purpose of this study was to examine the electrical and mechanical responses of cat middle cerebral arteries to electrical stimulation of the adventitial vs. intimal surface of the vessels and to determine the responses as a function of transmural pressure. Middle cerebral arteries were cannulated at both ends. Within each cannula was a stimulating electrode. Electrical stimulation (0.5-msec square current pulses at 0.5 Hz yielding 160 microA of current between electrodes) resulted in significant reduction in diameter that was greater at both 40 and 80 mm Hg vs. 100 or 140 mm Hg. Conversely, adventitial stimulation of perivascular nerves with transmural platinum stimulating electrodes resulted in significant vasodilation. The constrictor response to intimal stimulation, as well as the dilatory response to adventitial stimulation, was blocked by tetrodotoxin. The constrictor response to luminal stimulation was enhanced by scorpion toxin demonstrating a functional role for tissues containing fast Na+ channels. Perfusion with collagenase to disrupt the endothelium also abolished the constrictor response to luminal stimulation. The divergence of responses between adventitial and luminal surface stimulation may suggest that different cell layers within a blood vessel serve different functions, one to increase resistance and another to decrease resistance. For example, in cat middle cerebral arteries, the adventitial nerves (i.e., via reflexes) may increase flow, while blood-borne substances may mediate release of agents that reduce flow.

Topics: Animals; Biomechanical Phenomena; Cats; Cell Membrane; Cerebral Arteries; Dilatation, Pathologic; Electric Stimulation; Endothelium; Female; Male; Membrane Potentials; Muscle, Smooth, Vascular; Phentolamine; Pressure; Tetrodotoxin; Vasoconstriction