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F W Leung

Publications and source records attributed to F W Leung.

At least 19 recordsLinked to original sources
PubMed1995

Inhibition of endogenous nitric oxide reduces basal mesenteric vascular tone but does not alter intraduodenal hydrochloric acid-induced intestinal hyperemia in rats.

There are conflicting reports on the role of endogenous nitric oxide (NO) in the regulation of basal intestinal blood flow. The effect of inhibition of NO in intraduodenal hydrochloric acid (HCl) induced intestinal hyperemia remains to be confirmed. We investigated the effect of inhibition of endogenous NO on basal intestinal blood flow, HCl-induced intestinal hyperemia, and duodenal villous injury. Superior mesenteric artery blood flow in rats was measured by pulsed Doppler flowmetry and duodenal villous injury evaluated by histology. Intravenous NG-nitro-L-arginine methyl ester (L-NAME), or L-arginine or D-arginine followed by L-NAME, was given to show inhibition, reversal of inhibition of endogenous NO synthase, and stereospecificity, respectively. An intraduodenal 2 ml/kg bolus or perfusion for 30 min of 0.1 N HCl was given 15 min after L-NAME or vehicle. Mean arterial blood pressure was increased by L-NAME, which also significantly reduced intestinal blood flow under basal condition and after intraduodenal HCl. Basal mesenteric blood flow was not altered by L- or D- arginine. The L-NAME-induced increase in blood pressure and decrease in basal blood flow was attenuated by L- but not D-arginine. The villous damage and the magnitude of the peak hyperemia was unchanged by L-NAME, L- or D-arginine. Inhibition of endogenous NO by L-NAME is suggested by the significant rise in blood pressure. The rise in blood pressure and reduction in blood flow are attenuated by L- but not D-arginine, indicating stereospecificity. Inhibition of endogenous NO reduces basal mesenteric vascular tone but does not alter intraduodenal HCl-induced intestinal hyperemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Factors influencing reflectance spectrophotometric measurements of gastrointestinal mucosal blood flow.

Although the technique of endoscopic reflectance spectrophotometry has been applied in clinical studies, factors that modify the reproducibility of measurements have not been assessed systematically. To determine the limitations of the technique, measurements were made while endoscopic light intensity, systemic oxygen saturation, and orientation of the measuring probe were varied. The effects of hemorrhagic hypotension and exposure of the mucosa to 10% dextrose were also studied. When a large number (n = 480) of measurements in the human colon were considered, endoscopic light significantly decreased the index of oxygen saturation (ISO2) and increased the index of hemoglobin concentration (IHB). The decrease in ISO2, however, was small and unlikely to be of clinical importance despite being statistically significant. In one subject with chronic lung disease and baseline hypoxemia, administration of supplemental oxygen significantly increased oxygen saturation at the finger tip as measured by an oximeter and ISO2 of the buccal mucosa as measured by reflectance spectrophotometry. Varying the angle between the measuring probe and the gastric mucosa in rats from 90 degrees to 60 degrees did not affect ISO2 or IHB measurements. At 45 degrees, however, IHB but not ISO2 was significantly increased. Ischemia subsequent to induction of hemorrhagic hypotension and hyperemia induced by administration of 10% dextrose could be demonstrated reproducibly. We conclude that by lowering the intensity of endoscopic light and providing supplemental oxygen, errors in the measurement of IHB and ISO2, respectively, can be minimized. Minor deviations from the perpendicular orientation do not significantly affect ISO2 and IHB measurements. Attention to these details enhances the accuracy of endoscopic reflectance spectrophotometric recordings of ISO2 and IHB in clinical studies.

Animals↗
PubMed1995

Misoprostol reverses the inhibition of gastric hyperemia and aggravation of gastric damage by tobacco cigarette smoke in the rat.

BACKGROUND: Tobacco cigarette smoke attenuates injury-induced hyperemia, aggravates hypertonic saline-induced mucosal damage, inhibits ulcer margin hyperemia, and increases the size of the acetic acid-induced ulcer in the rat stomach. The inhibitory effect of tobacco cigarette smoke on gastric prostaglandin metabolism may be the basis for these observations. We have tested the hypothesis that exogenous prostaglandin (misoprostol) treatment will reverse these effects. METHODS: Rats with these two types of gastric injury were treated with tobacco cigarette smoke or breathed room air and were given intragastric misoprostol or vehicle. Gastric mucosal blood flow was measured by hydrogen gas clearance, and lesion score or ulcer size was measured by image analysis. RESULTS: Tobacco cigarette smoke attenuated the hyperemia and significantly aggravated the mucosal lesions and increased ulcer size. Treatment with intragastric misoprostol preserved the hyperemia and significantly attenuated the exacerbation of mucosal damage or increase in ulcer size produced by tobacco cigarette smoke. CONCLUSION: These data are consistent with the hypothesis that the attenuation of injury-induced or ulcer margin hyperemia by tobacco cigarette smoke is mediated by the inhibition of endogenous prostaglandins.

Acetates↗
PubMed1992

Superior mesenteric artery is more important than inferior mesenteric artery in maintaining colonic mucosal perfusion and integrity in rats.

Mucosal hemodynamics (by reflectance spectrophotometry) and mucosal damage (by histologic examination) following acute colonic ischemia were evaluated in different anatomic locations in the colon of anesthetized rats. The reflectance spectrophotometer provides an index of mucosal hemoglobin concentration (IHB) and an index of oxygen saturation of hemoglobin (ISO2). The patterns of ischemia without congestion (decreases IHB, decreases ISO2) during superior mesenteric artery occlusion, and ischemia with congestion (increases IHB, decreases ISO2) during portal vein occlusion, previously demonstrated in the stomach and duodenum, are also applicable to the colon. The significant linear correlations between changes (as percent of baseline) in IHB, ISO2, and hydrogen gas clearance suggest that changes in these indices are adequate indicators of changes in colonic mucosal perfusion. Superior mesenteric artery ligation produced significant reductions in both indices, and an increase in damage in the mucosa of the cecum, transverse colon, splenic flexure, and left colon, but not the rectum. Inferior mesenteric artery ligation produced only slight reduction in these indices and minimal damage only in the mucosa of the splenic flexure. These results support the hypothesis that the superior mesenteric artery is more important than the inferior mesenteric artery in maintaining colonic perfusion and colonic mucosal integrity in the rat.

Animals↗
PubMed1992

Intragastric nicotine protects against 40% ethanol-induced gastric mucosal injury despite pretreatment with propranolol or N-ethylmaleimide in rats.

We tested the hypotheses that the protective effect of intragastric nicotine against ethanol-induced gastric mucosal injury is dependent on propranolol- or N-ethylmaleimide-sensitive mechanisms. Propranolol was administered in doses (2 and 20 mg/kg) that provided dose-related blockade of beta-adrenoceptors (significant decreases in heart rate). N-Ethylmaleimide was administered in doses that previously had been shown to increase gastric vascular permeability (10 mg/kg) or inhibit gastric mucosal sulfhydryl compounds (50 mg/kg). At 0.5 hr after these or control subcutaneous pretreatments, the rats received intragastric nicotine (4 mg/kg) or vehicle. One hour later 40% ethanol was given intragastrically. The gastric corpus mucosal lesions were recorded by polaroid photographs after another hour, and their areas measured unbiasedly by computerized image analysis. The results showed that N-ethylmaleimide, but not propranolol, aggravated ethanol-induced gastric mucosal injury. The protective effect of intragastric nicotine was not modified by either pretreatment. We conclude that the mechanism mediating intragastric nicotine protection against 40% ethanol-induced gastric mucosal injury is independent of propranolol- or N-ethylmaleimide-sensitive mechanisms.

Animals↗
PubMed1992

Intragastric nicotine protection against 40% ethanol injury in rat stomach. Role of ganglionic stimulation or blockade.

Intragastric nicotine (4 mg/kg) protects against 40% ethanol-induced gastric mucosal injury and raises mean blood pressure. We postulated that this protective effect was mediated by the ganglionic stimulatory property of nicotine and therefore could be abolished by ganglionic blockers. Rats were pretreated with intraperitoneal hexamethonium (10 mg/kg) or mecamylamine (2 mg/kg) to block peripheral or central autonomic ganglia, respectively. Intragastric vehicle or nicotine (4 mg/kg) was then administered. The total lengths of the linear gastric corpus mucosal lesions induced by intragastric 40% ethanol were measured by an unbiased observer using a caliper. The results showed that both intraperitoneal hexamethonium and mecamylamine pretreatments protected against 40% ethanol-induced gastric mucosal injury. Neither modified the protective effect of intragastric nicotine. The protective effect of hexamethonium and mecamylamine was associated with a significant increase in the volume of gastric mucus and gastric juice. The increase in the volume of gastric content (mucus and juice) was partially responsible for the protective effect of these ganglionic blockers. In a separate experiment, intraperitoneal nicotine (4 mg/kg) also protected against 40% ethanol-induced gastric mucosal injury and raised mean blood pressure. These data indicate that the protection against 40% ethanol-induced gastric mucosal injury is not unique to intragastric nicotine. Such protection can be induced by ganglionic blocking doses of hexamethonium and mecamylamine, or a ganglionic stimulatory dose of intraperitoneally administered nicotine. Whether ganglionic stimulation or blockade plays a role in the mechanism of intragastric nicotine protection, however, remains to be determined.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Morphological and functional gastric cytoprotection by prostaglandin in rats receiving absolute ethanol orally.

Pretreatment with prostaglandins at non-antisecretory doses protects the gastric mucosa, including the parietal cells, from deep necrosis produced by intragastric administration of necrotising agents such as absolute ethanol. Whether the parietal cells also retained their ability to secrete acid when rats were pretreated with a prostaglandin, in spite of exposure to ethanol, was investigated. Gastric acid secretion was abolished 4 hours after ethanol, and secretion returned to control values only after 5-6 days. Pretreatment with a single, non-antisecretory dose of 16, 16-dimethyl prostaglandin E2 (dm PGE2) maintained acid secretion, in spite of exposure to absolute ethanol. Absolute ethanol caused histological changes - extensive gastric mucosal necrosis (through the muscularis mucosae), oedema, haemorrhages, polymorphonuclear infiltration, and formation of granulation tissue - that were maximal 24-48 hours after ethanol and persisted for 2 to 4 weeks. None of these changes were present in animals treated with the prostaglandin. It is concluded that a single oral pretreatment with dmPGE2 protects the gastric mucosa against not only the morphological damage of absolute ethanol (preventing necrosis, haemorrhages, and polymorphonuclear infiltration) but also the functional damage (maintaining the acid secretory function of parietal cells).

16,16-Dimethylprostaglandin E2↗
PubMed1992

Role of capsaicin-sensitive afferent nerves in mucosal injury and injury-induced hyperemia in rat colon.

Exposure of the colonic mucosa to 10% acetic acid results in ischemia and damage of the exposed mucosa and hyperemia in the adjacent unexposed and undamaged mucosa. We hypothesize that this hyperemia is mediated in part by capsaicin-sensitive afferent nerves, and absence of the hyperemia is associated with aggravation of damage in the exposed mucosa. In urethan-anesthetized rats, with the reflectance spectrophotometry probe in contact with the colonic mucosa, index of mucosal oxygen saturation (ISO2) was monitored before and for 5 min after 10% acetic acid was applied to the mucosa surrounding the measuring probe. Histological examination confirmed that the mucosa in contact with the measuring probe was undamaged, but the mucosa exposed to the 10% acetic acid was damaged. In the mucosa in contact with the reflectance spectrophotometry probe, a significant increase in ISO2 was observed in vehicle-pretreated rats, whereas a partial but significant reduction of such hyperemia was observed in capsaicin-pretreated rats. In the mucosa exposed to the 10% acetic acid, the depth of the mucosal lesion, but not the drop in ISO2, was significantly greater in the capsaicin-pretreated rats. The findings are consistent with the hypothesis that the colonic mucosal hyperemia in the undamaged mucosa adjacent to the mucosa damaged by the 10% acetic acid is mediated partially by capsaicin-sensitive afferent nerves. Attenuation of such hyperemia by capsaicin-pretreatment is associated with deeper mucosal damage, suggesting that the capsaicin-sensitive afferent nerves also contribute toward colonic mucosal protection against 10% acetic acid-induced injury in the exposed mucosa.

Acetates↗
PubMed1992

Regional differences in gut blood flow and mucosal damage in response to ischemia and reperfusion.

Ischemia and reperfusion of the small intestine and colon in rats were produced by reversible occlusion (for 30 min and 1 or 3 h) of the superior mesenteric artery and the aorta above the inferior mesenteric artery. Despite a greater reduction of mucosal perfusion in the colon than in the small intestine with 30 min of ischemia, the depth of mucosal damage was significantly smaller in the former than in the latter. Thirty minutes of ischemia followed by 1 h of reperfusion induced an increase in polymorphonuclear leukocyte infiltration in both locations. Exacerbation of mucosal injury occurred only in the small intestine, suggesting that reperfusion injury is independent of polymorphonuclear leukocyte infiltration. Reperfusion after 1 or 3 h of ischemia did not exacerbate mucosal damage in either location. Allopurinol significantly diminished the exacerbation of injury after reperfusion in the small intestine. The protective effect of allopurinol, however, was neither associated with an improvement in perfusion nor a reduction in polymorphonuclear leukocyte infiltration. These data indicate that there is a window (30 min) of reperfusion injury in the small intestine, but there is no evidence of reperfusion injury in the colon.

Allopurinol↗
PubMed1992

Modulation of autoregulatory escape by capsaicin-sensitive afferent nerves in rat stomach.

Visceral C fibers are stimulated by ischemia and hypoxia, which can be produced by intense vasoconstriction. Epinephrine applied to the gastric submucosa produces a marked vasoconstriction followed by autoregulatory escape. We hypothesize that the autoregulatory escape from epinephrine-induced vasoconstriction in the rat stomach is mediated partly by capsaicin-sensitive C fibers. Functional ablation of these afferent fibers by high-dose systemic capsaicin pretreatment will significantly reduce the magnitude of the autoregulatory escape. Rats received capsaicin (125 mg/kg sc) 10 days before blood flow studies to produce functional impairment of the capsaicin-sensitive afferent nerves. Control rats received vehicle. Under urethan anesthesia, a small area (2 mm diam) of the serosa from the anterior gastric wall was removed to expose the submucosa. The tip of a side-viewing laser-Doppler flow probe was placed inside the stomach directly beneath the exposed submucosa. At 20-min intervals, 20 microliters of buffer, 5 x 10(-4) M epinephrine, 1.6 x 10(-4) M capsaicin, or 3.3 x 10(-2) M histamine was applied topically to the exposed submucosa, with saline washes between applications at 10 min after each application. Blood pressure and laser-Doppler flow signals were monitored continuously. The escape index during the period of epinephrine application was significantly lower in the capsaicin-pretreated rats (0.239 +/- 0.046) than in the vehicle-pretreated rats (0.474 +/- 0.079). Functional ablation of the capsaicin-sensitive afferent fibers was confirmed by a significant blockade of the vasodilatation induced by topical capsaicin. Histamine-induced vasodilatation was unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1992

Pancreatic blood flow in cats with chronic pancreatitis.

Pancreatic blood flow and its relationship to pancreatic interstitial pressure were investigated in a model of chronic pancreatitis in cats using a hydrogen gas-clearance technique with an intraductal electrode. The intraductal technique correlated well with blood flow measurements made using gamma-labeled microspheres (r = 0.88, P less than 0.001). In control cats, the basal blood flow of 69.1 +/- 9.5 mL.min-1.100 g-1 increased by 25% to 86.2 +/- 11 mL.min-1.100 g-1 with secretory stimulation (P less than 0.05). Interstitial pressure was -0.02 +/- 0.3 mm Hg and did not change significantly with stimulation. In cats with chronic pancreatitis, basal interstitial pressure was 1.8 +/- 0.5 mm Hg and basal blood flow 39.9 +/- 4 mL.min-1.100 g-1 (P less than 0.05). Stimulation of the chronic pancreatitis gland increased the pressure to 3.0 +/- 0.4 mm Hg (P less than 0.01) and reduced flow 15% to 34.2 +/- 4 mL.min-1.100 g-1 (P less than 0.05). Papaverine increased blood flow in control and chronic pancreatitis cats without altering tissue pressure, suggesting that despite the reduced basal blood flow, the ability to increase blood flow was preserved in chronic pancreatitis. The increased interstitial pressure associated with secretion appeared to limit the gland's normal hyperemic response in this model of chronic pancreatitis.

Animals↗
PubMed1991

Mechanism of intragastric nicotine protection against ethanol-induced gastric injury.

To elucidate the mechanism of intragastric nicotine protection against ethanol-induced gastric mucosal injury seen in a previous report and in our preliminary study, the following studies were performed. Rats were pretreated with naloxone (8 mg/kg intraperitoneal, 0.5 hr prior to study) to block opiate receptors; or capsaicin (125 mg/kg subcutaneous 10 days prior to study) to denervate the afferent sensory fibers; or indomethacin (2.5 mg/kg intragastric or 5 mg/kg subcutaneous, 1 hr prior to study) to inhibit endogenous prostaglandin synthesis. At 1-hr intervals, nicotine (4 mg/kg) or vehicle and 40% ethanol were then given intragastrically. Total gastric corpus mucosal lesion length was measured unbiasedly. In separate studies, gastric mucosal blood flow (GMBF) was assessed by hydrogen gas clearance before and after intragastric nicotine or vehicle; luminal mucus volume, gastric juice volume, and acid output were measured 1 hr after either intragastric nicotine or vehicle administration. The results showed that the acute protective effect of intragastric nicotine was associated with a significantly larger luminal mucus volume. It was not blocked by naloxone, capsaicin, or indomethacin. There was no increase in GMBF. The larger gastric residual volume did not account for the protection. We conclude that the mechanism mediating nicotine protection is unique and is independent of opiate receptors, capsaicin-sensitive afferent sensory nerve fibers, endogenous prostaglandin generation, or dilution of the injurious agent. The increase in luminal gastric mucus volume may contribute to the protective effect of intragastric nicotine against gastric mucosal injury produced by 40% ethanol.

Animals↗
PubMed1991

Mucosal vascular stasis precedes loss of viability of endothelial cells in rat acetic acid colitis.

The hypothesis that a significant reduction in colonic mucosal perfusion, and hence ischemic injury, precedes the development of mucosal ulceration and inflammation is tested in this report. The microcirculatory changes in the rat colonic mucosa within 1 hr of topical exposure to 10% acetic acid were assessed. Colonic mucosal blood flow signals measured by laser Doppler flowmetry were significantly reduced to 61 +/- 8, 52 +/- 10, and 37 +/- 13% (mean +/- SEM) of baseline values at 1 min, 4 min, and 10 min after the colonic mucosa was exposed to 10% acetic acid, respectively, but not in controls exposed to saline. After the start of application of 10% acetic acid (for 4 min), in vivo microscopy studies demonstrated that colonic mucosal ischemia (stasis of the red blood cells in the mucosal capillaries) occurred at 9 +/- 5 min (mean +/- SEM). Evidence of endothelial cell death (failure to exclude a fluorescent dye, propidium iodide, by endothelial cells) developed at 25 +/- 10 min (mean +/- SEM). These findings indicate that within minutes after contact of the colonic mucosa with 10% acetic acid, colonic mucosal ischemia develops, followed shortly by death of endothelial cells. The data do not establish a cause-and-effect relationship between the reductions in mucosal blood flow and loss of endothelial cell viability in response to acetic acid. Nevertheless, because these events occur at such an early time point, they may play a pathogenetic role in the development of the subsequent inflammatory and ulcerative changes in this animal model of colitis. Further studies to define the potential causal relationships between these parameters are warranted.

Acetates↗
PubMed1991

Role of blood flow and alkaline secretion in acid-induced deep duodenal villous injury in rats.

The effect of 16,16-dimethylprostaglandin E2 (dmPGE2) and corticotropin-releasing factor (CRF) on duodenal blood flow, alkaline secretion, and acid-induced deep duodenal villous injury was studied. The duodena of anesthetized rats were prepared for simultaneous measurement of alkaline secretion by back titration, and blood flow by hydrogen gas clearance; or for perfusion with 0.1 N HCl and histological examination of villous injury. The results revealed that the dmPGE2-induced increase in basal alkaline secretion (due solely to an increase in the volume of secretion) appears to be a better predictor of protection against exogenous acid-induced deep duodenal villous injury than rise in duodenal blood flow, since CRF induces a similar rise in duodenal blood flow but does not enhance alkaline secretion or reduce acid-induced villous damage. The absence of a greater loss of H+ during acid perfusion of the duodenum in the dmPGE2-treated rats, however, suggests that the mechanism of the dmPGE2 protection against acid-induced deep duodenal villous injury cannot be explained entirely by its ability to increase basal duodenal alkaline secretion.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Mechanism of aggravation of mucosal injury by intravenous nicotine in rat stomach.

Endogenous prostaglandins and injury-induced hyperemia are important defense mechanisms in the gastric mucosa. In the rat stomach, we tested the hypotheses that an ulcer-promoting dose of intravenous nicotine 1) reduces ex vivo prostaglandin generation and 2) aggravates mucosal lesions by impairing injury-induced hyperemia. Anesthetized rats were given intravenous control or 4 or 40 micrograms.kg-1.min-1 nicotine infusion. In study 1, ex vivo generation of prostaglandin E2 and 6-ketoprostaglandin F1 alpha (stable metabolite of prostacyclin) was determined by vortexing the mucosal tissue, followed by radioimmunoassay. No significant difference in prostaglandin generation was found between the control and experimental groups. In study 2, intravenous nicotine (40 micrograms.kg-1.min-1) produced a significant rise (19 +/- 3%) in mean blood pressure and completely abolished the gastric hyperemia produced by intragastric saline (2 M). The extent of the associated gastric mucosal injury was significantly increased (from 5.3 +/- 0.8 to 17.4 +/- 5.2% of the corpus mucosa), while the maximum depth of the largest lesions was not affected by intravenous nicotine. The data confirm that the gastric hyperemia associated with gastric mucosal exposure to hypertonic saline plays an important role in limiting the extent of gastric mucosal damage. We conclude that in the rat stomach 1) an ulcer-promoting dose of intravenous nicotine does not significantly inhibit cyclooxygenase activity, and 2) the same does of intravenous nicotine exacerbates hypertonic saline-induced gastric mucosal injury by a mechanism that involves inhibition of injury-induced hyperemia.

6-Ketoprostaglandin F1 alpha↗
PubMed1990

Effect of submucosal epinephrine injection on local gastric blood flow. A study using laser Doppler flowmetry and reflectance spectrophotometry.

Clinical studies have demonstrated the efficacy of submucosal epinephrine injection in the control of bleeding ulcers. Since endoscopic techniques for assessing gastroduodenal blood flow are limited, we employed an animal model to study the mechanism of control of bleeding. The effect of submucosal epinephrine injection on local gastric blood flow was studied in the rat using laser Doppler flowmetry and reflectance spectrophotometry. Submucosal injection of 0.1 ml of 1/10,000 epinephrine caused a significantly greater drop in local gastric blood flow (laser Doppler flowmetry) compared with vehicle (10% sodium metabisulfite) injection. The reduction persisted for up to 120 min. This vasoconstrictive effect of epinephrine was confirmed by observations with reflectance spectrophotometry, which documented a pattern of ischemia without congestion (lower index of hemoglobin concentration, lower index of oxygen saturation). The autoregulatory escape from adrenergic vasoconstriction was not evident in either instance. We conclude that, after submucosal injection of epinephrine, the absence of autoregulatory escape from adrenergic vasoconstriction and the marked and prolonged decrease in local gastric blood flow enhance the homeostatic mechanisms (eg, platelets and other coagulative factors) to effect hemostasis in bleeding ulcers.

Animals↗
PubMed1990

Capsaicin-sensitive afferent fibers contribute to gastric mucosal blood flow response to electrical vagal stimulation.

Electrical stimulation of the peripheral vagus produces a noncholinergic increase in gastric mucosal blood flow (GMBF) via unknown mechanisms. The purpose of this study was 1) to investigate whether a portion of the increase in GMBF during prolonged electrical vagal stimulation involves a mechanism separate from augmented acid secretion and 2) to determine whether antidromic activation of afferent fibers contributes to the vascular or secretory responses to electrical vagal stimulation. Electrical vagal stimulation (40 V, 6 Hz, 2 ms) applied for 30 min to the distal cut end of the subdiaphragmatic ventral vagus significantly increased gastric acid secretion and GMBF measured by hydrogen gas clearance. Atropine (0.15 mg/kg iv) or omeprazole (10 mumol/kg iv) completely abolished the secretory response to electrical vagal stimulation, while a significant increase in GMBF remained. Pretreatment with perineural application of the sensory neurotoxin capsaicin to both cervical vagi significantly reduced by 48% the increase in GMBF but not gastric acid secretion; atropine completely abolished the remaining vascular response in capsaicin-treated rats. These results suggest that prolonged electrical vagal stimulation induces a sustained increase in GMBF partially independent of augmented acid secretion and that the noncholinergic portion of the vascular response is mediated by capsaicin-sensitive vagal afferent fibers.

Afferent Pathways↗