Laser-Doppler, H2 clearance, and microsphere estimates of mucosal blood flow

Kvietys, Peter R.; Shepherd, A. P.; Granger, D. Neil

doi:10.1152/ajpgi.1985.249.2.g221

Cited by 85 publications

(60 citation statements)

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“…The nature of the Doppler shift from an illuminated tissue depends on the velocity and number of moving red blood cells (31). The accuracy of the LaserDoppler flowmetry technique for gastrointestinal applications was described earlier (32,33). The laser probe was fixed to a micromanipulator and kept at a distance of 0.5-1 mm from the gastric mucosa in the chamber solution.…”

Section: Methodsmentioning

confidence: 99%

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Björne¹,

Petersson²,

Phillipson³

et al. 2004

J. Clin. Invest.

206

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Salivary nitrate from dietary or endogenous sources is reduced to nitrite by oral bacteria. In the acidic stomach, nitrite is further reduced to NO and related compounds, which have potential biological activity. We used an in vivo rat model as a bioassay to test effects of human saliva on gastric mucosal blood flow and mucus thickness. Gastric mucosal blood flow and mucus thickness were measured after topical administration of human saliva in HCl. The saliva was collected either after fasting (low in nitrite) or after ingestion of sodium nitrate (high in nitrite). In additional experiments, saliva was exchanged for sodium nitrite at different doses. Mucosal blood flow was increased after luminal application of nitrite-rich saliva, whereas fasting saliva had no effects. Also, mucus thickness increased in response to nitrite-rich saliva. The effects of nitrite-rich saliva were similar to those of topically applied sodium nitrite. Nitrite-mediated effects were associated with generation of NO and S-nitrosothiols. In addition, pretreatment with an inhibitor of guanylyl cyclase markedly inhibited nitrite-mediated effects on blood flow. We conclude that nitrite-containing human saliva given luminally increases gastric mucosal blood flow and mucus thickness in the rat. These effects are likely mediated through nonenzymatic generation of NO via activation of guanylyl cyclase. This supports a gastroprotective role of salivary nitrate/nitrite.

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Section: Methodsmentioning

confidence: 99%

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Björne¹,

Petersson²,

Phillipson³

et al. 2004

J. Clin. Invest.

206

View full text Add to dashboard Cite

show abstract

“…The blood flow was recorded continuously from the mucosal side of the gastric mucosa, with a probe fixed to a micromanipulator and kept at a distance of 0.5-1 mm above the surface of the mucosa, in the solution. This technique for measuring the gastric mucosal blood flow with laser-Doppler flowmetry has been well evaluated previously (25,29).…”

Section: Mucosal Blood Flowmentioning

confidence: 99%

Dietary nitrate increases gastric mucosal blood flow and mucosal defense

Petersson

Phillipson²,

Jansson³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

130

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Salivary nitrate from dietary or endogenous sources is reduced to nitrite by oral bacteria. In the acidic stomach, nitrite is further reduced to bioactive nitrogen oxides, including nitric oxide (NO). In this study, we investigated the gastroprotective role of nitrate intake and of luminally applied nitrite against provocation with diclofenac and taurocholate. Mucosal permeability ( 51 Cr-EDTA clearance) and gastric mucosal blood flow (laser-Doppler flowmetry) were measured in anesthetized rats, either pretreated with nitrate in the drinking water or given acidified nitrite luminally. Diclofenac was given intravenously and taurocholate luminally to challenge the gastric mucosa. Luminal NO content and nitrite content in the gastric mucus were determined by chemiluminescence. The effect of luminal administration of acidified nitrite on the mucosal blood flow was also investigated in endothelial nitric oxide synthasedeficient mice. Rats pretreated with nitrate or given nitrite luminally had higher gastric mucosal blood flow than controls. Permeability increased more during the provocation in the controls than in the nitrate-and nitrite-treated animals. Dietary nitrate increased luminal NO levels 50 times compared with controls. Nitrate intake also resulted in nitrite accumulation in the loosely adherent mucous layer; after removal of this mucous layer, blood flow was reduced. Nitrite administrated luminally in endothelial nitric oxide synthase-deficient mice increased mucosal blood flow. We conclude that dietary nitrate and direct luminal application of acidified nitrite decrease diclofenacand taurocholate-induced mucosal damage. The gastroprotective effect likely involves a higher mucosal blood flow caused by nonenzymatic NO production. These data suggest an important physiological role of nitrate in the diet. laser-Doppler flowmetry;51 chromium-labeled EDTA clearance; nitrite; rats; endothelial nitric oxide synthase deficient; gastric mucus THE ROLE OF NITRATE IN OUR diet has been a subject of great controversy over the years. The anxiety concerning nitrate consumption is related to the presumed association with gastrointestinal cancer. Today, however, there are more studies contradicting than supporting such a correlation (36). Several recent studies have in fact suggested that dietary nitrate has a gastroprotective role (6,16,31,32,35,38). Most of the nitrate in our diet originates from green leafy vegetables, a natural source of food for humans. Bacteria in the oral cavity reduce parts of the nitrate to nitrite, and human saliva therefore contains both of these anions (49). A large amount of nitric oxide (NO) is produced in the upper gut when swallowed nitrite reacts with hydrogen ions (6,35,37).

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“…The laser Doppler technique has been widely used to estimate gastrointestinal mucosal perfusion [7, 19, 20, 21, 22]. After the patient fasted overnight, we performed a routine endoscopic examination and measured the gastric mucosal blood flow (GMBF) by passing the endoscopic probe (PF-309; Perimed, Stockholm, Sweden) of the laser Doppler flowmeter (Periflux PF-3; Perimed) through the biopsy channel of the fiberscope.…”

Section: Methodsmentioning

confidence: 99%

Role of Vascular Endothelial Growth Factor in Portal Hypertensive Gastropathy

Tsugawa¹,

Hashizume

Migou³

et al. 2000

Digestion

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Background and Aims: Portal hypertensive gastropathy (PHG) is now recognized as a distinct entity; however, the angiogenesis in the portal hypertensive gastric mucosa has yet to be elucidated. Vascular endothelial growth factor (VEGF) is a potent angiogenic factor involved in both physiological and pathological angiogenesis. The aim of this study was thus to examine the function of VEGF in the portal hypertensive and non-portal hypertensive gastric mucosa. Method: Forty-five cirrhotic patients were divided into 3 groups as follows. Group I included 15 patients without PHG who were treated with 1.5 g teprenone/day for 8 weeks: PHG(–)-t. Group II included 15 patients with PHG who were not treated with teprenone: PHG(+)-n. Group III included 15 patients with PHG who were treated with teprenone for 8 weeks: PGH(+)-t. The gastric mucosal blood flow (GMBF), the concentration of gastric mucosal VEGF and hexosamine and the endoscopic findings were studied both before and after medication. Results: Before teprenone treatment, the GMBF in the antrum, fundus, fornix were significantly higher in PHG(+)-n than PHG(–)-t. After treatment, the GMBF in the fundus and fornix significantly decreased more than before treatment in the PHG(+)-t. After treatment, the GMBF in the antrum increased significantly more than before treatment in PHG(–)-t. The gastric VEGF and hexoxamine concentration in the antrum were significantly higher in PHG(+)-n than in PHG(–)-t. After treatment, the gastric VEGF and hexosamine concentration in the antrum significantly decreased in PHG(+)-t while no change in concentration was recognized in PHG(+)-n. In the endoscopic findings, a decrease in the PHG score was recognized in 2 patients in PHG(+)-t. Conclusion: Portal hypertensive gastric mucosal change was thus found to trigger a high concentration of VEGF and hexosamine. Such increased activity of VEGF and hexosamine may thus account for the presence of active congestion in PHG.

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Laser-Doppler, H2 clearance, and microsphere estimates of mucosal blood flow

Cited by 85 publications

References 0 publications

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Nitrite in saliva increases gastric mucosal blood flow and mucus thickness

Dietary nitrate increases gastric mucosal blood flow and mucosal defense

Role of Vascular Endothelial Growth Factor in Portal Hypertensive Gastropathy

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