Reflectance spectrophotometry for the assessment of gastroduodenal mucosal perfusion

Leung, Felix W.; Morishita, Tetsuo; Livingston, Edward H.; Reedy, Terry J.; Guth, Paul H.

doi:10.1152/ajpgi.1987.252.6.g797

Cited by 60 publications

(37 citation statements)

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“…The mHbO 2 values reported are the means of the last 5 min (150 spectra, 2 s each) of the respective intervention under steady state conditions. This method allows detection of splanchnic ischemia with similar precision as laser flowmetry (Leung et al 1987), intra-vital microscopy (Bellamy et al 1997), or hydrogen gas clearance (Machens et al 1995). The non-traumatic instrumentation and in particular nontraumatic access to the gastric mucosa allows the determination of mucosal oxygenation in the absence of surgical stress.…”

Section: Measurementsmentioning

confidence: 99%

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vollmer

Schwartges

Naber

et al. 2013

Journal of Endocrinology

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Hypercapnia (HC) improves systemic oxygen delivery (DO 2 ) and microvascular hemoglobin oxygenation of the mucosa (mHbO 2 ). Simultaneously, HC increases plasma levels of vasopressin. Although vasopressin is generally regarded a potent vasoconstrictor particularly in the splanchnic region, its effects on splanchnic microcirculation during HC is unclear. The aim of this study was to evaluate the role of endogenous vasopressin on gastric mucosal oxygenation and hemodynamic variables during physiological (normocapnia) and hypercapnic conditions. Five dogs were repeatedly anesthetized to study the effect of vasopressin V 1A receptor blockade ([Pmp 1 ,Tyr(Me) 2 ]-Arg 8 -Vasopressin, 35 mg/kg) on hemodynamic variables and mHbO 2 during normocapnia or HC (end-tidal CO 2 70 mmHg). In a control group, animals were subjected to HC alone. mHbO 2 was measured by reflectance spectrophotometry, systemic DO 2 was calculated from intermittent blood gas analysis, and cardiac output was measured by transpulmonary thermodilution. Data are presented as meanGS.E.M. for nZ5 animals. During HC alone, DO 2 increased from 12G1 to 16G1 ml/kg per min and mHbO 2 from 70G4 to 80G2%. By contrast, additional vasopressin V 1A receptor blockade abolished the increase in mHbO 2 (80G2 vs 69G2%) without altering the increase in DO 2 (16G1 vs 19G 2 ml/kg per min). Vasopressin V 1A receptor blockade (VB) during normocapnia neither affected DO 2 (13G1 vs 14G1 ml/kg per min) nor mHbO 2 (75G3 vs 71G5%). Vasopressin V 1A receptor blockade abolished the increase in mHbO 2 during HC independent of DO 2 . Thus, in contrast to its generally vasoconstrictive properties, the vasopressin V 1A receptors seem to mediate the increase in gastric microcirculatory mucosal oxygenation induced by acute HC.

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Section: Measurementsmentioning

confidence: 99%

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vollmer

Schwartges

Naber

et al. 2013

Journal of Endocrinology

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“…38 On the other hand, despite raising systemic blood pressure to the same extent as in the rats with PPVL, glybenclamide did not alter portal pressure in rats with SO. The observation suggests that K ϩ ATP channels play a role in regulating portal pressure possibly only in the presence of a stimulus to elevate portal pressure, e.g., after PPVL, which produces ischemia with congestion in the gastric mucosa 39 and reduces perfusion to the liver initially. We speculate that the hypoxic stimulus to both the stomach and liver triggers the opening of K ϩ ATP channels.…”

Section: Discussionmentioning

confidence: 99%

Potassium channels participate in gastric mucosal protection in rats with partial portal vein ligation

Tsui

Sung

et al. 1998

Hepatology

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Glybenclamide, an adenosine triphosphate-dependent potassium (K ؉ ATP ) channel blocker, lowered portal pressure and attenuated the hyperdynamic splanchnic circulation in rats with partial portal vein ligation (PPVL). The purpose of this report was to confirm these observations and to test the hypothesis that glybenclamide could reduce acidified ethanol-induced gastric mucosal injury in rats with PPVL. Gastric mucosal blood flow (hydrogen gas clearance), systemic blood pressure, and portal pressure were monitored in rats with PPVL or sham operation (SO). Intravenous glybenclamide (20 mg/kg) or vehicle was administered, followed by intragastric acidified ethanol (0.15 N HCl and 15% ethanol). The area of gastric mucosal lesions was assessed by image analysis. In contrast to published findings, there was no significant elevation of portal pressure after glybenclamide administration in rats with PPVL. Glybenclamide did not alter the gastric mucosal hyperemia in these rats. Glybenclamide significantly increased mucosal injury. The data are consistent with the hypothesis that K ؉ ATP channels play a role in protecting the gastric mucosa in rats with PPVL. (HEPATOLOGY 1998;27:1530-1535.)In rats with portal hypertension induced by partial portal vein ligation (PPVL), [1][2][3][4][5][6][7][8][9][10][11][12][13][14] there is an increase in splanchnic blood flow, 1,5,15 including gastric mucosal blood flow. 8,13,16 Reduction of the elevated portal pressure by ␤-adrenoceptor antagonists 1,10 in these rats is associated with a decrease in ethanol-induced gastric mucosal damage. 10 The observation suggests that lowering of the elevated portal pressure may be a marker of decreased susceptibility of the gastric mucosa to noxious damage in rats with PPVL. One report described preliminary data that glybenclamide, an inhibitor of adenosine triphosphate-dependent potassium (K ϩ ATP ) channels, reduced portal pressure, portal tributary blood flow, and hepatic arterial blood flow, and increased portal territory and hepatic arterial vascular resistance in rats with PPVL. 5 The reproducibility of these observations has not been confirmed. If the increased gastric perfusion and elevated portal pressure in rats with PPVL play a role in modulating the susceptibility of the gastric mucosa to noxious damage, attenuation of such changes, as suggested by results of infusing ␤-adrenoceptor antagonist, 10 should lead to a change in the resistance of the mucosa to damage. We tested the hypothesis that glybenclamide, an inhibitor of K ϩ ATP channels, could attenuate gastric mucosal injury produced by intragastric acidified ethanol in rats with PPVL. MATERIALS AND METHODSAnimal Preparation. Male Sprague-Dawley rats weighing 220 to 300 g were kept in a room with controlled temperature of 23°C and humidity. They were fed laboratory rodent diet 5001 (Purina Mills Inc., St. Louis, MO) and tap water. After an overnight fast, rats of comparable weights were randomized to undergo PPVL or sham operation (SO). They were anesthetized with intraperitoneal pe...

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“…With this system, the largest values of IHb and ISO2 can be obtained be cause the pressure on the gastric mucosal capillaries by the sensor tip decreases IHb and ISO2; and when the tip of the sensor does not touch the gastric mucosa, the reading of IHb and ISO2 decreases. Using the reflect ance spectrophotometry system, Leung et al reported that IHb increased and ISO2 decreased when the portal vein was ligated, and IHb and ISO2 decreased when the celiac artery was occluded in anesthetized rats (14). The former therefore indicated mucosal congestion and the latter indicated ischemia.…”

Section: Discussionmentioning

confidence: 99%

Cetraxate Improves Ethanol-Induced Gastric Mucosal Congestion in Anesthetized Dogs.

et al. 1992

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Gastric mucosal microcirculatory disturbance in experimental animals is stressed as an important factor in the development of gastric ulceration induced by ethanol. In this study, we used a reflectance spectrophotometry system to investigate the effect of cetraxate on ethanol-induced gastric mucosal hemodynamics in anesthetized dogs. Forty percent ethanol caused a significant increase in the mucosal blood volume and a significant decrease in mucosal hemoglobin oxygenation. The changes in these parameters indicated mucosal congestion and tissue hypoxia. Topical administration of cetraxate (200 mg in 10 ml saline) prevented the increase in mucosal blood volume and decrease in mucosal hemoglobin oxygenation which had been induced by ethanol loading in the stomach. In conclusion, cetraxate showed a protective effect on mucosal microcirculation that resulted in the maintenance of the gastric mucosal integrity against ethanol loading in the gastric mucosa.

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Reflectance spectrophotometry for the assessment of gastroduodenal mucosal perfusion

Cited by 60 publications

References 0 publications

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Vasopressin V1A receptors mediate the increase in gastric mucosal oxygenation during hypercapnia

Potassium channels participate in gastric mucosal protection in rats with partial portal vein ligation

Cetraxate Improves Ethanol-Induced Gastric Mucosal Congestion in Anesthetized Dogs.

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