Physiology of gastric circulation

2011 ◽  
Author(s):  
Paul H. Guth ◽  
Felix W. Leung ◽  
Gordon L. Kauffman
Keyword(s):  
Gastric Circulation

Concentration of biogenic amines in stomach tissues of rats with reduced gastric circulation

1983 ◽  
Vol 96 (1) ◽  
pp. 902-904
Author(s):  
L. K. Gavrovskaya ◽  
V. M. Sedov ◽  
A. K. Gusyakov ◽  
E. N. Kharchevnikova
Keyword(s):  
Biogenic Amines ◽  
Gastric Circulation

Gastric circulation and gastric secretion

1972 ◽  
Vol 7 (2) ◽  
pp. 205-206
Author(s):  
T. Takahashi ◽  
J. Inoue ◽  
S. Yasuda ◽  
Y. Maruyama ◽  
S. Hida ◽  
...  
Keyword(s):  
Gastric Secretion ◽  
Gastric Circulation

Studies on portal circulation (X) With special reference to its relation to gastric circulation

1971 ◽  
Vol 6 (1) ◽  
pp. 36-37
Author(s):  
T. Takahashi ◽  
J. Inoue ◽  
S. Yasuda ◽  
Y. Maruyama ◽  
S. Hida ◽  
...  
Keyword(s):  
Special Reference ◽  
Portal Circulation ◽  
Gastric Circulation

Pancreatic polypeptide stimulates gastric acid secretion through a vagal mechanism in rats

1995 ◽  
Vol 269 (5) ◽  
pp. R983-R987 ◽  
Author(s):  
D. M. McTigue ◽  
R. C. Rogers
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Pancreatic Polypeptide ◽  
Acid Output ◽  
Arterial Infusion ◽  
Efferent Limb ◽  
Cervical Vagotomy ◽  
The Central Nervous System ◽  
Gastric Circulation

The present study examined the effect of pancreatic polypeptide (PP) on gastric acid secretion. A 45-min infusion of PP was delivered into the jugular vein of urethan-anesthetized rats. Rat PP (100 pmol) significantly increased acid secretion over baseline; bilateral cervical vagotomy or peripheral atropine both eliminated this acid response. Neither intraperitoneal infusion nor close intra-arterial infusion of 100 pmol PP into the gastric circulation altered acid secretion. These results suggest that although PP requires intact vagal reflexes to stimulate acid output, it does not act on afferent or presynaptic efferent terminals of the vagus or directly within the stomach. Given that vagal reflexes consist of an afferent limb, an efferent limb, and a central relay, it may be that the target of circulating PP lies within the central nervous system. Indeed, previous studies from our laboratory have shown that microinjection of PP into the dorsal vagal complex results in long-lasting vagal-dependent elevation of gastric acid secretion.

scholarly journals Quantitative serosal and mucosal optical imaging perfusion assessment in gastric conduits for esophageal surgery: an experimental study in enhanced reality

2020 ◽  
Author(s):  
Manuel Barberio ◽  
Eric Felli ◽  
Margherita Pizzicannella ◽  
Vincent Agnus ◽  
Mahdi Al-Taher ◽  
...  
Keyword(s):  
Capillary Density ◽  
Esophageal Surgery ◽  
Confocal Laser Endomicroscopy ◽  
Confocal Laser ◽  
Sodium Fluorescein ◽  
Significant Difference ◽  
Gastric Circulation ◽  
Perfusion Assessment ◽  
Greater Curvature ◽  
Enhanced Reality

Abstract Introduction/objective Gastric conduit (GC) is used for reconstruction after esophagectomy. Anastomotic leakage (AL) incidence remains high, given the extensive disruption of the gastric circulation. Currently, there is no reliable method to intraoperatively quantify gastric perfusion. Hyperspectral imaging (HSI) has shown its potential to quantify serosal StO2. Confocal laser endomicroscopy (CLE) allows for automatic mucosal microcirculation quantification as functional capillary density area (FCD-A). The aim of this study was to quantify serosal and mucosal GC’s microperfusion using HSI and CLE. Local capillary lactate (LCL) served as biomarker. Methods GC was formed in 5 pigs and serosal StO2% was quantified at 3 regions of interest (ROI) using HSI: fundus (ROI-F), greater curvature (ROI-C), and pylorus (ROI-P). After intravenous injection of sodium-fluorescein (0.5 g), CLE-based mucosal microperfusion was assessed at the corresponding ROIs, and LCLs were quantified via a lactate analyzer. Results StO2 and FCD-A at ROI-F (41 ± 10.6%, 3.3 ± 3.8, respectively) were significantly lower than ROI-C (68.2 ± 6.7%, p value: 0.005; 18.4 ± 7, p value: 0.01, respectively) and ROI-P (72 ± 10.4%, p value: 0.005; 15.7 ± 3.2 p value: 0.001). LCL value at ROI-F (9.6 ± 4.7 mmol/L) was significantly higher than at ROI-C (2.6 ± 1.2 mmol/L, p value: 0.04) and ROI-P (2.6 ± 1.3 mmol/L, p value: 0.04). No statistically significant difference was found in all metrics between ROI-C and ROI-P. StO2 correlated with FCD-A (Pearson’s r = 0.67). The LCL correlated negatively with both FCD-A (Spearman’s r =  − 0.74) and StO2 (Spearman’s r =  −  0.54). Conclusions GC formation causes a drop in serosal and mucosal fundic perfusion. HSI and CLE correlate well and might become useful intraoperative tools.

Role of L-arginine-derived nitric oxide in cholinergic dilation of gastric arterioles

1993 ◽  
Vol 265 (6) ◽  
pp. H2110-H2116
Author(s):  
R. Y. Chen ◽  
G. Ross ◽  
K. Y. Chyu ◽  
P. H. Guth
Keyword(s):  
Nitric Oxide ◽  
Vascular Tone ◽  
Topical Administration ◽  
Microscopy Technique ◽  
No Formation ◽  
Resistance Vessels ◽  
Gastric Circulation ◽  
Arteriolar Diameter

The role of L-arginine-derived nitric oxide (NO) in cholinergic vasodilation of resistance vessels was studied in the intact stomach of the rat, utilizing an in vivo microscopy technique. Two L-arginine analogues, NG-monomethyl-L-arginine (L-NMMA) and nitro-L-arginine methyl ester (L-NAME), were used to block NO synthesis. Cholinergic dilation of gastric submucosal arterioles was induced by topical application of various concentrations of acetylcholine (ACh) (10(-7)-10(-4) M). Intravenous but not topical administration of L-NMMA and L-NAME caused an increase in arterial pressure. Intravenous or topical L-NAME reduces resting arteriolar diameter. These findings support the contention that NO formation modulates basal vascular tone and suggest that NO release may play a significant role in the regulation of the gastric circulation. L-Arginine analogues attenuated the arteriolar dilating effect of ACh but not adenosine or nitroglycerin. Substantial arteriolar responses to ACh remained after systemic or topical treatment with either L-NMMA or L-NAME. These results indicate that the L-arginine-NO pathway accounts only in part for ACh-induced vasodilation in gastric resistance vessels in vivo.

Primate gastric circulation: effects of catecholamines and adrenergic blockade

1976 ◽  
Vol 230 (2) ◽  
pp. 346-350 ◽  
Author(s):  
MJ Zinner ◽  
JC Kerr ◽  
DG Reynolds
Keyword(s):  
Blood Flow ◽  
Gastrointestinal Bleeding ◽  
Upper Gastrointestinal Bleeding ◽  
Gastric Blood Flow ◽  
Adrenergic Blockade ◽  
Beta Adrenergic ◽  
Before And After ◽  
Gastric Circulation ◽  
Autoregulatory Escape ◽  
Upper Gastrointestinal

The effects of intra-arterial injections and infusions of epinephrine, norepinephrine, and isoproterenol on gastric blood flow were studied in anesthetized baboons. Blood flow was measured electromagnetically before and after adrenergic blockade. The results for injected epinephrine and norepinephrine indicate these agents to be pure vasoconstrictors in the primate gastric circulation, and this response is attenuated by alpha-adrenergic blockade with phenoxybenzamine. Isoproterenol is a pure vasodilator, and its response is attenuated following beta-adrenergic blockade with propranolol. Intra-arterial infusions of epinephrine and norepinephrine (.05 mug kg-1 min-1) resulted in sustained vasoconstriction with no evidence of autoregulatory escape and no postinfusion "over-shoot." This study suggests that epinephrine and norepinephrine might provide alternatives to vasopressin as a vasoconstrictor for the control of upper gastrointestinal bleeding.

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