Physiology of gastric circulation

Author(s):  
Paul H. Guth ◽  
Felix W. Leung ◽  
Gordon L. Kauffman
Keyword(s):  
1983 ◽  
Vol 96 (1) ◽  
pp. 902-904
Author(s):  
L. K. Gavrovskaya ◽  
V. M. Sedov ◽  
A. K. Gusyakov ◽  
E. N. Kharchevnikova

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

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

1995 ◽  
Vol 269 (5) ◽  
pp. R983-R987 ◽  
Author(s):  
D. M. McTigue ◽  
R. C. Rogers

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.


Author(s):  
Manuel Barberio ◽  
Eric Felli ◽  
Margherita Pizzicannella ◽  
Vincent Agnus ◽  
Mahdi Al-Taher ◽  
...  

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.


1993 ◽  
Vol 265 (6) ◽  
pp. H2110-H2116
Author(s):  
R. Y. Chen ◽  
G. Ross ◽  
K. Y. Chyu ◽  
P. H. Guth

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.


1976 ◽  
Vol 230 (2) ◽  
pp. 346-350 ◽  
Author(s):  
MJ Zinner ◽  
JC Kerr ◽  
DG Reynolds

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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