Oral Carbohydrate Solution Ameliorates Endotoxemia-Induced Splanchnic Ischemia

Male rats consumed much more of an intraorally administered mixed protein, fat and carbohydrate solution than of a carbohydrate solution. Injection of cholecystokinin octapeptide (CCK-8, 0.6-5.0 microgram) suppressed intake of both solutions, but the CCK-A receptor antagonist L-364, 718 (20-40 micrograms) facilitated only carbohydrate intake. Blood levels of CCK-8 were higher after intake of the carbohydrate than the mixed solution. Blood levels of isoleucine, leucine, lysine, threonine, valine, and tryptophan increased only after intake of the mixed solution. Injection of these amino acids suppressed intake of both solutions. Blood levels of amino acids were also less after the seventh than after the first session ingesting the mixed solution. Treatment with CCK-8 or amino acids inhibits intake of any diet, but when secreted endogenously, these signals may terminate the meal in a diet-dependent manner.

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Technique of Celiac Blockade for Relief of Splanchnic Ischemia

JAMA ◽

10.1001/jama.1965.03080200018004 ◽

1965 ◽

Vol 192 (7) ◽

pp. 600 ◽

Cited By ~ 1

Author(s):

Amos Nahor

Keyword(s):

Splanchnic Ischemia

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II. Nitric oxide protects in intestinal inflammation

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1999.276.3.g572 ◽

1999 ◽

Vol 276 (3) ◽

pp. G572-G575 ◽

Cited By ~ 8

Author(s):

Allan M. Lefer ◽

David J. Lefer

Keyword(s):

Nitric Oxide ◽

Intestinal Inflammation ◽

Ischemia Reperfusion ◽

Protective Agent ◽

No Donors ◽

Beneficial Effects ◽

Splanchnic Ischemia ◽

Inflammatory State ◽

Or Gene ◽

Oxide Synthase

This article examines the evidence for nitric oxide (NO) as a protective agent in splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation. Four major points emerge from this body of data. First, acute intestinal inflammation results in an early (i.e., <5 min) and severe decrease in endothelium-derived NO. Thus the early trigger event in this condition is a functional loss of NO. Second, administration of exogenous NO, NO donors, or NO precursors ameliorate splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation (i.e., splanchnic trauma). These beneficial effects occur at physiological levels of NO when given early in the course of the inflammatory state. Third, blockade of nitric oxide synthase (NOS) or gene deletion of NOS exacerbates intestinal inflammation. Fourth, there are a variety of signaling mechanisms that may mediate the protective effect of NO.

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Downstream effects of splanchnic ischemia-reperfusion injury on renal function and eicosanoid release

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.2.530 ◽

1997 ◽

Vol 83 (2) ◽

pp. 530-536 ◽

Cited By ~ 23

Author(s):

Patricia Rothenbach ◽

Richard H. Turnage ◽

Jose Iglesias ◽

Angela Riva ◽

Lori Bartula ◽

...

Keyword(s):

Blood Flow ◽

Renal Function ◽

Reperfusion Injury ◽

Renal Blood Flow ◽

Ischemia Reperfusion Injury ◽

Ischemia Reperfusion ◽

Inulin Clearance ◽

Downstream Effects ◽

Splanchnic Ischemia ◽

Eicosanoid Release

Rothenbach, Patricia, Richard H. Turnage, Jose Iglesias, Angela Riva, Lori Bartula, and Stuart I. Myers. Downstream effects of splanchnic ischemia-reperfusion injury on renal function and eicosanoid release. J. Appl. Physiol.82(2): 530–536, 1997.—This study examines the hypothesis that intestinal ischemia-reperfusion (I/R) injury contributes to renal dysfunction by altered renal eicosanoid release. Anesthetized Sprague-Dawley rats underwent 60 min of sham or superior mesenteric artery (SMA) occlusion with 60 min of reperfusion. The I/R groups received either allopurinol, pentoxifylline, 1-benzylimidazole, or carrier before SMA occlusion. In vivo renal artery blood flow was measured by Transonic flow probes, the kidneys were then perfused in vitro for 30 min, and the effluent was analyzed for eicosanoid release and renal function. Intestinal I/R caused a twofold increase in the ratio of renal release of thromboxane B2to prostaglandin E2and to 6-ketoprostaglandin F1αcompared with the sham level, with a corresponding 25% decrease in renal sodium and inulin clearance and renal blood flow. Pentoxifylline or allopurinol pretreatment restored renal eicosanoid release and renal sodium and inulin clearance to the sham level but did not alter renal blood flow. Pretreatment with 1-benzylimidazole restored renal function, eicosanoid release, and renal blood flow to sham levels. These data suggest that severe intestinal I/R contributes to the downregulation of renal function. The decrease in renal function is due in part to toxic oxygen metabolites, which occur in the milieu of altered renal eicosanoid release, reflecting a decrease in vasodilator and an increase in vasoconstrictor eicosanoids.

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The effect of human SOD on the survival rate in rats with temporary splanchnic ischemia

Journal of Anesthesia ◽

10.1007/s0054080020041 ◽

1988 ◽

Vol 2 (1) ◽

pp. 41-45 ◽

Cited By ~ 3

Author(s):

Ryo Ogawa ◽

Hiroyasu Bitoh ◽

Yoshiyuki Ohi

Keyword(s):

Survival Rate ◽

Splanchnic Ischemia

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Composite versus single transportable carbohydrate solution enhances race and laboratory cycling performance

Applied Physiology Nutrition and Metabolism ◽

10.1139/h2012-013 ◽

2012 ◽

Vol 37 (3) ◽

pp. 425-436 ◽

Cited By ~ 34

Author(s):

David S. Rowlands ◽

Marilla Swift ◽

Marjolein Ros ◽

Jackson G. Green

Keyword(s):

High Intensity ◽

Peak Power ◽

Endurance Performance ◽

Cycling Performance ◽

Mountain Bike ◽

Gastrointestinal Discomfort ◽

Recorded Data ◽

Intestinal Transporters ◽

Maltodextrin Solution ◽

Carbohydrate Solution

When ingested at high rates (1.8–2.4 g·min–1) in concentrated solutions, carbohydrates absorbed by multiple (e.g., fructose and glucose) vs. single intestinal transporters can increase exogenous carbohydrate oxidation and endurance performance, but their effect when ingested at lower, more realistic, rates during intermittent high-intensity endurance competition and trials is unknown. Trained cyclists participated in two independent randomized crossover investigations comprising mountain-bike races (average 141 min; n = 10) and laboratory trials (94-min high-intensity intervals followed by 10 maximal sprints; n = 16). Solutions ingested during exercise contained electrolytes and fructose + maltodextrin or glucose + maltodextrin in 1:2 ratio ingested, on average, at 1.2 g carbohydrate·kg–1·h–1. Exertion, muscle fatigue, and gastrointestinal discomfort were recorded. Data were analysed using mixed models with gastrointestinal discomfort as a mechanism covariate; inferences were made against substantiveness thresholds (1.2% for performance) and standardized difference. The fructose–maltodextrin solution substantially reduced race time (–1.8%; 90% confidence interval = ±1.8%) and abdominal cramps (–8.1 on a 0–100 scale; ±6.6). After accounting for gastrointestinal discomfort, the effect of the fructose–maltodextrin solution on lap time was reduced (–1.1%; ±2.4%), suggesting that gastrointestinal discomfort explained part of the effect of fructose–maltodextrin on performance. In the laboratory, mean sprint power was enhanced (1.4%; ±0.8%) with fructose–maltodextrin, but the effect on peak power was unclear (0.7%; ±1.5%). Adjusting out gastrointestinal discomfort augmented the fructose–maltodextrin effect on mean (2.6%; ±1.9%) and peak (2.5%; ±3.0%) power. Ingestion of multiple transportable vs. single transportable carbohydrates enhanced mountain-bike race and high-intensity laboratory cycling performance, with inconsistent but not irreconcilable effects of gut discomfort as a possible mediating mechanism.

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