Is the beneficial effect of prior exercise on postprandial lipaemia partly due to redistribution of blood flow?

Preprandial aerobic exercise lowers postprandial lipaemia (a risk factor for coronary heart disease); however, the mechanisms responsible are still not clear. The present study investigated whether blood flow to skeletal muscle and/or the liver was increased in the postprandial period after exercise, relative to a control trial, and whether this resulted from increased cardiac output or redistribution of flow. Eight overweight inactive males, aged 49.4±10.5 years (mean±S.D.), acted as their own controls in a counterbalanced design, either walking briskly for 90 min at 60% V̇O2max (maximal oxygen uptake), or resting in the lab, on the evening of day 1. The following morning, a fasting blood sample was collected, participants consumed a high-fat breakfast, and further venous blood samples were drawn hourly for 6 h. Immediately after blood sampling, Doppler ultrasound was used to measure cardiac output and blood flow through both the femoral artery of one leg and the hepatic portal vein, with the ultrasonographer blinded to trial order. The total postprandial triacylglycerol response was 22% lower after exercise (P=0.001). Blood flow through the femoral artery and the hepatic portal vein was increased by 19% (P<0.001) and 16% (P=0.033), respectively, during the 6-h postprandial period following exercise; however, postprandial cardiac output did not differ between trials (P=0.065). Redistribution of blood flow, to both exercised skeletal muscle and the liver, may therefore play a role in reducing the plasma triacylglycerol response to a high-fat meal on the day after an exercise bout.

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Systemic effects of NaHCO3 in experimental lactic acidosis in dogs

AJP Renal Physiology ◽

10.1152/ajprenal.1982.242.6.f586 ◽

1982 ◽

Vol 242 (6) ◽

pp. F586-F591 ◽

Cited By ~ 5

Author(s):

A. I. Arieff ◽

W. Leach ◽

R. Park ◽

V. C. Lazarowitz

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Lactic Acidosis ◽

Portal Vein ◽

Blood Lactate ◽

Lactate Production ◽

Systemic Effects ◽

Arterial Ph ◽

Hepatic Portal Vein ◽

Hepatic Portal

Lactic acidosis is characterized by metabolic acidosis due to accumulation of H+ ions from lactic acid with blood lactate of at least 5 mM. The standard treatment is intravenous NaHCO3, with resultant mortality in excess of 50%. Despite the high mortality, the metabolic and systemic effects of NaHCO3 used in the treatment of lactic acidosis have not been extensively studied. The present experiments in diabetic dogs were designed to address these questions. Dogs with phenformin-induced lactic acidosis (blood lactate above 5 mM, arterial pH below 7.20) were treated with equimolar amounts of either NaCl or NaHCO3 or received no therapy. Intravenous NaHCO3 resulted in a decline of cardiac output and intracellular pH (pHi) of liver and erythrocytes, whereas treatment with NaCl did not. With NaHCO3 but not with NaCl infusion gut lactate production increased almost stoichiometrically, with no change in arterial pH or bicarbonate but with a doubling of lactate. Bicarbonate also resulted in a decrease of hepatic portal vein blood flow. The mean survival time and percent mortality were similar in NaCl- vs. NAHCO3(-) treated animals. Although both groups lived longer than did animals receiving no therapy, the differences were not significant. Thus, treatment of experimental lactic acidosis with either NaCl or NaHCO3 or with no therapy results in no change of blood pH and bicarbonate and in a similar mortality. In terms of systemic effects, however, NaHCO3 results in significant decrements of liver and erythrocyte pHi, hepatic portal vein blood flow, and cardiac output and in significant increments of gut lactate production, whereas NaCl does not. The data suggest that the rationale for therapy of lactic acidosis with NaHCO3 should probably be reevaluated.

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Effect of exercise intensity on blood flow of the hepatic portal vein measured by a semipermanently embedded electromagnetic blood flow meter.

Kanzo ◽

10.2957/kanzo.36.173 ◽

1995 ◽

Vol 36 (3) ◽

pp. 173-174

Author(s):

RISA YANO

Keyword(s):

Blood Flow ◽

Portal Vein ◽

Exercise Intensity ◽

Flow Meter ◽

Hepatic Portal Vein ◽

Hepatic Portal

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The effect of high-molecular-weight guar gum on net apparent glucose absorption and net apparent insulin and gastric inhibitory polypeptide production in the growing pig: relationship to rheological changes in jejunal digesta

British Journal Of Nutrition ◽

10.1079/bjn19950157 ◽

1995 ◽

Vol 74 (4) ◽

pp. 539-556 ◽

Cited By ~ 112

Author(s):

P. R. Ellis ◽

F. G. Roberts ◽

A. G. Low ◽

L. M. Morgan

Keyword(s):

Molecular Weight ◽

Blood Flow ◽

Guar Gum ◽

Gastric Inhibitory Polypeptide ◽

Glucose Absorption ◽

Growing Pigs ◽

Zero Shear Viscosity ◽

Postprandial Period ◽

Hepatic Portal Vein ◽

Hepatic Portal

The present study was designed to determine the quantitative effects of starchy meals containing guar gum on rates of net apparent glucose absorption and net apparent insulin and gastric inhibitory polypeptide (GIP) production in growing pigs. The effects of these meals on the viscosity of jejunal digesta were also examined and correlated to changes in glucose absorption. Four growing pigs were each given either a low-fat semi-purified diet (control) or the same diet supplemented with a high-molecular-weight guar gum at concentrations in the diet of 20 or 40 g/kg. Blood samples were removed simultaneously via indwelling catheters from the mesenteric artery and the hepatic portal vein. Samples of jejunal digesta were removed via a T-piece cannula and used immediately for viscosity measurements at 39°. The ‘zero-shear’ viscosity of each sample was then calculated. Blood-flow measurements were made using an ultrasonic flow probe fitted to the hepatic portal vein. All measurements were made at intervals of 10 or 30 min during a 4 h postprandial period. Meals containing guar gum significantly increased (P < 0·05) the viscosity of jejunal digesta, an effect that was strongly dependent on the concentration of guar gum in the original diet. No significant differences in blood-flow rates were found between the control and guar-containing diets. Both concentrations of guar gum significantly reduced (P < 0·05) glucose absorption and insulin and GIP secretion rates over the 4 h postprandial period. An inverse relationship between the rate of glucose absorption and the ‘zero-shear’ viscosity of jejunal digesta was found. This study also provides direct evidence for the important role played by the entero-insular axis in modifying the glycaemic response to a meal containing guar gum.

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Quantification of in vitro and in vivo energy metabolism of the gastrointestinal tract of fed or fasted sheep

Canadian Journal of Animal Science ◽

10.4141/cjas93-088 ◽

1993 ◽

Vol 73 (4) ◽

pp. 855-868 ◽

Cited By ~ 9

Author(s):

J. M. Kelly ◽

B. G. Southorn ◽

C. E. Kelly ◽

L. P. Milligan ◽

B. W. McBride

Keyword(s):

Blood Flow ◽

Gastrointestinal Tract ◽

Portal Blood Flow ◽

Whole Body ◽

Hepatic Portal Vein ◽

Flow Through ◽

Hepatic Portal ◽

Ouabain Inhibition

The effect of level of nutrition on in vitro and in vivo O2 consumption by the gastrointestinal tract in four nonlactating, nonpregnant ewes catheterized in the anterior mesenteric vein, hepatic portal vein and mesenteric artery with duodenal cannulae was investigated. Animals were fed a pelleted ration at maintenance (M) or twice maintenance (2M) or fasted (F) subsequent to the M measurement. Duodenal in vitro O2, ouabain-sensitive O2 (OSO2) and cycloheximide-sensitive O2 (CSO2) consumption was determined polarographically using a YSI O2 monitor; whole-gut O2 consumption was determined as (arterio-venous difference of O2 concentration) × (blood flow through the PV). Whole-body O2 consumption was determined using indirect calorimetry. Ewes fed 2M exhibited higher (P < 0.10) whole-body O2 consumption than either M or F ewes. Ewes fed M and 2M had higher (P < 0.10) duodenal in vitro O2 and ouabain-insensitive O2 (OIO2) consumption than F ewes. Hepatic portal blood flow was directly proportional to level of intake (P < 0.10): it was lowest for F ewes (81.0 L h−1), intermediate for M ewes (97.7 L h−1) and highest for 2M ewes (122.5 L h−1). Ouabain inhibition of O2 consumption by portal-drained viscera (PDV) was highest in M ewes and lowest in 2M ewes (P < 0.10). CSO2 consumption by the entire PDV was not affected by level of intake, corresponding to no change in OIO2 consumption by the PDV. As a proportion of whole-body O2 consumption, total O2, OSO2 and cycloheximide-insensitive O2 consumption by the PDV was higher in F ewes than in 2M ewes (P < 0.10). Fasted ewes expended a greater proportion of whole-body O2 consumption on gastrointestinal energetics than did 2M ewes. Key words: Sheep, gastrointestinal oxygen consumption, sodium–potassium ATPase, protein synthesis

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Permanent cannulation of the hepatic portal vein and carotid artery in laboratory animals without disruption of blood flow

Cryobiology ◽

10.1016/0011-2240(74)90266-1 ◽

1974 ◽

Vol 11 (6) ◽

pp. 582

Author(s):

R. Sablé

Keyword(s):

Blood Flow ◽

Carotid Artery ◽

Portal Vein ◽

Laboratory Animals ◽

Hepatic Portal Vein ◽

Hepatic Portal

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Blood flow, vascular resistance, and blood volume after hemorrhage in conscious adrenalectomized rat

Journal of Applied Physiology ◽

10.1152/jappl.1997.83.5.1648 ◽

1997 ◽

Vol 83 (5) ◽

pp. 1648-1653 ◽

Cited By ~ 12

Author(s):

Daniel N. Darlington ◽

Majid J. Tehrani

Keyword(s):

Blood Flow ◽

Portal Vein ◽

Hepatic Artery ◽

Blood Volume ◽

Vascular Resistance ◽

Cardiovascular Collapse ◽

Artery Blood Flow ◽

Hepatic Portal Vein ◽

Small Intestines ◽

Hepatic Portal

Darlington, Daniel N., and Majid J. Tehrani. Blood flow, vascular resistance, and blood volume after hemorrhage in conscious adrenalectomized rat. J. Appl. Physiol. 83(5): 1648–1653, 1997.—Hemorrhage leads to cardiovascular collapse and death in adrenal-insufficient animals. To determine whether the cardiovascular collapse is due to vasodilation and/or failure to restore blood volume, we used radiolabeled microspheres and 125I-labeled albumin to measure blood flow and blood volume in conscious adrenalectomized (ADX) rats after 15 ml ⋅ kg−1 ⋅ 3 min−1 hemorrhage. In ADX rats, hemorrhage led to a greater fall than in sham rats in blood flow in the stomach, small intestines, cecum, colon, spleen, hepatic portal vein, kidney, testis, lung, thymus, bone, fat, forebrain, cerebellum, and brainstem. The greater fall in blood flow was caused by an increase in vascular resistance in these organs except brain and hepatic artery. Sham rats maintained or increased brain and hepatic artery blood flow after hemorrhage whereas flow decreased and remained depressed in ADX rats. ADX rats failed to restore blood volume, whereas sham rats completely restored blood flow by 2 h. We conclude that cardiovascular collapse in ADX rats does not result from vasodilatation but may result from a failure to restore blood volume. The failure to restore blood volume and the low blood flow to organs, especially brain and liver, may contribute to mortality in ADX rats after hemorrhage.

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