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

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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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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