Hepatic Portal Vein Blood Flow Research Articles

Evaluation of hepatic uptake clearance of tetrodotoxin in the puffer fish Takifugu rubripes

In this study, we investigated the hepatic uptake clearance (CL uptake) of tetrodotoxin (TTX) in the marine puffer fish Takifugu rubripes by integration plot analysis after a single bolus injection of 0.25 mg TTX/kg body weight into the hepatic vein at 20 °C. The blood concentration of TTX decreased over time after the injection, from 1451 ± 45 ng/mL at 10 min to 364 ± 59 ng/mL at 60 min. TTX concentrations in the spleen and kidney decreased in parallel with the blood concentrations, whereas those in the muscle and skin remained almost the same throughout the experiment. In contrast, the TTX concentration in the liver gradually increased, reaching 1240 ± 90 ng/g liver at 60 min after injection. The amount of TTX that had accumulated in the liver 60 min after injection accounted for 63 ± 5% of the administered dose. Integration plot analysis indicated a CL uptake of 3.1 mL/min/kg body weight in the liver for TTX, a rate far below that of the hepatic portal vein blood flow rate (at most, 9%). This finding is consistent with negligible extraction of TTX by the liver. The results demonstrated conclusively that the liver-specific distribution of TTX in T. rubripes is achieved by removal from the systemic circulation, but not by the hepatic first-pass effect.

Portal net appearance of amino acids in growing pigs fed a barley-based diet with inclusion of three different forage meals

The net absorption of amino acids (AA) in young pigs fed a barley-based control diet (C) and diets where barley was replaced by 200 g/kg fresh weight of dried lucerne (Medicago sativa; L20), white clover (Trifolium repens; W20) or perennial ryegrass (Lolium perenne; PR20) meal was studied. Castrated male pigs were fitted with permanent catheters in the hepatic portal vein and mesenteric artery, and the hepatic portal net absorption of AA was estimated from the porto-arterial plasma concentration differences and the hepatic portal-vein blood flow. In general, the essential AA (EAA) concentrations in the hepatic portal vein reached peak levels 90 min after feeding and thereafter exhibited a transient decline. Maximum porto-arterial differences were reached between 1 and 3 h postprandially for most of the AA. The cumulative net absorption of non-essential AA (NEAA) and EAA did not differ significantly between the barley-based diet and diets W20 and PR20. Due to a lower intake of AA on diet L20, the cumulative net absorption of NEAA and EAA was significantly (P < 0.05) lower than diet C. With the exceptions of the EAA arginine, cystine and valine, and the NEAA glutamic acid + glutamine and glycine, there were no significant differences in the absorption coefficients for the EAA and NEAA between the diets. In addition, the pattern of the total EAA in the mixture absorbed postprandially did not differ significantly between the diets. The present study gives support to the contention that the replacement of barley AA with forage meal AA in a barley-based diet for growing pigs should be expected to result in minor differences in the net portal flux of AA.

Oxygen consumption by portal vein-drained organs and by whole animal in conscious growing swine.

A method was developed to measure simultaneously the O2 consumption (VO) by the whole animal and by the hepatic portal vein-drained organs (PVDO), including the gastrointestinal tract, spleen, and pancreas in conscious 3.5- to 4-month-old swine. The method was used to determine (i) the effect of feeding on hepatic portal vein blood flow rate (Qpv) and VO by PVDO and by the whole animal, and (ii) the significance of PVDO on the oxidative demand in the pig. Chronic cannulas were placed in the hepatic portal vein, carotid artery, and ileal vein. The Qpv was determined by an indicator dilution technique employing continuous constant infusion of 1% p-aminohippuric acid into the ileal vein. The VO2 by PVDO was estimated by multiplying Qpv by arterial-portal vein O2 difference measured with an arterial-venous O2 difference analyzer connected to the carotid artery and portal vein cannulas. Whole animal VO2 was measured with an open circuit indirect calorimeter. In seven pigs (3.5- to 4-month-old, 37.4 +/- 0.8 kg) trained to be fed once daily, feeding (1.2 kg of feed mixed with 1.2 liter of H2O) caused postprandial (6 hr) Qpv to increase more than 34 +/- 15% above the preprandial value of 34.5 +/- 4.2 ml.min-1.kg-1 body wt. The postprandial VO2 by PVDO was elevated more than 46 +/- 12% above the value of 1.52 +/- 0.20 ml.min-1.kg-1 body wt observed during the preprandial period. Whole animal VO2 increased 45 +/- 9 and 33 +/- 7% above the preprandial value of 6.23 +/- 0.57 ml.min-1.kg-1 body wt for the first 6 hr and the 7 to 12 hr after feeding, respectively. Although PVDO represent only 5% of body weight, they used 25% of whole body VO2. The study clearly illustrates the significance of PVDO on the whole animal oxidative demand in conscious growing swine.

Systemic effects of NaHCO3 in experimental lactic acidosis in dogs.

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.