Ethanol-induced increase in portal blood flow: role of adenosine

1988 ◽  
Vol 254 (4) ◽  
pp. G495-G501 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
V. Saldivia ◽  
H. G. Giles ◽  
S. Sandrin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Maximal Effect ◽  
Dependent Manner ◽  
Dose Dependent Increase ◽  
Dose Dependent

The mechanism by which ethanol induces an increase in portal vein blood flow was studied in rats using radiolabeled microspheres. Ethanol (2 g/kg) by gavage resulted in an increase of 50-70% in portal vein blood flow. The ethanol-induced increase in portal blood flow was suppressed by the adenosine receptor blocker 8-phenyltheophylline [ethanol, 61.8 +/- 4.1 ml.kg-1.min-1; ethanol + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 44.2 +/- 2.0 ml.kg-1.min-1; P less than 0.05]. By itself, 8-phenyltheophylline (0.2 mg.kg-1.min-1) was without effect on cardiac output or portal blood flow. Adenosine infusion resulted in a dose-dependent increase in portal blood flow with a maximal effect at a dose of 0.17 mg.kg-1.min-1 (control, 41.3 +/- 2.3; adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; P less than 0.05). This adenosine-induced increase in portal blood flow was inhibited by 8-phenyltheophylline in a dose-dependent manner [adenosine, 81.7 +/- 8.0 ml.kg-1.min-1; adenosine + 8-phenyltheophylline (0.2 mg.kg-1.min-1), 49.8 +/- 6.6 ml.kg-1.min; P less than 0.05]. Both alcohol and adenosine significantly reduced preportal vascular resistance by 40% (P less than 0.02) and 60% (P less than 0.01), respectively. These effects were fully suppressed by 8-phenyltheophylline. It is concluded that adenosine is a likely candidate to mediate the ethanol-induced increase in portal vein blood flow. It is suggested that an increase in circulating acetate and liver hypoxia may mediate the effects of alcohol by increasing tissue and interstitial adenosine levels.

New insights on the mechanism of the alcohol-induced increase in portal blood flow

1988 ◽  
Vol 66 (1) ◽  
pp. 1-9 ◽  
Author(s):  
H. Orrego ◽  
F. J. Carmichael ◽  
Y. Israel
Keyword(s):  
Blood Flow ◽  
Alcohol Dehydrogenase ◽  
Portal Blood Flow ◽  
Protective Role ◽  
Portal Blood ◽  
Acute Administration ◽  
Direct Role ◽  
Potent Vasodilator ◽  
Dose Dependent Increase

Acute administration of ethanol increases portal blood flow by 40–60%. This increase in blood flow compensates for the increase in O2 consumption that follows alcohol intake and may play a protective role against hypoxic hepatocellular necrosis. We have investigated the mechanism of this hemodynamic effect of ethanol in the rat using the labeled microsphere technique. We ruled out a direct role of systemic glucagon and of acetaldehyde in mediating the increase in portal flow. However, the increase in flow is maximal at a blood ethanol concentration of 3.5 mM, corresponding to that required to achieve the Vmax of alcohol dehydrogenase, and is suppressed by 4-methylpyrazole, an inhibitor of alcohol dehydrogenase. Alcohol ingestion results in zonal liver hypoxia and in increases in acetate, both of which have been shown to increase the levels of adenosine, a potent vasodilator, in blood and tissues. Ethanol produces a 400% increase in arterial adenosine. Adenosine infusion leads to a dose-dependent increase in portal blood flow of up to 100%, an effect that is suppressed by administration of 8-phenyltheophylline, an antagonist of adenosine at A1 and A2 receptors. Similarly, the ethanol-induced increase in portal blood flow is fully suppressed by 8-phenyltheophylline. In conclusion, adenosine appears to play an important role in the mechanism by which ethanol increases portal blood flow.

scholarly journals Portal Vein Dopplerflowmetry in healthy sheep according to age

2017 ◽  
Vol 37 (10) ◽  
pp. 1172-1176 ◽  
Author(s):  
Alexandra F. Belotta ◽  
Bianca P. Santarosa ◽  
Danilo O.L. Ferreira ◽  
Sílvia M.F. Carvalho ◽  
Roberto C. Gonçalves ◽  
...  
Keyword(s):  
Blood Flow ◽  
Portal Vein ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Mean Values ◽  
Pulsed Doppler Ultrasound ◽  
Healthy Sheep ◽  
Vein Diameter ◽  
Congestion Index ◽  
Post Hoc

ABSTRACT: Pulsed Doppler ultrasound was used to evaluate portal blood flow, portal velocity and portal congestion index in 24 healthy sheep divided into groups (lambs, yearlings and ewes), according to age. Measurements were performed at the 11th right intercostal space using ideal insonation angle and uniform insonation method. Mean values obtained in each group were compared with one-way ANOVA, followed by Tukey post-hoc test. Portal velocity and portal blood flow were statistically similar between the groups (P>0.05). Mean portal velocity were 17.75; 17.13 and 16.75; while mean portal blood flow were 26.65; 31.04 and 24.32 for lambs, yearlings and ewes, respectively. Portal congestion index was statistically distinct between the groups and values for lambs, yearlings and ewes were 0.009; 0.058 and 0.09, respectively (P<0.01). Statistical differences were observed in portal vein diameter, portal vein area and portal congestion index between the groups, presumably due to influence of weight and not to age.

scholarly journals Correction of extrahepatic portal hypertension in pediatric patient after liver transplantation

2017 ◽  
Vol 19 (1) ◽  
pp. 47-51
Author(s):  
A. R. Monakhov ◽  
B. L. Mironkov ◽  
T. A. Dzhanbekov ◽  
K. O. Semash ◽  
Kh. M. Khizroev ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Blood Flow ◽  
Portal Hypertension ◽  
Portal Vein ◽  
Pediatric Patient ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Positive Trend ◽  
Portal Vein Stenosis ◽  
Vein Stenosis

Introduction. Liver transplantation is a multi-component and complex type of operative treatment. Patients undergoing such a treatment sometimes are getting various complications. One of these complications is a portal hypertension associated with portal vein stenosis.Materials and methods. In 6 years after the left lateral section transplantation from living donor in a pediatric patient the signs of portal hypertension were observed. Stenosis of the portal vein was revealed. Due to this fact percutaneous transhepatic correction of portal vein stenosis was performed.Results. As a result of the correction of portal blood flow in the patient a positive trend was noted. According to the laboratory and instrumental methods of examination the graft had a normal function, portal blood flow was adequate. In order to control the stent patency Doppler ultrasound and MSCT of the abdominal cavity with intravenous bolus contrasting were performed. Due to these examinations the stent function was good, the rate of blood flow in the portal vein due to Doppler data has reached 80 cm/sec, and a decrease of the spleen size was noted.Conclusion. Diagnosis and timely detection of portal vein stenosis in patients after liver transplantation are very important for the preservation of graft function and for the prevention of portal hypertension. In order to do that, ultrasound Doppler fluorimetry examination needs to be performed to each patient after liver transplantation. In cases of violation of the blood flow in the portal vein CT angiography performance is needed. Percutaneous transhepatic stenting of portal vein is a minimally invasive and highly effective method of correction of portal hypertension. Antiplatelet therapy and platelet aggregation control are the prerequisites for successful stent function.

Postprandial intestinal hyperemia: role of bile salts in the ileum

1981 ◽  
Vol 241 (6) ◽  
pp. G469-G477 ◽  
Author(s):  
P. R. Kvietys ◽  
J. M. McLendon ◽  
D. N. Granger
Keyword(s):  
Blood Flow ◽  
Oxygen Uptake ◽  
Bile Salt ◽  
Bile Salts ◽  
Dependent Manner ◽  
Salt Solutions ◽  
Dose Dependent ◽  
Oxygen Difference ◽  
Artificial Pressure

In an autoperfused dog ileum preparation, artificial pressure, venous outflow pressure, blood flow, and arteriovenous oxygen difference were measured while bile and bile salt solutions, at physiological concentrations, were placed in the lumen. Intraluminal placement of endogenous bile, synthetic bile, or bile salt solutions increased ileal blood flow (99 +/- 10, 94 +/- 20, and 104 +/- 17%, respectively) and oxygen uptake (30 +/- 5, 36 +/- 9, and 28 +/- 5%, respectively). Endogenous bile pretreated with cholestyramine, a bile salt-sequestering resin, did not alter ileal blood flow, yet increased ileal oxygen uptake by 11 +/- 3%, a response similar to that observed while Tyrode's solution (the vehicle) was in the lumen. Intra-arterial infusion of bile salts increased ileal blood flow in a dose-dependent manner, while not significantly altering ileal oxygen uptake. The results of the present study indicate that bile salts play an important role in the functional (postprandial) hyperemia in the ileum by 1) directly dilating the ileal vasculature and 2) enhancing ileal metabolism during their active absorption.

Role of Nitric Oxide towards Vasodilator Effects of Substance P and ATP in Human Forearm Vessels

1997 ◽  
Vol 92 (2) ◽  
pp. 123-131 ◽  
Author(s):  
Masanari Shiramoto ◽  
Tsutomu Imaizumi ◽  
Yoshitaka Hirooka ◽  
Toyonari Endo ◽  
Takashi Namba ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Substance P ◽  
Sodium Nitroprusside ◽  
Forearm Blood Flow ◽  
Dependent Manner ◽  
Human Forearm ◽  
Before And After ◽  
Dose Dependent

1. It has been shown in animals that substance P as well as acetylcholine releases endothelium-derived nitric oxide and evokes vasodilatation and that ATP-induced vasodilatation is partially mediated by nitric oxide. The aim of this study was to examine whether vasodilator effects of substance P and ATP are mediated by nitric oxide in humans. 2. In healthy volunteers (n = 35), we measured forearm blood flow by a strain-gauge plethysmograph while infusing graded doses of acetylcholine, substance P, ATP or sodium nitroprusside into the brachial artery before and after infusion of NG-monomethyl-l-arginine (4 or 8 μmol/min for 5 min). In addition, we measured forearm blood flow while infusing substance P before and during infusion of l-arginine (10 mg/min, simultaneously), or before and 1 h after oral administration of indomethacin (75 mg). 3. Acetylcholine, substance P, ATP or sodium nitroprusside increased forearm blood flow in a dose-dependent manner. NG-Monomethyl-l-arginine decreased basal forearm blood flow and inhibited acetylcholine-induced vasodilatation but did not affect substance P-, ATP-, or sodium nitroprusside-induced vasodilatation. Neither supplementation of l-arginine nor pretreatment with indomethacin affected substance P-induced vasodilatation. 4. Our results suggest that, in the human forearm vessels, substance P-induced vasodilatation may not be mediated by either nitric oxide or prostaglandins and that ATP-induced vasodilatation may also not be mediated by nitric oxide.

Dose-Dependent Effects of Meclofenamate on Peripheral Vasculature of Conscious Rabbits

1983 ◽  
Vol 64 (5) ◽  
pp. 471-474 ◽  
Author(s):  
R. A. Banks ◽  
L. J. Beilin ◽  
J. Soltys
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Organ Blood Flow ◽  
Hepatic Circulation ◽  
Peripheral Vasculature ◽  
Conscious Rabbits ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
The Brain ◽  
Intravenous Sodium

1. Changes in systemic haemodynamics and organ blood flow were measured in conscious rabbits after various doses of intravenous sodium meclofenamate, an inhibitor of prostaglandin cyclo-oxygenase. 2. Meclofenamate had no effect on arterial pressure or cardiac output but caused a dose-dependent fall in renal blood flow. 3. Meclofenamate also reduced adrenal perfusion but, in contrast, caused a dose-dependent increase in blood flow to the brain, bronchial and hepatic circulation and to the testis. No effect was demonstrated on other organs studied. 4. The effect on the cerebral circulation was observed at the lowest dose of meclofenamate (0.75 mg/kg). Higher total doses were necessary for an effect on the renal and bronchial (3 mg/kg) and testicular and hepatic arteries (6 mg/kg). 5. The results suggest a variety of local vasomotor influences of renal and non-renal prostaglandins in conscious rabbits.

Haemodynamic Effects of Eating: The Role of Meal Composition

1996 ◽  
Vol 90 (4) ◽  
pp. 269-276 ◽  
Author(s):  
U. Høst ◽  
H. Kelbaek ◽  
H. Rasmusen ◽  
M. Court-Payen ◽  
N. Juel Christensen ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Portal Vein ◽  
Forearm Blood Flow ◽  
Plasma Catecholamines ◽  
Left Ventricular ◽  
Gastric Distension ◽  
Left Ventricular Volumes ◽  
Portal Vein Flow

1. The purpose of this study was to investigate the effect of fractional meal stimulation on postprandial haemodynamic changes, the possible correlation between these changes and the potential mediating role of circulating catecholamines and insulin. 2. Healthy young subjects were studied before and after ingestion of isocaloric, isovolumetric high-protein, carbohydrate or fat meals (80–85% of total energy), 60 kJ per kg of body weight. Multigated radionuclide cardiography with autologous 99mTc-labelled erythrocytes was performed for assessment of cardiac output, venous occlusion plethysmography to obtain forearm blood flow and Doppler-ultrasonography for portal vein flow. Plasma levels of catecholamines and insulin were determined by radioimmunoassay. 3. Cardiac output increased considerably after each meal, including the control meal (water) with only minor differences in extent and timing. Left ventricular volumes increased after food intake, most pronounced after carbohydrate and protein. Forearm blood flow increased only after carbohydrate and protein. Portal vein flow increased after all meals, especially after fat, but also after the control meal. There was a significant correlation between the increment in cardiac output and changes in forearm and portal vein flow, but no correlation between either haemodynamic response and plasma catecholamines or insulin. 4. Postprandial cardiovascular changes are not substantially different after various isocaloric and isovolumic meal compositions. Gastric distension seems to play a role in the increase in cardiac output, accomplished by ventricular dilatation. These changes seem to some extent to be linked to changes in muscle and splanchnic flow.

scholarly journals Role of Mas Receptor Antagonist A799 in Renal Blood Flow Response to Ang 1-7 after Bradykinin Administration in Ovariectomized Estradiol-Treated Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Aghdas Dehghani ◽  
Shadan Saberi ◽  
Mehdi Nematbakhsh
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Wistar Rats ◽  
Group Versus ◽  
Dependent Manner ◽  
Mas Receptor ◽  
Flow Response ◽  
Renal Vascular ◽  
Dose Dependent

Background. The accompanied role of Mas receptor (MasR), bradykinin (BK), and female sex hormone on renal blood flow (RBF) response to angiotensin 1-7 is not well defined. We investigated the role of MasR antagonist (A779) and BK on RBF response to Ang 1-7 infusion in ovariectomized estradiol-treated rats.Methods. Ovariectomized Wistar rats received estradiol (OVE) or vehicle (OV) for two weeks. Catheterized animals were subjected to BK and A799 infusion and mean arterial pressure (MAP), RBF, and renal vascular resistance (RVR) responses to Ang 1-7 (0, 100, and 300 ng kg−1 min−1) were determined.Results. Percentage change of RBF (%RBF) in response to Ang1-7 infusion increased in a dose-dependent manner. In the presence of BK, when MasR was not blocked, %RBF response to Ang 1-7 in OVE group was greater than OV group significantly (P<0.05). Infusion of 300 ng kg−1 min−1Ang 1-7 increased RBF by6.9±1.9% in OVE group versus0.9±1.8% in OV group. However when MasR was blocked, %RBF response to Ang 1-7 in OV group was greater than OVE group insignificantly.Conclusion. Coadministration of BK and A779 compared to BK alone increased RBF response to Ang 1-7 in vehicle treated rats. Such observation was not seen in estradiol treated rats.

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