scholarly journals Circulatory effects of graded diversion of portal blood flow to the systemic circulation in rats: Role of nitric oxide

Hepatology ◽  
1997 ◽  
Vol 26 (2) ◽  
pp. 262-267 ◽  
Author(s):  
C Bernadich ◽  
J C Bandi ◽  
C Piera ◽  
J Bosch ◽  
J Rodes
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Portal Blood Flow ◽  
Systemic Circulation ◽  
Portal Blood ◽  
Circulatory Effects

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.

Evidence for involvement of nitric oxide in the regulation of hypothalamic portal blood flow

Neuroscience ◽  
1992 ◽  
Vol 51 (4) ◽  
pp. 769-772 ◽  
Author(s):  
S. Ceccatelli ◽  
J.M. Lundberg ◽  
J. Fahrenkrug ◽  
D.S. Bredt ◽  
S.H. Snyder ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Portal Blood Flow ◽  
Portal Blood

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.

Role of Nitric Oxide on Papillary Blood Flow and Pressure Natriuresis

Hypertension ◽  
1995 ◽  
Vol 25 (3) ◽  
pp. 408-414 ◽  
Author(s):  
Francisco J. Fenoy ◽  
Paloma Ferrer ◽  
Luis Carbonell ◽  
Miguel García-Salom
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Pressure Natriuresis

Portal Blood Flow as Measured by the Doppler Shift Technique in Sheep Fed Chopped Forages

1975 ◽  
Vol 41 (2) ◽  
pp. 596-600 ◽  
Author(s):  
L. R. Prewitt ◽  
D. R. Jacobson ◽  
R. W. Hemken ◽  
R. H. Hatton
Keyword(s):  
Blood Flow ◽  
Doppler Shift ◽  
Portal Blood Flow ◽  
Portal Blood ◽  
Shift Technique
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