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Biomedical subjects

A Braillon

Publications and source records attributed to A Braillon.

At least 19 recordsLinked to original sources
PubMed1993

Reduced splanchnic vasoconstriction to angiotensin II in conscious rats with biliary cirrhosis.

Decreased pressor reactivity to angiotensin II has been demonstrated in portal hypertension due to cirrhosis. The present study investigated the respective roles of portal hypertension and cirrhosis and the hemodynamic mechanisms of the depressor response in different models of portal hypertension in conscious rats. Dose-pressor curves were studied in sham-operated, portal vein stenosed (portal hypertension without cirrhosis) and biliary cirrhotic rats following angiotensin II administration. Decreased pressor response was observed in cirrhotic rats but not in portal vein stenosed rats. The hemodynamic effects of angiotensin II administration (11 ng.100 g-1 body wt.min-1, i.v.) were studied in conscious sham-operated and biliary cirrhotic rats (radioactive microsphere method). The percentage of change from basal values following angiotensin II administration were significantly more marked in sham-operated rats than in cirrhotic rats for mean arterial pressure (+34 vs. +6%), cardiac index (-36 vs. -22%), systemic vascular resistance (+117 vs. +40%). After angiotensin II, portal tributary and hepatic artery blood flows significantly decreased in sham-operated rats (-31 and -14%, respectively) but not in cirrhotic rats (+1 and +23%), whereas changes in renal blood flow were not significantly different between the two groups (-44 vs. -34%). In conclusion, in biliary cirrhotic rats, decreased pressor response to angiotensin II depends on the presence of liver disease rather than on portal hypertension or basal hemodynamic alterations. It also depends on the decreased vasoconstrictive effect which predominates in the splanchnic vascular bed.

Angiotensin II↗
PubMed1993

Renal hemodynamics in patients with cirrhosis: relationship with ascites and liver failure.

In patients with cirrhosis and ascites decreased renal blood flow might be related to the severity of liver disease but the relationship between the severity of cirrhosis and renal perfusion has not yet been established. Thus we measured renal, systemic and splanchnic hemodynamics in 63 patients with ascites and in 28 without ascites. When compared to patients without ascites, patients with ascites had lower renal blood flow (1,170 +/- 100 vs. 935 +/- 55 ml/min/1.73 m2; mean +/- SEM, p < 0.05) and renal perfusion pressure (78 +/- 2 vs. 72 +/- 1 mm Hg, p < 0.05 and higher inferior vena cava pressure (6.5 +/- 0.7 vs. 10.7 +/- 0.7 mm Hg, p < 0.05). Patients with ascites had significantly higher serum bilirubin concentrations, hepatic venous pressure gradient and lower serum albumin concentrations, indocyanine green (ICG) extraction than patients without ascites. Renal vascular resistance, glomerular filtration rate, mean arterial pressure, cardiac index and systemic vascular resistance were not significantly different between the two groups. By multiple regression analysis no significant correlation was found between liver tests (i.e., prothrombin time, serum bilirubin and albumin concentrations, ICG extraction), hepatic venous pressure gradient, cardiac index and systemic vascular resistance on the one hand and renal blood flow on the other. No significant correlation was found between glomerular filtration rate and liver tests. In conclusion, in patients with cirrhosis and ascites, renal hypoperfusion is not related to the severity of liver disease.

Ascites↗
PubMed1992

Plasma catecholamine concentrations are a reliable index of sympathetic vascular tone in patients with cirrhosis.

In patients with cirrhosis, the significance of elevated plasma catecholamine concentrations is unclear. Thus we investigated the relationship between plasma catecholamine concentrations and the hemodynamic effect of pindolol (an index of sympathetic vascular tone) in 10 patients with cirrhosis. Systemic and splanchnic hemodynamics and plasma catecholamine concentrations in the pulmonary artery and the splanchnic veins (hepatic and azygos veins) were studied before and after the oral administration of pindolol (20 mg). In basal conditions patients exhibited a hyperkinetic circulatory syndrome and elevated plasma catecholamine concentrations. Alterations in basal hemodynamics were correlated with plasma epinephrine concentrations but not with norepinephrine. Pindolol administration significantly decreased heart rate and increased right atrial pressure. After pindolol administration, individual hemodynamic changes (cardiac index, systemic vascular resistance, wedged hepatic venous pressure) were significantly correlated with plasma catecholamine concentrations. In conclusion, this study shows that in cirrhotic patients epinephrine may play a role in hemodynamic alterations, and plasma catecholamine concentrations are an index of sympathetic vascular tone.

Epinephrine↗
PubMed1992

Hemodynamic effects of terbutaline, a beta 2-adrenoceptor agonist, in conscious rats with secondary biliary cirrhosis.

The hemodynamic responses to terbutaline - a selective beta 2-adrenoceptor agonist - were studied in conscious normal rats and in conscious rats with secondary biliary cirrhosis. Compared with those of normal rats, dose-response curves in cirrhotic rats indicated significantly decreased reactivity in arterial pressure and heart rate. Half-maximal effective dose was not significantly different between the two groups. Terbutaline induced significant, dose-dependent decreases in portal pressure in both normal rats (9.3%) and cirrhotic rats (13.8%). In normal rats, terbutaline administration (32 micrograms.min-1.kg-1 body wt) increased both cardiac output and portal tributary blood flow, thus mimicking hemodynamic changes in cirrhotic rats. In cirrhotic rats, despite a significant increase in portal tributary blood flow (from 19.9 +/- 1.7 ml/min to 22.7 +/- 1.5 ml/min), terbutaline decreased portal pressure from 17.4 +/- 1.0 mm Hg to 15.0 +/- 0.8 mm Hg. This study indicates that increased beta 2-adrenoceptor stimulation in cirrhotic rats may be involved in hyperdynamic circulation. The association of a decreased portal pressure and increased splanchnic blood flow suggests that beta 2-adrenoceptor stimulation may modulate hepatic and portal collateral vascular resistance.

Adrenergic beta-Agonists↗
PubMed1992

Hemodynamic effects of calibrated stenosis of the superior mesenteric artery in conscious rats with portal vein stenosis.

Because superior mesenteric arterial blood flow is increased in portal hypertension and plays a role in elevated portal pressure, mechanical reduction of artery diameter should induce decreases in portal pressure and superior mesenteric arterial blood flow. In this study, calibrated superior mesenteric artery stenosis (induced with a 22-gauge needle) was performed in rats simultaneously with portal vein stenosis or 2 wk after creation of portal vein stenosis. Hemodynamic studies were performed 3 wk after induction of portal vein stenosis in conscious, unrestrained rats. At that time, neither weight loss nor digestive tract alterations were observed in rats with arterial stenosis. In neither group of rats with arterial stenosis was portal tributary blood flow significantly different from that of normal rats; nor was it significantly lower than in rats with portal vein stenosis without arterial stenosis. In both groups of rats with arterial stenosis, portal pressure was significantly lower (12.1 +/- 1.6 mm Hg and 12.5 +/- 1.8 mm Hg, respectively) than in rats subjected to portal vein stenosis (15.4 +/- 1.5 mm Hg) but significantly higher than in controls (7.2 +/- 1.0 mm Hg). In rats with arterial stenosis, cardiac index was also significantly lower than that in rats with portal vein stenosis but higher than that in controls. In conclusion, this study shows that both early and late superior mesenteric artery stenosis significantly reduce the degree of portal hypertension and the hyperkinetic state of rats with extrahepatic portal hypertension. Thus we can speculate that superior mesenteric artery stenosis might provide a new therapeutic approach for portal hypertension.

Analysis of Variance↗
PubMed1992

Persistence of a hyperdynamic circulation in cirrhotic rats following removal of the sympathetic nervous system.

The sympathetic nervous system is thought to play a role in the pathogenesis of the hyperdynamic circulation associated with portal hypertension. However, the extent of this role is unknown. After elimination of all neurological control by pithing, systemic and regional hemodynamics were studied in rats with portal hypertension caused by either portal vein stenosis or biliary cirrhosis. In normal rats, pithing induced a two-thirds decrease in mean arterial pressure and cardiac index. Compared with pithed normal rats, pithed portal vein-stenosed rats showed similar values for mean arterial pressure, cardiac index, and portal tributary blood flow. In contrast, pithed cirrhotic rats still showed hyperdynamic circulation with increased cardiac index and portal tributary blood flow. Although pithing dramatically reduced portal pressure in all groups, portal pressure remained significantly higher in portal hypertensive rats than in normal rats. These results indicate that in rats with portal vein stenosis, the sympathetic nervous system plays a major role in hemodynamic alterations, whereas in rats with cirrhosis, nonneurogenic factors participate in the pathogenesis of the hyperdynamic circulation.

Animals↗
PubMed1992

Hemodynamic effects of endotoxin and platelet activating factor in cirrhotic rats.

Acute infections may influence the hemodynamic alterations of liver disease. Therefore, the hemodynamic effects of endotoxin (LPS E. coli 0111:B4) in conscious, normal, and cirrhotic rats were compared. Endotoxin decreased cardiac index in cirrhotic but not in normal rats. Although the effect of endotoxin on portal tributary blood flow was minor in all animals, a reduction in portal pressure was found in cirrhotic rats. Because the most marked hemodynamic effects were observed in cirrhotic rats, the second part of our study investigated whether platelet activating factor played a role in endotoxin-induced hemodynamic alterations in the cirrhotic model. Platelet activating factor reduced cardiac index and kidney blood flow but did not influence portal tributary blood flow. Two antagonists to platelet activating factor reduced the adverse renal blood flow lowering effects of endotoxin in cirrhotic rats. Thus, it is suggested that the hemodynamic changes observed in cirrhosis may be aggravated during acute infections. Under this condition, antagonists to platelet activating factor may be of benefit in the prevention of hemodynamic complications induced by endotoxin.

Animals↗
PubMed1992

Ursodeoxycholic acid limits liver histologic alterations and portal hypertension induced by bile duct ligation in the rat.

Chronic administration of ursodeoxycholic acid (UDCA) has recently been suggested as a potential treatment for cholestatic liver disease. The purpose of this study was to examine the effects of chronic oral administration of UDCA on the histological, biochemical, and hemodynamic abnormalities induced by bile duct ligation in the rat. Fifty-one rats with ligation-section of the common bile duct were randomly and blindly assigned to receive UDCA (25 mg/kg each day) or placebo by gavage for 4 weeks. At the end of the treatment period, morphometric analysis showed that in rats treated with UDCA, hepatocyte and sinusoidal volume fractions were significantly higher than in rats receiving placebo [41.9 +/- 3.2% vs. 28.1 +/- 1.8%, (mean +/- SE) and 7.4 +/- 0.1% vs. 4.3 +/- 0.3%, respectively], whereas bile duct volume fraction (reflecting bile ductular proliferation) and connective tissue fraction were significantly lower in rats treated with UDCA than in rats receiving placebo (14.2 +/- 1.5% vs. 20.0 +/- 1.0% and 35.4 +/- 2.4% vs. 47.6 +/- 1.7%, respectively). Serum aminotransferase and alkaline phosphatase activities, and total serum bile acids and individual bile acid concentrations were not significantly different between the two groups. Portal pressure (12.7 +/- 0.5 mm Hg vs. 17.1 +/- 0.5 mm Hg), portal tributary blood flow (5.7 +/- 0.4 vs. 9.3 +/- 0.4 mL.min-1.100 g-1 body weight), and cardiac index (41.1 +/- 1.8 vs. 50.6 +/- 1.4 mL.min-1.100 g-1 body weight) were significantly lower in UDCA-treated rats than in placebo-treated animals. In portal vein stenosed rats, chronic administration of UDCA had no hemodynamic effects, a finding that suggests UDCA has no direct vasoactive effect on splanchnic circulation. It is concluded that in rats with bile duct ligation UDCA limits the severity of liver disease and consequently of portal hypertension and hyperkinetic circulation.

Animals↗
PubMed1992

Hemodynamic and sympathetic responses to human atrial natriuretic peptide infusion in patients with cirrhosis.

To determine the potential usefulness of atrial natriuretic peptide (ANP) in patients with cirrhosis, we examined the effects of the infusion of a low dose of alpha-human ANP (alpha hANP, 25 ng.kg-1.min-1 for 30 min) on renal, splanchnic, systemic hemodynamics and sympathetic outflow in eight patients. Pulmonary arterial plasma ANP concentrations increased from 59 +/- 9 to 328 +/- 41 pg/ml (mean +/- S.E., p less than 0.05). Mean values of glomerular filtration rate and renal plasma flow were not significantly changed. Individual renal plasma flow responses differed from one patient to another. Renal plasma flow increased in two patients, decreased in three and did not change in the other patients. Renal plasma flow changes were correlated with basal renal plasma flow values (r = -0.938, p less than 0.05) but not with arterial pressure changes or renal vein plasma norepinephrine concentration changes. Azygos blood flow increased from 0.43 +/- 0.10 to 0.63 +/- 0.13 l/min (p less than 0.05) and the hepatic-venous pressure gradient decreased from 19.9 +/- 1.5 to 17.5 +/- 2.9 mmHg in post-infusion (p less than 0.05). Mean arterial pressure decreased significantly by 18% and cardiac output by 12%. Systemic vascular resistance and pulmonary arterial plasma norepinephrine concentrations were not significantly modified. Thus, in patients with cirrhosis, alpha hANP appears to have a direct vasodilating action on renal arterioles when basal renal vascular tone is high. In addition, although alpha hANP might exert a portal hypotensive action, alpha hANP induced arterial hypotension as a result of both low cardiac output and a lack of increased sympathetic vascular tone. The arterial hypotensive action may, thus, limit the therapeutic use of low doses of alpha hANP in cirrhotic patients.

Aldosterone↗
PubMed1992

[Effects of halogenated anesthetics on splanchnic hemodynamic in normo- and hypovolemic cirrhotic rats].

The effects of 1 MAC of either halothane, enflurane or isoflurane on splanchnic haemodynamics were studied in cirrhotic rats that were either normovolaemic or hypovolaemic from haemorrhage. A group of conscious rats acted as the control group. Bile duct ligation had been carried out in all the rats four weeks previously to induce cirrhosis. At the time of the study, all the rats were anaesthetized with ether for catheterization of the left femoral artery and vein, and the left ventricle via the right carotid. The control group was allowed to awake. When the other rats started to recover, they were artificially ventilated with room air and 1 MAC of the halogenated agent. Heart rate and mean arterial blood pressure were monitored continuously. Once the animals had remained steady for one hour, 1.25 ml of blood for 100 g body weight was removed over a 10 min period. PaO2, PaCO2, arterial pH, heart rate, mean arterial blood pressure, cardiac index and regional blood flows (RBF) were measured before, and thirty minutes after the haemorrhage. Cardiac output and RBF were measured using the radioactive-labelled microsphere method. Only 32 animals were finally included, eight in each group. Splanchnic, portal and hepatic arterial blood flows were similar in conscious rats and in those receiving isoflurane or halothane, and were higher than in those receiving enflurane. The lowest splanchnic and portal venous blood flows were found in those rats receiving enflurane. After haemorrhage, these RBF decreased significantly in all groups except in the enflurane group.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, Inhalation↗
PubMed1992

[Renal sympathetic nervous activity in patients with cirrhosis].

This study was designed to evaluate the renal contribution to overall sympathetic nerve hyperactivity and the relationships between renal sympathetic activity and systemic, splanchnic or renal hemodynamics in a series of 55 cirrhotic patients. Plasma noradrenaline concentrations were significantly higher in the renal vein than in the pulmonary artery (803 +/- 54 vs 608 +/- 47 pg/ml, P less than 0.01). These two concentrations were significantly correlated, which suggests that renal sympathetic activity and overall sympathetic activity increase in parallel in patients with cirrhosis. However, the estimated renal net release of noradrenaline was not correlated with plasma noradrenaline concentration in the pulmonary artery, suggesting that overall sympathetic nerve activity is not directly dependent on renal contribution in patients with cirrhosis. Neither plasma noradrenaline concentration in the renal vein nor renal net release of noradrenaline were correlated with systemic. splanchnic or renal hemodynamics. Thus, this study did not show a major role of renal sympathetic activity in the hemodynamic changes in cirrhosis.

Adult↗
PubMed1992

Long-term sympathetic and hemodynamic responses to clonidine in patients with cirrhosis and ascites.

The aim of the present study was to examine the short- and long-term effects of the alpha 2-agonist clonidine on sympathetic overactivity, systemic, splanchnic, and renal circulation changes, and abnormal renal sodium excretion in cirrhotic patients with ascites. Of 17 patients, 8 received clonidine and 9 a placebo. Measurements were taken before and after either a single dose of clonidine (150 micrograms) and placebo or a 1-week treatment with clonidine (150 micrograms/day) and placebo. Clonidine but not placebo induced significant short- and long-term decreases in plasma norepinephrine concentrations in the pulmonary artery and the right renal vein. Acute clonidine administration induced a significant reduction in cardiac output, heart rate, arterial pressure, and hepatic venous pressure gradient but had no effect on renal hemodynamics. Long-term clonidine administration induced a significant decrease in the hepatic venous pressure gradient from 20.1 +/- 1.9 to 17.6 +/- 2.0 mm Hg (mean +/- SEM) but had no significant effects on systemic or renal hemodynamics or renal excretion of sodium. It is concluded that long-term clonidine administration in cirrhotic patients induced a sustained decrease in sympathetic nervous activity and portal pressure. In contrast, clonidine had no prolonged effect on systemic hemodynamics. In addition, short- and long-term clonidine administration did not modify renal hemodynamics or induce a natriuretic response in patients with ascites.

Ascites↗
PubMed1991

Variability of hemodynamic values and plasma catecholamine concentrations over a one-hour period in conscious, restrained rats.

Restrained conscious rats have been widely used for physiological and pharmacological hemodynamic studies. In this condition, the variability of the circulation is unclear. Repeated measurements in restrained normal rats showed stable systemic hemodynamics (cardiac output ranging from 130 +/- 14 to 174 +/- 10 mL/min, mean arterial pressure ranging from 109 +/- 9 to 117 +/- 5 mmHg) and splanchnic hemodynamics (splanchnic blood flow ranging from 8.51 +/- 1.89 to 13.01 +/- 1.45 mL min-1 100 g-1 body wt) over a period of 1 hr. Slight but not significant hemodynamic variations, however, occurred in pulmonary blood flow. Similarly, plasma noradrenaline concentrations did not vary over this period (plasma noradrenaline level ranging from 186 +/- 36 to 358 +/- 64 pg/mL). These plasma noradrenaline concentrations were similar to those measured in a group of conscious unrestrained rats 3 hr after recovery from surgery (292 +/- 60 pg/mL). A significant correlation was observed between plasma noradrenaline concentration and heart rate.

Animals↗
PubMed1991

Regional sympathetic activity, severity of liver disease and hemodynamics in patients with cirrhosis.

One hundred and eight patients with cirrhosis (23 grade A, 46 grade B and 39 grade C, according to Pugh's classification) underwent hemodynamic studies and plasma catecholamine concentration measurements. Blood samples were withdrawn from the pulmonary artery (n = 108), the hepatic vein (n = 108), the azygos vein (n = 59), the right renal vein (n = 66), the right jugular vein (n = 34) and the femoral vein (n = 33). Plasma noradrenaline concentrations in the pulmonary artery and the hepatic vein were more elevated in grade B (607 +/- 52 and 402 +/- 42 pg/ml, respectively) and C patients (630 +/- 59 and 475 +/- 53 pg/ml, respectively) than in grade A patients (411 +/- 51 and 243 +/- 40 pg/ml, respectively). Plasma noradrenaline concentrations from these two vessels were negatively correlated with indocyanine green clearance. These results indicate that both overall and splanchnic sympathetic activities are dependent on altered hepatic function. Significant correlations were found between the wedged hepatic venous pressure and plasma noradrenaline concentrations from either the pulmonary artery, the hepatic vein or the azygos vein. These correlations indicate that both overall and splanchnic sympathetic activities are dependent on the degree of portal hypertension. Moreover, significant correlations were found between hepatic venous plasma noradrenaline concentrations and systemic hemodynamic values, suggesting that splanchnic sympathetic nervous activity could either play a role in the systemic hyperkinetic syndrome or be a consequence of this hyperkinetic syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Divergent circulatory effects of betaxolol in conscious and anesthetized normal and portal hypertensive rats.

We aimed to define the circulatory effects of beta 1-blockade in conscious normal and portal hypertensive rats and determine if pentobarbital anesthesia affected these responses. A selective beta 1-antagonist, betaxolol, was given to four groups: conscious and anesthetized sham-operated and portal hypertensive rats. Cardiac output and splanchnic organ blood flows were measured by radioactive microspheres twice in each rat, before and 15 min after betaxolol. Both groups of conscious rats maintained mean arterial pressure despite significant decreases in cardiac output and heart rate, by increasing total peripheral resistance. Anesthetized rats were unable to do this and thus also diminished arterial pressure significantly, with portal hypertensive rats showing greater decreases than sham-operated rats. Portal tributary flow and portal pressure decreased only in the anesthetized rats. Autoregulation of splanchnic blood flow was not uniform between groups or organs: although splenic flow decreased in all four groups, intestinal blood flow decreased only in anesthetized portal hypertensive rats. The greatest decreases in several splanchnic organ blood flows were seen in this latter group. These results indicate that: (i) pentobarbital markedly changes systemic and splanchnic responses to beta 1-blockade; (ii) splanchnic autoregulation is not uniform--the intestinal circulation enjoys more protection than the splenic; and (iii) portal hypertensive rats seem to be more vulnerable to the circulatory effects of beta 1-blockade.

Animals↗
PubMed1991

PAF increases hepatic vascular resistance and glycogenolysis in vivo.

Administration of platelet-activating factor (PAF) to portal venous circulation of anesthetized fed rats produced decreases in mean arterial pressure and increases in hepatic portal pressure and blood glucose concentration. These responses to PAF were dose dependent with ED50 values of 0.02-0.05 micrograms/kg and specific as lyso- and enantio-PAF did not reproduce effects of PAF. Specific PAF receptor antagonist SRI 63-675 (75 micrograms/kg) inhibited significantly these PAF (0.1 micrograms/kg)-induced responses in rats. Administration of prazosin (500 micrograms/kg) and propranolol (400 micrograms/kg) to rats abolished phenylephrine (50 micrograms/kg)-induced increases in mean arterial pressure, hepatic portal pressure, and blood glucose concentration but did not prevent PAF (1 microgram/kg)-induced alterations in these parameters. Glycogen phosphorylase alpha levels were increased significantly in livers of rats after administration of PAF (1 microgram/kg) or phenylephrine (50 micrograms/kg). Administration of prazosin and propranolol to rats inhibited phenylephrine- but not PAF-induced activation of hepatic glycogen phosphorylase. Hepatic adenosine 3',5'-cyclic monophosphate (cAMP) concentration was increased slightly by PAF, but these increases were eliminated by adrenergic blockade, suggesting that activation of hepatic glycogen phosphorylase by PAF is not dependent on increases in cAMP. Increases in hepatic portal pressure and blood glucose concentration in response to PAF (0.1 micrograms/kg) were not attenuated in adrenalectomized rats. Moreover, PAF (0.1 micrograms/kg) stimulated increases in hepatic portal pressure after administration of the ganglionic blocking agent chlorisondamine (2.5 mg/kg) to adrenalectomized rats. Administration of PAF (0.05 micrograms/kg) to rats instrumented with pulse Doppler flow probes produced decreases in hepatic arterial and portal vein blood flow and increases in hepatic arterial and portal vascular resistance. These observations provide direct evidence that PAF regulates hepatic hemodynamics and glycogenolysis in vivo. It is suggested that PAF plays an important role in regulating hepatic blood flow and supplying extrahepatic tissues with energy substrates by sympathetic-independent mechanism(s) after its release in acute pathophysiological situations.

Animals↗
PubMed1991

Adenosine and hemodynamic alterations in cirrhotic rats.

This study evaluated the hypothesis that adenosine may participate in the hemodynamic alterations observed in conscious unrestrained cirrhotic rats. In sham-operated rats, adenosine (20 micrograms.100 g body wt-1.min-1 iv) induced hyperdynamic circulation and significantly increased portal pressure, mimicking the hemodynamic changes observed in cirrhosis. Although adenosine significantly increased hyperdynamic circulation and portal pressure in cirrhotic rats, these changes were significantly less marked than in sham-operated rats. 8-Phenyltheophylline (20 micrograms.100 g body wt-1.min-1 iv), a specific and potent adenosine antagonist, significantly decreased portal tributary blood flow in sham-operated rats (-18.0 +/- 5.6%) but did not have a significant effect in cirrhotic rats. The limited effect of 8-phenyltheophylline was not due to an insufficient dose, since the dose administered antagonized the hemodynamic effect of exogenous adenosine up to 40 micrograms.100 g body wt-1.min-1. We conclude that in certain circumstances, although adenosine may aggravate the hyperdynamic circulation, in normal conditions, the hemodynamic alterations observed in cirrhotic rats are not mediated by adenosine.

Adenosine↗