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Biomedical subjects

D Lebrec

Publications and source records attributed to D Lebrec.

At least 109 records · Page 6Linked to original sources
PubMed1996

Role of sympathetic cardiovascular tone in control of arterial pressure in rats with cirrhosis.

Although an increase in sympathetic nervous activity has been recognized in cirrhosis, the contribution of this overactivity to the regulation of arterial pressure is unknown. The arterial pressure response to increasing doses of hexamethonium (0.05 to 3.2 mg.kg-1.min-1), a ganglionic blocker that decreases sympathetic cardiovascular tone, was explored in normal rats and in two models of portal hypertension, i.e., rats with cirrhosis and rats with portal vein stenosis. Changes in plasma norepinephrine concentrations were greater in rats with cirrhosis (356 +/- 50 vs 166 +/- 30 pg/ml, p = 0.04) than in normal rats (186 +/- 23 vs 86 +/- 31 pg/ml, p = 0.06) and rats with portal vein stenosis (103 +/- 37 vs 93 +/- 5 pg/ml, p = 0.10). The maximum decrease in arterial pressure was obtained at a dose of 1.6 mg.kg-1.min-1 in each group. However, the decrease in arterial pressure was significantly greater in rats with cirrhosis (-25 +/- 2%) than in normal rats (-11 +/- 1%) and in rats with portal vein stenosis (-13 +/- 2%) (p = 0.04). In conclusion, the results of this study suggest that the sympathetic cardiovascular tone is more important for the maintenance of arterial pressure in rats with cirrhosis than in normal rats and in rats with portal vein stenosis.

Animals↗
PubMed1996

Systemic and splanchnic hemodynamic changes in patients with hepatic schistosomiasis.

Although hepatic schistosomiasis is a common cause of portal hypertension, only a few hemodynamic studies, in humans, have been published on this subject. The aim of this study was to determine the systemic and splanchnic hemodynamic changes in hepatic schistosomiasis and to evaluate the influence of liver fibrosis on these changes. A retrospective analysis of a series of 13 patients with hepatic schistosomiasis who had undergone hemodynamic studies was performed. Portal or perisinusoidal fibrosis was present at liver biopsy in 8 patients. The control group included 22 patients with chronic hepatitis and normal hepatic venous pressure gradients. Patients with schistosomiasis exhibited high cardiac index (4.11 +/- 1.15 l.min-1.m-2 vs 2.99 +/- 0.85 l.min-1.m-2; p < 0.05) and low systemic vascular resistance (1039 +/- 316 dyn.s.cm-5 vs 1334 +/- 336 dyn.s.cm-5; p < 0.05). The hepatic venous pressure gradient and hepatic blood flow were normal. Azygos blood flow was markedly increased (0.90 +/- 0.66 l.min-1 vs 0.13 +/- 0.04 l.min-1; p < 0.05). Hemodynamic values were not significantly different between patients with liver fibrosis and those without fibrosis at liver biopsy. In conclusion, patients with hepatic schistosomiasis had a hyperkinetic systemic and splanchnic circulation. In patients with esophageal varices, a normal hepatic venous pressure gradient confirmed presinusoidal portal hypertension. The presence of portal or perisinuoidal fibrosis did not influence hyperdynamic splanchnic state.

Adult↗
PubMed1996

Validation of transit-time ultrasound flow probes to directly measure portal blood flow in conscious rats.

Direct measurement of portal venous blood flow is technically difficult, yet crucial for accurate assessment of liver hemodynamic and metabolic functions. The aim of this investigation was to assess the feasibility of implanting transit-time ultra-sound (TTUS) perivascular flow probes on the portal vein of the rat and to validate this technique as a means of directly measuring portal blood flow in conscious rats. A TTUS flow probe was implanted on the portal veins of 10 rats. One week later, portal flow was measured under basal conditions in these rats by TTUS probes and after pharmacological manipulation of portal flow by intravenous injections of Glypressin or infusions of adenosine while the rats were conscious. Portal flow was simultaneously measured in the same rats using radioactive microspheres. Basal systemic hemodynamics, regional blood flows to splanchnic organs, and portal blood pressure were not significantly modified by the presence of the probe on the portal vein compared with a control group of rats not instrumented with flow probes. Basal portal flows measured by the TTUS and microsphere techniques were not different (20.6 +/- 2.6 and 17.6 +/- 1.3 ml/min). After Glypressin, portal flows measured by the TTUS and microsphere techniques were 12.3 +/- 2.9 and 9.3 +/- 1.9 ml/min and, in response to adenosine, increased to 27.2 +/- 3.4 and 31.3 +/- 4.1 ml/min. There was no significant difference between the TTUS and microsphere flows. Both the relationship between absolute flows and the relationship between changes in flows measured by the two techniques were linear with slopes approaching 1.0. Thus TTUS flow probes can be used to directly measure portal flow from the portal vein in conscious rats. This methodology is as effective as the standard technique of radioactive microspheres. More importantly, the TTUS technique allows for continuous direct measurement of portal flow and eliminates the hazards and sources of error associated with the radioactive microsphere technique.

Animals↗
PubMed1996

Long-term hemodynamic effects of portocaval shunt and Sugiura procedure in patients with cirrhosis.

Systemic and splanchnic hemodynamics were studied before and six months after a portal systemic shunt (n = 6) or a Sugiura procedure (n = 9) in 15 patients with cirrhosis and a past history of variceal bleeding. Hepatic blood flow was estimated by hepatic extraction and clearance of continuous indocyanine green infusion. Azygos blood flow was measured with a continuous thermodilution catheter. After portocaval shunt, the cardiac index increased significantly from 4.0 +/- .4 to 5.4 +/- 0.8 l/min m2 (p < 0.05), the hepatic venous pressure gradient and hepatic blood flow were significantly decreased from 21 +/- 3 to 13 +/- 5 mm Hg (p < 0.05) and from 1.20 +/- 0.35 to 0.37 +/- 0.16 l/min (p < 0.05) respectively. The decrease in azygos blood flow was not significant (0.51 +/- 0.31 vs 0.25 +/- 0.33 l/min; p = 0.1). After Sugiura procedure, there was no significant change in cardiac index, hepatic venous pressure gradient, hepatic blood flow or azygos blood flow. This is the first study to show the long-term maintenance of splanchnic and systemic hemodynamics in patients with cirrhosis after Sugiura procedure. The absence of long-term hemodynamic alterations could explain the absence of encephalopathy after this procedure.

Azygos Vein↗
PubMed1996

[Hepatic encephalopathy after injection of lanreotide, a somatostatin analog].

We report one case of hepatic encephalopathy following the administration of a somatostatin analogue (lanreotide) in a patient with a pancreatic endocrine tumor and liver metastases. Hepatic insufficiency was absent. The diagnosis of hepatic encephalopathy relied upon a positive re-challenge test, elevated veinous ammonemia, suggestive findings on electroencephalogram and lack of recurrence after lanreotide discontinuation. Encephalopathy was thought to be due to a significant decrease in hepatic blood flow caused by lanreotide; an associated thrombosis of the portal vein may have played a facilitating role.

Aged↗
PubMed1995

Ischemic hepatitis due to obstructive sleep apnea.

The case of an obese patient who developed massive centrilobular liver cell necrosis, severe coagulopathy, acute renal failure, and encephalopathy is presented. Hypovolemia and heart failure were absent, but the acute liver disease was associated with severe arterial hypoxemia due to obstructive sleep apnea that was shown by the nocturnal blood oxygen desaturation, the results of the polysomnographic study, and normal baseline pulmonary function tests. In this obese patient, liver cell necrosis was caused by severe liver cell hypoxia secondary to severe arterial hypoxemia as a consequence of obstructive sleep apnea associated with a Pickwickian syndrome. This observation is consistent with the hypothesis that liver ischemia was directly related to severe arterial hypoxemia.

Female↗
PubMed1995

Effects of superior mesenteric artery stenosis on splanchnic and systemic hemodynamics in conscious rats with biliary cirrhosis.

BACKGROUND/AIMS: Since portal tributary blood flow is increased in portal hypertension due to cirrhosis, a reduction in mesenteric arterial blood flow should decrease portal pressure. METHODS: Calibrated stenosis of the superior mesenteric artery was performed in bile duct ligated rats, using a 22-gauge needle. Arterial stenosis was performed 4 weeks after bile duct ligation. Hemodynamic studies were performed in the 5th week following bile duct ligation in conscious rats. RESULTS: At that time, no digestive tract alterations were observed. In rats with mesenteric arterial stenosis, portal pressure was 12.2 +/- 2.0 mmHg; this value was lower than in rats with cirrhosis without arterial stenosis (14.5 +/- 1.1 mmHg) but higher than normal rats (5.8 +/- 0.7 mmHg). In rats with cirrhosis with mesenteric arterial stenosis, portal tributary and mesenteric blood flows were lower than in rats with cirrhosis without arterial stenosis and not significantly different from normal rats. In rats with mesenteric stenosis, cardiac index was significantly lower than in rats with cirrhosis and not significantly different from normal rats. CONCLUSION: This study shows that calibrated superior mesenteric arterial stenosis normalized portal tributary blood flow and reduced but did not normalize the degree of portal hypertension.

Animals↗
PubMed1995

Plasma endotoxin and tumor necrosis factor-alpha in the hyperkinetic state of cirrhosis.

BACKGROUND/AIMS: The factors which trigger the hyperdynamic circulation in cirrhosis remain poorly defined. Plasma levels of the potent vasodilators endotoxin and tumor necrosis factor-alpha may be elevated in patients with cirrhosis, and therefore the potential role of these substance was assessed in the hyperkinetic circulation in cirrhosis. METHODS: Forty-nine patients in stable condition underwent systemic and hepatic hemodynamic measurements, and right atrial blood sampling for endotoxin and tumor necrosis factor-alpha assays. Patients were divided into three groups according to the severity of the disease: group 1 consisted of eight patients with normal liver or mild hepatic fibrosis, and groups 2 and 3 contained 17 and 24 patients with Child A and Child B or C cirrhosis, respectively. RESULTS: Systemic vascular resistance decreased and cardiac index increased from group 1 to 3: 1530 +/- 196 dyn.s.cm-5 to 990 +/- 72 dyn.s.cm-5 (mean +/- S.E.; p<0.05) and 3.1 +/- 0.3 l.min-1.m-2 to 4.2 +/- 0.2 l.min-2.m-2, respectively. Endotoxin was not detectable in any of the groups and tumor necrosis factor-alpha was increased in one patient from group 1, six from group 2 and six from group 3. Mean tumor necrosis factor-alpha levels were not different among the groups (10 +/- 5, 18 +/- 5 and 17 +/- 7 pg/ml in groups 1, 2 and 3, respectively). Systemic vascular resistance and cardiac index were not correlated to plasma tumor necrosis factor-alpha levels; patients with increased levels of this cytokine did not have worse hyperdynamic circulation in any of the groups. CONCLUSIONS: These results suggest that tumor necrosis factor-alpha and endotoxin do not play a role in the maintenance of the hyperkinetic state of cirrhosis.

Hemodynamics↗
PubMed1995

Endogenous pulmonary nitric oxide production measured from exhaled air is increased in patients with severe cirrhosis.

BACKGROUND/AIMS: Endogenous pulmonary nitric oxide production may be increased in severe cirrhosis and contribute to pulmonary vasodilation. This study assessed pulmonary nitric oxide production by measuring nitric oxide in the exhaled air in patients with severe cirrhosis and examined the relationship between exhaled nitric oxide and pulmonary hemodynamics in these patients. METHODS: Nitric oxide concentrations and production were measured in the exhaled air in six Child-Pugh class C patients with cirrhosis and 21 non-smoking healthy controls. Systemic and pulmonary hemodynamics were measured in patients only. RESULTS: Nitric oxide concentration (32.0 +/- 1.7 (mean +/- SEM) vs. 8.9 +/- 1.0 ppb) and production (9.2 +/- 1.3 vs. 3.1 +/- 0.3 nmol/min) in exhaled air were significantly higher in patients than in controls. Patients had high cardiac output (8.5 +/- 0.9 l/min), low pulmonary and systemic vascular resistance (57 +/- 10 and 767 +/- 93 dyn.s.cm-5, respectively) under baseline conditions. A significant negative correlation was found between pulmonary vascular resistance and exhaled nitric oxide production (r=0.943, p=0.05) but not between cardiac output or systemic vascular resistance and nitric oxide measured in exhaled air. CONCLUSIONS: Endogenous pulmonary nitric oxide production measured from exhaled air is increased in patients with cirrhosis and liver failure. Increased in patients with cirrhosis and liver failure. Increased nitric oxide production may also contribute to cirrhosis-induced pulmonary vasodilatation.

Female↗
PubMed1995

Blunted natriuresis and abnormal systemic hemodynamic responses to C-type and brain natriuretic peptides in rats with cirrhosis.

BACKGROUND/AIMS: The effects of C-type and brain natriuretic peptides (CNP and BNP, respectively) on renal excretion of sodium and hemodynamics have not yet been studied in cirrhosis. METHODS: This study aimed to examine the effects of saline, CNP (300 ng.kg-1.min-1 i.v. for 30 min) and BNP (600 ng.kg-1.min-1 i.v. for 30 min) on natriuresis and diuresis in normal and rats with cirrhosis. Moreover, regional and systemic hemodynamics were measured prior to and following CNP and BNP administration in normal rats and rats with cirrhosis with ascites. RESULTS: In rats with cirrhosis, the effects of CNP or BNP or natriuresis and diuresis did not significantly differ from the effects of saline. CNP significantly decreased portal pressure and systemic vascular resistance and significantly increased the cardiac index. BNP significantly decreased portal tributary blood flow, portal pressure and cardiac index. In normal rats, natriuresis and diuresis were significantly higher with CNP and BNP than with saline. Systemic hemodynamics were not changed by CNP. A decrease in arterial pressure was the sole BNP-induced hemodynamic change. CONCLUSIONS: In conclusion, this study shows that the natriuretic response to pharmacological doses of CNP and BNP is blunted in rats with cirrhosis. This blunting may be related to an activation of the endogenous antinatriuretic systems secondary to systemic vasodilation (by CNP) or to a decreased cardiac index (by BNP). Finally, this study shows that CNP and BNP have a portal hypotensive action.

Animals↗
PubMed1995

Lack of vascular hyporesponsiveness to the L-type calcium channel activator, Bay K 8644, in rats with cirrhosis.

BACKGROUND/AIMS: In cirrhosis, the mechanism(s) for vascular hyporesponsiveness to vasoconstrictors such as, alpha 1-adrenoceptor agonists, vasopressin and angiotensin II, are unclear. Moreover, vascular reactivity to substances such as L-type calcium channel activators is unknown. METHODS: Thus, pressor dose-response curves to vasoconstrictors [phenylephrine (an alpha 1-agonist, 0.1-500 micrograms/kg) angiotensin II (10-500 ng/kg), vasopressin (0.01-5 IU/kg), and Bay K 8644 (an L-type calcium channel activator, 0.5-50 micrograms/kg)] were obtained in normal rats and in rats with secondary biliary cirrhosis. All experiments were performed in ganglionic-blocked animals to limit the influence of cardiovascular reflexes. Doses of vasoconstrictor necessary to obtain a 40 mmHg increase in arterial pressure (D40) were calculated. RESULTS: Compared to normal animals, rats with cirrhosis had significantly higher D40 values for angiotensin II (171 +/- 57 vs. 344 +/- 41 ng/kg), phenylephrine (2.6 +/- 0.2 vs. 26.4 +/- 10.7 micrograms/kg) and vasopressin (73 +/- 19 vs. 401 +/- 150 mU/kg). Pressor responses to Bay K 8644 did not differ between normal rats and rats with cirrhosis (8.8 +/- 0.9 vs. 10.5 +/- 2.1 micrograms/kg). CONCLUSIONS: In conclusion, this study shows that cirrhosis produces vascular hyporeactivity to phenylephrine, vasopressin and angiotensin II but not to Bay K 8644. Therefore, cirrhosis impairs certain constrictor mechanisms which are shared by phenylephrine, angiotensin II and vasopressin but which do not contribute to the vascular response to Bay K 8644.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1995

Haemodynamic assessment.

The degree of portal hypertension and its haemodynamic complications can be easily determined. However, the interpretation of these values is not entirely clear and further clinical and experimental studies are needed to explain why some patients with portal hypertension bleed from oesophageal varices while others do not.

Hemodynamics↗
PubMed1995

Short-term cardiovascular effects of somatostatin in patients with cirrhosis.

Somatostatin is used to treat variceal hemorrhage in patients with cirrhosis and portal hypertension. Its systemic hemodynamic effects, however, are not yet well defined. Since cardiomyopathy or pulmonary artery hypertension may occur in patients with cirrhosis, definition of the systemic hemodynamic effects of somatostatin or its analogue octreotide is of clinical importance. The aim of this study was to evaluate the effects of somatostatin, at different doses and under different conditions of administration, on the systemic hemodynamics in 17 patients with cirrhosis. Two sets of experiments were performed. In the first, eight patients received two different bolus doses (100 and 250 micrograms) of somatostatin. The second set of experiments was designed to study the hemodynamic effects of the combination of a bolus and an infusion of somatostatin. Nine other patients received one bolus of 250 micrograms of somatostatin, followed by a 250 micrograms/h infusion for 65 min. A second bolus of 250 micrograms of somatostatin was injected in these patients after 35 min of infusion. Before and for 30 min after each bolus, systemic hemodynamics were measured. Following a bolus of somatostatin, a dose-dependent decrease in heart rate (from 77 +/- 3 to 73 +/- 5 beats/min with 100 micrograms, and from 78 +/- 4 to 68 +/- 5 beats/min with 250 micrograms, p < 0.05) and increases in systemic and pulmonary artery pressures were observed. The combination of an infusion and a bolus of somatostatin significantly reduced the increases in systemic and pulmonary artery pressures.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Validation of 1- and 2-mm transit-time ultrasound flow probes on mesenteric artery and aorta of rats.

The aim of this investigation was to validate and calibrate the 1- and 2-mm transit-time ultrasound, perivascular flow probes on the superior mesenteric artery and aorta of the rat by using an in vivo and in situ calibration system. The baseline blood flows measured by the flowmeter zero-flow function and the true-zero flow measurement, after complete occlusion of the vessels, were not different. The probes were then calibrated, in situ, by timed-volume measurements with a blood/saline pump-perfused circuit. The relationship between measured flow and true flow was linear for both probes. The slope of the 1-mm probe data was not significantly different from the line of identity, whereas the 2-mm probe data slightly overestimated the true flow (slope = 1.2, y-intercept = -3.2 ml/min). The slope of the middle region of the 2-mm probe data, however, was not significantly different from the line of identity, suggesting that the 2-mm probe has a window of accuracy over this range of flows. Progressive elimination of the low and high data points varying the most from the line of identity and reanalysis of the data revealed that the window of accuracy for the 2-mm probe, under our experimental conditions, was between 10.4 and 45.1 ml/min.

Animals↗
PubMed1994

Blood and plasma 5-hydroxytryptamine levels in patients with cirrhosis.

Serotoninergic mechanisms are thought to play a role in portal hypertension. Because this biomine is metabolized by the liver, peripheral blood and plasma levels of 5-hydroxytryptamine and 5-hydroxyindole acetic acid (the main metabolite of 5-hydroxytryptamine) were measured in 30 patients with cirrhosis. Whole-blood 5-hydroxytryptamine levels were significantly lower in patients with cirrhosis (158 +/- 28 nM) than in age-matched controls (332 +/- 19 nM), and no correlation was found between these levels and the severity of cirrhosis. Unconjugated plasma 5-hydroxytryptamine levels, an indication of the active form of 5-hydroxytryptamine, were significantly higher in patients with cirrhosis than in controls (6.8 +/- 1.7 nM and 3.4 +/- 0.5 nM, respectively), and in patients with cirrhosis these levels were higher in Pugh grade A than in Pugh grade C patients. Conjugated-plasma 5-hydroxytryptamine levels were not significantly different between patients with cirrhosis (32.2 +/- 8.1 nmol/L) and controls (16.4 +/- 1.4 nmol/L). Plasma 5-hydroxyindole acetic acid was significantly lower in patients with cirrhosis than in controls (1.5 +/- 0.1 nmol/L and 2.3 +/- 0.1 nmol/L, respectively). In conclusion, this study shows that serotoninergic mechanisms are altered in patients with cirrhosis.

Hepatic Veins↗