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Biomedical subjects

R Moreau

Publications and source records attributed to R Moreau.

At least 163 records · Page 9Linked to original sources
PubMed1989

Relationship between oxygen transport and oxygen uptake in patients with cirrhosis: effects of vasoactive drugs.

To elucidate the relationship between oxygen transport and uptake in cirrhosis, we studied the effects of three vasoactive drugs that change O2 transport. Systemic hemodynamics, blood gases and lactate concentration were measured in patients with alcoholic cirrhosis before and after intravenous dobutamine, propranolol and nitroglycerin. Nine patients received successively dobutamine and then propranolol. Ten patients received nitroglycerin. Three other patients without cirrhosis (controls) received dobutamine. In patients with cirrhosis, dobutamine infusion was accompanied by a significant increase in cardiac output (+21%), systemic O2 transport (+21%) and O2 uptake (+12%), whereas O2 extraction ratio and arterial lactate concentration did not change significantly. Propranolol administration was followed by a significant decrease in cardiac output (-24%) and systemic O2 transport (-25%) and a significant increase in O2 extraction ratio (+19%), whereas O2 uptake and arterial lactate concentration did not change. Nitroglycerin infusion was accompanied by a significant decrease in cardiac output (-21%), systemic O2 transport (-26%) and O2 uptake (-10%), whereas O2 extraction ratio (+18%) and arterial lactate concentration (+31%) significantly increased. In control patients, dobutamine infusion was accompanied by an increase in cardiac output and in systemic O2 transport and by a decrease in O2 extraction ratio, whereas O2 uptake was not modified. These results suggest that O2 uptake may be abnormally dependent on O2 transport in patients with cirrhosis.

Biological Transport↗
PubMed1989

Low dose of nitroglycerin failed to improve splanchnic hemodynamics in patients with cirrhosis: evidence for an impaired cardiopulmonary baroreflex function.

High doses of nitroglycerin may decrease portal pressure in patients with cirrhosis with untoward effects such as arterial hypotension and a decrease in systemic O2 uptake. In the present study, low doses of nitroglycerin (7 to 15 micrograms per min, i.v.) were administered in 11 patients with cirrhosis in order to unload cardiopulmonary baroreceptor--one of the possible mechanisms by which nitroglycerin may improve splanchnic hemodynamics--and moreover to avoid deleterious systemic effects. Nitroglycerin significantly decreased right atrial pressure (-35%) and pulmonary wedged pressure (-27%) with significant increase in plasma norepinephrine concentration (+23%), which indicated that cardiopulmonary baroreceptor unloading was achieved. Changes in systemic hemodynamics were slight, although significant, with a decrease in arterial pressure (-8%) and an increase in heart rate (+8%); this indicates a minimal effect on high-pressure baroreflexes. In contrast, no significant change was observed in hepatic venous pressure gradient, hepatic blood flow and azygos blood flow. However, the fraction of cardiac output reaching the azygos system significantly increased by 18%. Plasma renin activity did not change significantly. Moreover, O2 transport and uptake were significantly decreased. These findings show that low doses of nitroglycerin failed to improve splanchnic hemodynamics in patients with cirrhosis. These results suggest an impaired cardiopulmonary baroreflex function which is probably located on the efferent arch.

Adult↗
PubMed1989

Effects of oxygen inhalation on tissue oxygenation in patients with cirrhosis. Evidence for an impaired arterial baroreflex control.

In patients with cirrhosis, O2 uptake, i.e., O2 consumption, is abnormally decreased. We administered 50% O2 for 30 min in eight patients with alcoholic cirrhosis to determine whether the subsequent increase in arterial O2 content may correct the low O2 consumption. In addition, we studied in these patients the reflex control of cardiac output and blood pressure by arterial baroreceptors, as O2 inhalation induces a systemic vasoconstriction. Arterial O2 tension, oxyhaemoglobin saturation and arterial O2 content significantly increased as well as systemic vascular resistance and arterial pressure. In contrast, O2 consumption (which was below normal values) under basal conditions, O2 transport, O2 extraction ratio, heart rate, right atrial and pulmonary wedged pressures, cardiac output, hepatic venous pressures, hepatic and azygos blood flows were unaffected by O2 administration. In three patients receiving air, no significant change was observed. Our results show that, in patients with cirrhosis, inhalation of 50% O2 does not correct O2 consumption. We may conclude that reflex control of cardiac output and arterial pressure by arterial baroreceptors is impaired in these patients.

Blood Pressure↗
PubMed1989

Reduction of portal pressure by acute administration of furosemide in patients with alcoholic cirrhosis.

In patients with cirrhosis, it has been demonstrated that blood volume and degree of portal hypertension are correlated. Hence, a reduction of blood volume by furosemide could decrease portal pressure and could thereby be useful in the treatment of portal hypertension. Splanchnic and systemic haemodynamics were evaluated before and 1 h after intravenous administration of furosemide (0.75 mg/kg) in 10 patients with cirrhosis. Furosemide significantly increased haemoglobin from 12.4 to 13.0 g/dl and patients passed more than 1 l of urine within the 3 h following furosemide administration. These findings confirm that blood volume decreased after diuretic administration. Cardiac output significantly decreased from 6.6 +/- 2.3 to 5.5 +/- 2.2 l/min, while arterial pressure and heart rate did not change significantly. Furosemide significantly decreased wedged hepatic venous pressure from 31.1 +/- 6.2 to 27.7 +/- 5.2 mmHg, but not free hepatic venous pressure. Accordingly, the hepatic venous pressure gradient significantly decreased from 22.1 +/- 5.4 to 19.5 +/- 4.0 mmHg. Azygos blood flow and hepatic blood flow also significantly decreased from 0.40 +/- 0.17 to 0.31 +/- 0.13 l/min and from 1.49 +/- 0.50 to 0.82 +/- 0.30 l/min, respectively. These results show that diuretic therapy markedly influences splanchnic haemodynamics.

Adult↗
PubMed1989

Hyperkinetic circulatory syndrome in patients with presinusoidal portal hypertension. Effect of propranolol.

This study evaluates systemic and splanchnic haemodynamics and the effect of propranolol in 15 patients with presinusoidal portal hypertension (portal vein obstruction, n = 11; schistosomiasis, n = 4). These patients exhibited a hyperkinetic circulatory syndrome characterized by high cardiac index (4.4 +/- 1.61.min-1.m-2, mean +/- S.D.) and by low systemic vascular resistance despite normal liver function and sinusoidal pressure. Hepatic blood flow was decreased in half of the patients with portal vein obstruction. Azygos blood flow, an estimate of superior portal-systemic collateral circulation, was markedly increased in all patients (0.46 +/- 0.19 l/min, upper limit of normal: 0.19 l/min). Therefore, in these patients with normal hepatic venous pressure gradient, azygos blood flow measurement provides an index of splanchnic haemodynamic changes. Propranolol administration (15 mg, i.v.) reduced the hyperkinetic circulatory syndrome, with a significant decrease in heart rate (-17 +/- 6%), cardiac index (-25 +/- 12%) and azygos blood flow (-40 +/- 26%) and a significant increase in systemic vascular resistance (+40 +/- 40%). These results suggest that the hyperkinetic circulatory syndrome observed in these patients, could be related to an increase in beta-adrenergic activity. The decrease in azygos blood flow, after propranolol administration, was significantly correlated (r = 0.94) with the increase in right atrial pressure. This finding suggests that propranolol may act through an increase in portal-systemic collateral venous tone. These haemodynamic results justify, in patients with presinusoidal portal hypertension, clinical trials investigating the beneficial effect of beta-blockers on gastrointestinal bleeding caused by portal hypertension.

Adult↗
PubMed1989

Occult gastrointestinal bleeding in high-risk intensive care unit patients receiving antacid prophylaxis: frequency and significance.

Gastroccult reagent was used every 4 h to detect blood in gastric juice in 41 ICU patients at risk of GI bleeding (GB) and receiving antacid prophylaxis (gastric pH greater than 3.5). Of the present patients, 27% (11/41) had at least one episode of occult GB (three consecutive positive determinations; a total of 14 episodes). Endoscopy identified acute gastroduodenal mucosal lesions (stress ulcers) as the most frequent lesion in this group (eight patients). Sepsis was the most frequent underlying condition associated with occult GB due to stress ulcer. Hematemesis occurred in 36% (4/11) of patients with occult GB and was due to stress ulcer in three patients and to benign gastric tumor in one. No overt GB occurred in the absence of previous occult GB. We conclude that: a) risk of GB persists in critically ill ICU patients in spite of antacid prophylaxis (gastric pH greater than 3.5); b) high-risk patients can be identified through periodic testing for the presence of blood in gastric juice using the reagent; c) when occult GB occurs, treatment should be based on the endoscopy results. In the absence of acute gastroduodenal mucosal lesions, antacid prophylaxis should not be modified, and specific treatment of the identified lesion(s) should be initiated. In the presence of stress lesions, antacid prophylaxis should be reinforced if the pH of the gastric content is less than 3.5 and a septic complication should be actively sought if the pH is greater than 3.5.

Adult↗
PubMed1989

Comparison of two simplified severity scores (SAPS and APACHE II) for patients with acute myocardial infarction.

The Simplified Acute Physiology Score (SAPS), the Acute Physiology and Chronic Health Evaluation II (APACHE II), the Acute Physiology Score (APS), and the Coronary Prognostic Index (CPI), calculated within the first 24 h of ICU admission, were compared in 76 patients with acute myocardial infarction (AMI). Sixteen (21%) patients subsequently died in the ICU. The nonsurvivors had significantly higher SAPS, APACHE II, and CPI scores than the survivors. ROC curves drawn for each severity index were in a discriminating position. There were no significant differences either between the areas under the ROC curves drawn for SAPS, APACHE II, and CPI, or between the overall accuracies of these indices. APS provided less homogeneous information. We conclude that SAPS and APACHE II, two severity indices which are easy to use, assess accurately the short-term prognosis, i.e., the ICU outcome, of patients with AMI.

Aged↗
PubMed1989

[Tissue hypoxia and hepatocellular insufficiency in patients with cirrhosis].

To determine whether tissue hypoxia occurred in cirrhosis, oxygen contents, mixed venous and hepatic venous lactate concentrations as well as systemic hemodynamics were studied in 53 patients with cirrhosis. The influence of liver failure on tissue oxygenation was also studied. Cardiac index and mixed venous and hepatic venous lactate concentrations were significantly higher in patients with cirrhosis than in 20 control subjects. Oxygen consumption, oxygen extraction ratio and mixed venous and hepatic venous carbon dioxide tensions were significantly lower in the former than in the latter. Oxygen transport was not significantly different between the two groups. Cardiac index and oxygen transport were not significantly different between grade A (Pugh's classification) and grade C patients. Mixed venous as well as hepatic venous lactate concentrations were significantly higher while oxygen consumption, oxygen extraction ratio and carbon dioxide tensions were significantly lower in grade C than in grade A patients. We conclude that tissue hypoxia occurs in patients with cirrhosis and hepatic insufficiency. This tissue hypoxia might be due to arteriovenous shunting-related limitation of tissue oxygen extraction.

Adult↗
PubMed1989

[Fulminant hepatitis induced by disulfiram in a patient with alcoholic cirrhosis. Survival after liver transplantation].

Fulminant hepatitis was observed in a 44-year-old patient with cirrhosis, 38 days after the beginning of a treatment by disulfiram. Hepatitis was associated with fever and hypereosinophilia. Liver transplantation was performed with success. We reviewed 15 previously published cases of disulfiram-induced hepatitis. They occurred from 10 to 180 days after the beginning of the treatment by disulfiram, aminotransferases were increased whereas alkaline phosphatases were not markedly changed; there was either focal or widespread necrosis. Fulminant hepatitis was observed mainly in patients with alcoholic chronic liver disease or in patients who continued to ingest disulfiram while jaundice was already present. An immunoallergic mechanism is thought to be responsible for disulfiram-induced hepatitis.

Adult↗
PubMed1989

[Influence of ascites on splanchnic and systemic hemodynamics in patients with alcoholic cirrhosis].

The effect of ascites on splanchnic and systemic hemodynamics was retrospectively studied in 256 patients with alcoholic cirrhosis. The patients were divided into 3 classes: no ascites, moderate ascites, and large ascites. They were also classed into 3 groups according to a modified Pugh classification (ascites was not taken into account). In patients without ascites, cardiac output was positively related to the severity of liver disease. This result was not found in patients with large ascites. Similarly, in patients with no or moderate ascites, the degree of portal hypertension estimated by the hepatic venous pressure gradient was associated with liver failure. In patients with large ascites, hepatic venous pressure gradient was higher than in patients without ascites but this relation was observed only in patients without liver failure. These results show that ascites reduces the relation between cardiac output and liver failure and increases the degree of portal hypertension but not cardiac output.

Ascites↗
PubMed1988

Liver hypermetabolism during alcohol withdrawal in humans. Role of sympathetic overactivity.

Catecholamines, which are elevated during alcohol withdrawal, can alter hepatic blood flow and increase hepatic oxygen consumption. We hypothesized that, in the withdrawal state, hepatic oxygen consumption and delivery could be altered in relation to an increased sympathetic activity. Thirteen chronic alcoholics were studied 34-72 h after withdrawal and 10 days later (control period) using conventional hemodynamic methods. As compared with the control period, splanchnic oxygen uptake was elevated at withdrawal (74.5 +/- 27.1 vs. 59.2 +/- 16.8 ml/min, p less than 0.025) and its variation was correlated with that of plasma epinephrine (r = 0.70, p less than 0.01). The hepatic venous oxygen content was reduced at withdrawal (113 +/- 22 vs. 126 +/- 21 ml/L, p less than 0.025) and correlated inversely with plasma norepinephrine levels (r = 0.56, p less than 0.01). We conclude that, during alcohol withdrawal in humans, hepatic energy expenditure may be elevated in relation to epinephrine secretion and that sympathetic overactivity may hinder the adaptive response in hepatic blood flow. The wide range in sympathetic nervous response to alcohol withdrawal could explain some differences in individual susceptibility to liver damage caused by alcohol.

Energy Metabolism↗
PubMed1988

Abnormal tissue oxygenation in patients with cirrhosis and liver failure.

Systemic haemodynamic and hepatic venous pressures, arterial and mixed venous gases and arterial lactate concentration were measured in 35 patients with histologically proven alcoholic cirrhosis who had been classified into three groups (A, B and C). Eight alcoholic patients without cirrhosis on liver biopsy were also studied. Compared with group A patients, group C patients had significantly higher hepatic venous pressure gradient, cardiac index, O2 transport and arterial lactate concentration and significantly lower systemic vascular resistance, arteriovenous O2 content difference and O2 uptake. In group B patients, corresponding values fell between those of groups A and C. Group A patients, unlike group C patients, were not significantly different from patients without cirrhosis with respect to cardiac index, systemic vascular resistance, O2 uptake and arterial lactate concentration. Our results suggest that in patients with cirrhosis, liver failure-associated hyperdynamic circulation may be accompanied by an abnormal tissue oxygenation.

Acid-Base Equilibrium↗
PubMed1987

Oxygen and bile acid content in the azygos blood. Clues to the azygos derivation in patients with portal hypertension.

In patients with cirrhosis, elevation of azygos blood flow has been attributed on indirect grounds to cephalad portosystemic collaterals. To gather more information on the origin of the azygos blood, we studied the oxygen and bile acid content of the azygos and mixed venous blood in patients with portal hypertension. Azygos oxygen saturation was 59.6 +/- 6.0% in 8 controls, and significantly higher in 35 patients with cirrhosis (76.7 +/- 7.6%; P less than 0.01) as well as in 6 patients with noncirrhotic portal hypertension (84.0 +/- 8.2%; P less than 0.01). High oxygen saturation, however, was not correlated to azygos blood flow in patients with cirrhosis. In cirrhotic patients, total bile acid concentrations were 28.1 +/- 20.4 mumol/l in the pulmonary artery and 25.9 +/- 17.6 mumol/l in the azygos vein, giving an azygos to mixed venous ratio of 0.95 +/- 0.18. These results provide new evidence that elevated azygos blood flow in patients with portal hypertension is derived from the portal system, and perhaps predominantly from the splenic territory.

Azygos Vein↗
PubMed1987

Naloxone does not alter haemodynamics in cirrhosis. Studies in humans and rats.

In order to test the hypothesis that endogenous opioids may mediate some of the circulatory derangements in cirrhosis, we studied the haemodynamic effects of naloxone, an opioid antagonist, in patients and in a rat model of biliary cirrhosis. In 9 patients with alcoholic cirrhosis and 5 control patients without significant liver disease, cardiac output, systemic vascular resistance, mean arterial pressure, heart rate, hepatic venous pressures and O2 content, hepatic and azygos blood flows and serum catecholamines were measured before and 30 min after naloxone 3.2 mg i.v. bolus. No significant changes were observed in either group of patients. Similarly in 16 conscious rats, 8 sham-operated and 8 with cirrhosis due to bile duct ligation, cardiac output, systemic vascular resistance, mean arterial pressure, heart rate, and splanchnic organ blood flows were measured by radioactive microspheres, before and 20 min after naloxone 1 mg/kg i.v. bolus. No significant changes were observed in either group. We failed to detect any evidence that endorphins are involved in tonic haemodynamic control in cirrhosis.

Adult↗