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Biomedical subjects

J Bosch

Publications and source records attributed to J Bosch.

At least 271 records · Page 15Linked to original sources
PubMed1990

Effects of propranolol on arterial oxygenation and oxygen transport to tissues in patients with cirrhosis.

Patients with cirrhosis may show ventilation-perfusion (VA/Q) inequality in the absence of any intrinsic heart or lung disease. However, the high cardiac output of cirrhosis generally prevents or minimizes the appearance of a severe degree of arterial hypoxemia. Propranolol has been used to reduce cardiac output and portal pressure in these patients. We wondered whether it might alter arterial oxygenation and reduce O2 transport to tissues. We studied eight patients (three women) 54 +/- 3 (SEM) yr of age before and after intravenous propranolol (0.1 mg/kg followed by 2 mg/h). Cardiac output (QT) fell from 7.8 +/- 0.7 to 6.0 +/- 0.7 L/min (p less than 0.05), and portal pressure was reduced (22 +/- 2 to 19 +/- 2 mm Hg, p less than 0.01). Arterial PO2 did not change (88 +/- 4 to 89 +/- 5 mm Hg) because the fall in mixed venous PO2 (43 +/- 1 to 40 +/- 1 mm Hg, p less than 0.01) that followed the lower QT was counterbalanced by a lower intrapulmonary shunt (multiple inert gas technique) (4 +/- 2 to 2 +/- 1%, p less than 0.05) and a shift of the VA/Q distributions toward a higher VA/Q ratio. Paralleling the fall in QT, oxygen transport to tissues (QO2) was reduced (19 +/- 2 to 14 +/- 1 ml/min/kg, p less than 0.01). However, O2 uptake (VO2) remained constant (3.4 +/- 0.2 to 3.6 +/- 0.2 ml/min/kg) because O2 extraction by the tissues increased appropriately (22 +/- 2 to 28 +/- 1%, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1990

[Uremic hemolytic syndrome induced by mitomycin C. Presentation of a series of 5 cases and review of the literature].

Five new cases of hemolytic uremic syndrome associated mitomycin C treatment in neoplastic patients are presented and clinical, biological, histological therapeutic and the evolution data of 92 other cases from the literature are analyzed. The results point out the high incidence of GI adenocarcinomas (65%), its rare appearance with total mitomycin doses below 50 mg/m2, its frequent clinical presentation with cardiovascular manifestations, the therapeutical difficulties and the possibility of a better prognosis with an early diagnosis.

Adenocarcinoma↗
PubMed1989

[Churg-Strauss syndrome: 8 cases in the last 10 years].

The clinical and histopathological findings of 8 patients with a diagnosis of Churg-Strauss syndrome seen in our institution in a 10 year period have been reviewed. All patients had asthma and hypereosinophilia (mean eosinophil count 7.64 x 10(9); range: 0.748 x 10(9)-31.46 x 10(9) eosinophils/l). The organs and systems involved in the late phase of the syndrome (vasculitic phase) were: nervous system (16 cases), respiratory system (5 cases), skin and subcutaneous tissue (5 cases), heart (3 cases), digestive system (3 cases) and kidney (1 case). The diagnosis was made on the basis of the clinical and histopathological findings. In 7 cases necrotizing angiitis was shown, tissue eosinophilia in 4, and extravascular granulomas in 2. In most cases, corticosteroid therapy resulted in a favorable course, but cyclophosphamide was required in two patients. In the discussion, the evolution of the criteria for the diagnosis of this condition is analyzed.

Adolescent↗
PubMed1989

Hemodynamic effects of blood volume restitution following a hemorrhage in rats with portal hypertension due to cirrhosis of the liver: influence of the extent of portal-systemic shunting.

The present study investigated whether, in rats with portal hypertension due to cirrhosis of the liver induced by carbon tetrachloride, blood volume restitution following a hemorrhage produces an increase of portal pressure beyond control values, as observed in rats with prehepatic portal hypertension. Since carbon tetrachloride-induced cirrhosis caused mild portal-systemic shunting, in some of the cirrhotic rats (12 of 29 rats) portal-systemic shunting was enhanced by a transient (4 days) partial constriction of the portal vein, which was removed 1 week prior to the study. After baseline measurements of portal pressure and arterial pressure, 15 ml per kg of blood were withdrawn at a rate of 0.3 ml per min and reinfused 15 min later. After blood reinfusion, portal pressure and arterial pressure were measured again, and cardiac output, regional blood flows and portal-systemic shunting were determined using radioactive microspheres. Portal-systemic shunting was 78 +/- 11% of total blood flow in the cirrhotic rats that had temporary portal vein constriction, but only 5 +/- 2% (p less than 0.001) in those that did not. Blood volume restitution in low-portal-systemic shunting rats did not produce any significant modification in splanchnic or systemic hemodynamics. However, in rats with high portal-systemic shunting, blood volume restitution produced a significant increase in portal pressure (from 9.9 +/- 0.9 to 13.5 +/- 0.9 mmHg, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Beta-blockade with propranolol and hepatic artery blood flow in patients with cirrhosis.

In patients with cirrhosis and portal hypertension, propranolol administration reduces heart rate and cardiac output and diminishes portal pressure and collateral blood flow. However, there is little information on the possible effects of propranolol on hepatic artery blood flow. The present study addressed this question in 12 cirrhotic patients with end-to-side portacaval shunt, in whom all of the liver blood flow represents the hepatic artery blood flow. Hepatic artery blood flow (continuous infusion of indocyanine green), cardiac output (thermal dilution), heart rate and mean arterial pressure were measured before and 20 min after the intravenous infusion of 10 to 15 mg of propranolol. beta-Adrenergic blockade caused a significant reduction of cardiac output (from 9.1 +/- 2.1 to 7.1 +/- 1.4 liters per min, p less than 0.001) (mean +/- S.D.) and heart rate (from 85 +/- 10 to 71 +/- 7 beats per min, p less than 0.001), and a significant increase of systemic vascular resistance (from 9.0 +/- 2.1 to 11.7 +/- 2.7 mmHg per liter per min, p less than 0.001), whereas mean arterial pressure did not change (77 vs. 78 mmHg). Propranolol significantly reduced hepatic artery blood flow (from 0.65 +/- 0.20 to 0.55 +/- 0.14 liters per min, p less than 0.01). However, reduction of hepatic artery blood flow (-12.9 +/- 7.3%) was significantly less than reduction of cardiac output (-21.1 +/- 5.2%, p less than 0.01). As a result, the fraction of the cardiac output delivered to the liver was significantly greater after propranolol (8.0 +/- 1.7%) than before (7.3 +/- 1.7%, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1989

Propranolol decreases portal pressure without changing portocollateral resistance in cirrhotic rats.

Propranolol decreases portal pressure by reducing portal blood inflow. Studies in rats with prehepatic portal hypertension due to portal vein stenosis (a model with extensive portosystemic shunting) have shown that propranolol increases the portocollateral resistance, which hinders the fall in portal pressure. The present study examined the effects of propranolol on splanchnic and systemic hemodynamics in rats with portal hypertension due to cirrhosis of the liver, a model which is characterized by mild portosystemic shunting. Two groups of rats with CCl4-induced cirrhosis were studied: the propranolol group (n = 8), which received a propranolol infusion of 2 mg per 15 min, and controls (n = 9), which received a placebo (saline) infusion. Hemodynamic measurements were done using radiolabeled microspheres. Propranolol-treated rats had significantly lower cardiac output (-31%) and heart rate (-26%) than controls (p less than 0.001). Hepatic artery flow was not modified by propranolol. Propranolol caused splanchnic vasoconstriction, manifested by increased splanchnic resistance (+57%) and by a significant fall in portal blood inflow (4.8 +/- 0.4 vs. 6.3 +/- 0.5 ml per min.100 gm in controls, p less than 0.05). In contrast with rats with prehepatic portal hypertension, propranolol did not increase portal resistance in cirrhotic rats [2.0 +/- 0.2 vs. 2.0 +/- 0.1 mmHg per ml per min.100 gm body weight (not significant)]. Hence, the fall in portal pressure (-19%) was expected from the decrease in portal inflow (-24%). These results suggest that increased portal resistance in rats with prehepatic portal hypertension may represent an intrinsic effect of propranolol on the portocollateral vessels, since beta-blockade does not modify portal vascular resistance in cirrhosis.

Animals↗
PubMed1989

Association of transdermal nitroglycerin to vasopressin infusion in the treatment of variceal hemorrhage: a placebo-controlled clinical trial.

The aim of this study was to evaluate, using a double-blind technique, the efficacy of the association of transdermal nitroglycerin to vasopressin infusion for the treatment of variceal bleeding. Sixty-nine cirrhotic patients with active variceal bleeding were randomly allocated to receive vasopressin (0.4 to 0.8 unit per min until variceal bleeding has been controlled for 12 hr) associated with nitroglycerin administered transdermically in a slow-release preparation (10 mg in 24 hr) or placebo. An initial control of variceal hemorrhage was achieved in 83% of the patients receiving vasopressin-nitroglycerin and in 74% in the vasopressin-placebo group. Owing to a lower frequency of recurrent bleeding during therapy (18 vs. 42%, p = 0.11), vasopressin-nitroglycerin achieved a definitive control of bleeding in a higher proportion of patients than vasopressin-placebo (73 vs. 54%, p = 0.13). The group treated with the drug combination showed favorable results in relation to transfusion requirements (2.9 +/- 0.4 vs. 4.2 +/- 0.5 units, p = 0.05), total dose of vasopressin required (453 +/- 47 vs. 587 +/- 50 units, p less than 0.05), need of balloon tamponade (6 vs. 15, p less than 0.05) and requirement for emergency surgery (0 vs. 4, p = 0.07). There were no significant differences in the undesirable effects associated with treatment, observed in 37 and 49% of cases, respectively. Hospital mortality was similar (33 vs. 25%). This study demonstrates that transdermal nitroglycerin improves the effectiveness of vasopressin for controlling variceal hemorrhage.

Administration, Cutaneous↗
PubMed1989

Calcified ovarian fibromas in prepubertal girls.

Ovarian fibromas in prepubertal girls are rare. We describe two girls aged 8 and 11 years with extensively calcified ovarian fibromas. One patient had a single unilateral fibroma with metaplastic bone formation in the calcified area. The other patient had bilateral nodular fibromas suggesting the possibility of naevoid basal-cell carcinoma syndrome although broader manifestations are lacking at present.

Calcinosis↗
PubMed1989

Reduction of portal pressure by isosorbide-5-mononitrate in patients with cirrhosis. Effects on splanchnic and systemic hemodynamics and liver function.

The results of a study to characterize the effects of the oral administration of isosorbide-5-mononitrate (Is-5-Mn), the active metabolite of isosorbide dinitrate, on portal hypertension in 23 patients with cirrhosis are reported. Patients received 20 mg of Is-5-Mn (n = 10), 40 mg (n = 9), or a placebo (n = 4). No significant changes were observed after the administration of the placebo. However, both doses of Is-5-Mn significantly reduced portal pressure, as evaluated by measurements of the hepatic venous pressure gradient. The fall in portal pressure averaged 10% after the 20-mg dose and 18% after 40 mg and was maintained for the 2 h of observation. Reduction of portal pressure was due to a decrease in the wedged hepatic vein pressure, with no changes in the free hepatic venous pressure. After the 20-mg dose, the decrease in portal pressure was associated with an increase in hepatic blood flow (16%), suggesting a fall in hepatic vascular resistance. However, after the 40-mg dose, a reflex splanchnic vasoconstriction elicited by the fall in arterial pressure (-19%) appeared to contribute to the greater reduction in portal pressure, as suggested by a significant decrease in azygos blood flow (-15%). These beneficial effects on portal pressure were not associated with adverse effects on liver function, as evaluated by measurements of the hepatic clearance of indocyanine green and the hepatic intrinsic clearance. Neither dose of Is-5-Mn caused significant changes in these quantitative parameters of liver function. These findings suggest that Is-5-Mn could be a potentially useful and safe agent in the treatment of portal hypertension.

Adult↗
PubMed1989

Portal hypertension.

Portal hypertension is a frequent syndrome characterized by a chronic increase in portal venous pressure and by the formation of portal-systemic collaterals. Its main consequence is massive bleeding from ruptured esophageal and gastric varices. Bleeding is promoted by increased portal and variceal pressure, and is favored by dilatation of the varices. The evaluation of the portal hypertensive patient should include the assessment of portal vein patency by ultrasonography, endoscopic evaluation of the presence, size, and extent of esophageal varices, and hemodynamic studies with measurements of portal pressure and of portal-collateral blood flow. The preferred techniques are hepatic vein catheterization and measurement of azygos blood flow. Endoscopic measurements of variceal pressure and estimations of portal blood velocity by the Doppler technique have recently been introduced, but are still research procedures. Acute variceal hemorrhage should be treated under intensive care. Specific therapy to arrest variceal bleeding includes balloon tamponade, vasopressin, somatostatin, sclerotherapy, and emergency surgery. Treatment of portal hypertension is aimed at preventing variceal hemorrhage and bleeding-related deaths. Pharmacologic prophylaxis is based on the use of drugs that cause a sustained reduction in portal pressure; most studies have used propranolol. Surgery and endoscopic sclerotherapy can also be used to prevent rebleeding.

Acute Disease↗
PubMed1989

Pulmonary hemodynamics and gas exchange during exercise in liver cirrhosis.

We have recently shown that ventilation-perfusion (VA/Q) mismatching at rest in cirrhosis is due to an abnormal pulmonary vascular tone. It has been suggested that in patients with cirrhosis, O2 transfer might become diffusion-limited during exercise. This study examined pulmonary hemodynamics and mechanisms modulating gas exchange during exercise (60 to 70% VO2max) in six patients (41 +/- 5 yr, mean +/- SEM) with cirrhosis but with normal lung function tests. At rest, QT was high (8.4 +/- 0.5 L/min), pulmonary vascular resistance (PVR) was low (0.61 +/- 0.17 mm Hg/L/min), and there was mild to moderate VA/Q mismatching (LogSD Q, 0.79 +/- 0.09; normal range, 0.3 to 0.6). However, hyperventilation (PaCO2, 29 +/- 2 mm Hg) and high QT (thus, high PVO2, 41 +/- 2 mm Hg) contributed to the maintenance of PaO2 within normal values (99 +/- 7 mm Hg). Exercise VO2 (1,278 +/- 122 ml/min) was normal relative to work load, but, contrary to that in normal subjects, QT was higher and PVR did not fall. During exercise, PaO2 showed a trend to decrease (to 90 +/- 5 mm Hg) and PaCO2 to rise (to 35 +/- 2 mm Hg), but the differences failed to reach statistical significance (p = 0.07 each). PVO2 fell significantly with exercise (41 +/- 2 to 33 +/- 0.3 mm Hg, p less than 0.05), but neither AaPO2 (15 +/- 7 to 21 +/- 6 mm Hg) nor VA/Q inequality (LogSD Q, 0.82 +/- 0.11) changed. No systemic difference was noticed between predicted and measured PaO2 values, suggesting no O2 diffusion impairment during exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Sepsis and neonatal meningitis].

The epidemiological, clinical and bacteriological data of 38 infants under 28 days of age with a diagnosis of neonatal meningitis (13 patients), early neonatal sepsis (17 patients) or late neonatal sepsis (8 patients) were retrospectively reviewed. 52.6% of patients were premature and/or low weight neonates, 76.3% had an unfavorable obstetrical history and 39.4% had one or more underlying diseases. The clinical features were predominantly neurological (81.5%), cardiac or respiratory (71%) and gastrointestinal (34.2); the most outstanding laboratory data were positive CRP, hyperbilirubinemia and abnormalities in leukocyte differential count. The major microorganisms involved were E. coli (11 patients), S. agalactiae (9), S. aureus (5), L. monocytogenes (3) and coagulase-negative Staphylococcus (3). The overall incidence of these disorders was 3.33 cases/1000 live neonates, and the mortality rate was 7.9%.

Female↗
PubMed1989

Evaluation of the portal hypertensive patient.

Portal hypertension is characterized by a chronic increase in portal venous pressure. This is initiated by an increased vascular resistance to portal blood flow. In advanced stages, however, blood flow increases and contributes to worsen and maintain portal hypertension. Increased pressure and blood flow within the portal system promotes the appearance and dilation of portal-systemic collaterals and oesophageal varices, which are responsible for the main complication of portal hypertension: massive gastrointestinal haemorrhage. In recent years there have been several major innovations in the evaluation of portal hypertension. These include the application of new endoscopic, ultrasonographic and haemodynamic techniques that allow a better evaluation of the portal hypertensive patient, especially when prophylactic medical therapy is considered. Ultrasonography is very useful to assess the patency of the portal vein. The association of a pulsed Doppler flowmeter increases its accuracy and allows the non-invasive estimation of the direction and magnitude of portal blood flow. In addition to the measurement of portal pressure, measurement of azygos venous blood flow has proven very useful in the haemodynamic evaluation of portal hypertension. Azygos blood flow represents an index of blood flow through gastro-oesophageal collaterals and varices draining in the azygos vein. Its main application has been the assessment of the effects of pharmacological therapy. Endoscopic measurements of variceal pressure, either by direct puncture or using non-invasive pressure gauges, have contributed significantly to the understanding of the mechanism of variceal haemorrhage. This technique allows the calculation of the variceal wall tension as the product of the transmural pressure at the varices and the radius of the varix.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1989

Endoscopic measurement of variceal pressure in cirrhosis: correlation with portal pressure and variceal hemorrhage.

This study evaluated the clinical application of a pressure-sensitive gauge that allows the noninvasive measurement of the pressure of esophageal varices at endoscopy. The study was performed in 70 patients with cirrhosis and portal hypertension. Among them, 47 had bled from the varices and 23 had varices but had not bled. In addition to measurements of variceal pressure, the size of the varices was estimated semiquantitatively at endoscopy. This allowed an estimate of the tension on the wall of the varices as the product of the transmural pressure and the estimated radius of the varices. Most patients had a standard hemodynamic evaluation of portal hypertension, with measurements of wedged and free hepatic venous pressures, and of azygos blood flow. These were performed within 24 h of the variceal pressure measurements. Variceal pressure was significantly higher in bleeders than in nonbleeders (15.7 +/- 2.8 vs. 12.1 +/- 2.6 mmHg, p less than 0.001) in spite of a similar portal pressure in both groups (20.1 +/- 5.1 vs. 20.4 +/- 7.6 mmHg, NS). More than 60% of the bleeders, but only 22% of the nonbleeders had a variceal pressure greater than or equal to 15 mmHg (p less than 0.005). Among nonbleeders, variceal pressure was higher in patients with large varices (13.9 +/- 2 mmHg, n = 9) than in those with small varices (10.9 +/- 2.4 mmHg, n = 14) (p less than 0.01). Estimates of variceal wall tension further exaggerated the differences between bleeders and nonbleeders (66.1 +/- 22.6 vs. 32.0 +/- 19.8 mmHg.mm, p less than 0.001). More than 50% of bleeders, but just 9% of nonbleeders had an estimated variceal tension greater than 50 mmHg.mm (p less than 0.001). Our findings support the role of an increased variceal pressure in the pathogenesis of variceal hemorrhage, and suggest that this noninvasive technique can be valuable in assessing the risk of variceal hemorrhage in patients with portal hypertension.

Endoscopes↗