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Biomedical subjects

J Bosch

Publications and source records attributed to J Bosch.

At least 235 records · Page 13Linked to original sources
PubMed1992

Hepatic, splanchnic and systemic haemodynamic abnormalities in portal hypertension.

Portal hypertension is characterized by a pathological increase in portal venous pressure that leads to the formation of portosystemic collaterals that divert portal blood to the systemic circulation, bypassing the liver. Increased vascular resistance to portal blood flow is the initiating factor in portal hypertension. Increased resistance along the hepatic and portocollateral circulation is in part modifiable by pharmacological agents. An additional factor is splanchnic vasodilatation with increased portal blood inflow, which contributes to the maintenance and aggravation of the portal hypertension. Endogenous vasodilators are thought to be responsible for the splanchnic hyperaemia of portal hypertension. Vasodilatation is also prominent in the stomach and lungs, and plays an important role in the pathophysiology of portal hypertensive gastropathy and of the hepatopulmonary syndrome. The systemic circulation is markedly hyperkinetic, with reduced arterial pressure and peripheral resistance and increased cardiac output. The plasma volume is expanded due to renal sodium retention. The expanded plasma volume enables the increase in cardiac output, and represents another mechanism contributing to the increase in portal pressure.

Blood Flow Velocity↗
PubMed1992

Effects of inhibiting nitric oxide biosynthesis on the systemic and splanchnic circulation of rats with portal hypertension.

1. The effects of inhibiting endogenous nitric oxide (NO) synthesis with NG-monomethyl-L-arginine (L-NMMA) on the systemic and splanchnic circulation have been investigated in rats with experimental chronic portal hypertension, anaesthetized with ketamine. 2. Portal hypertension was induced by partial portal vein ligation, 2 weeks prior to study. This procedure induced a reduction in systemic arterial blood pressure (MAP), an increase in cardiac output as measured by radiolabelled microspheres, a reduction in peripheral and splanchnic vascular resistance and an increased portal venous inflow (PVI) and portal pressure, as compared to control non-ligated rats. 3. L-NMAA (6.25 and 50 mg kg-1, i.v.) dose-dependently increased MAP, reduced cardiac output and PVI, and increased peripheral and splanchnic vascular resistance. With L-NMMA (50 mg kg-1), PVI and the vascular resistances returned to values comparable to those determined in control non-ligated anaesthetized rats under resting conditions. 4. Porto-collateral resistance was also increased by these doses of L-NMMA, whereas portal pressure was unchanged. The increase in renal blood flow and decrease in renal vascular resistance also seen in portal-hypertensive rats was reversed by L-NMMA (50 mg kg-1). 5. These effects of L-NMMA (50 mg kg-1) were inhibited by prior administration of L-arginine (300 mg kg-1, i.v.). 6. These findings indicate that the chronic hyperdynamic circulatory characteristics following portal vein stenosis can be attenuated by L-NMMA. Thus, the excessive formation of endogenous NO may be implicated in the pathogenesis of the haemodynamic disturbances and splanchnic vasodilatation associated with chronic portal hypertension.

Animals↗
PubMed1992

Portal hypertension in acute liver failure.

Twenty five patients with acute liver failure were measured for hepatic venous pressure gradient as an index of portal pressure during the course of a transjugular liver biopsy. Hepatic venous pressure gradient ranged from 4 to 24.5 mm Hg with a mean of 12.8 (5.3) mm Hg (normal values less than 5 mm Hg). All patients but one had increased portal pressure gradient. Portal hypertension correlated with the degree of architectural distortion of the liver, as suggested by a direct correlation between hepatic venous pressure gradient and the area of reticulin collapse, evaluated by means of a morphometric analysis on Sirius red stained liver slides (r = 0.43, p less than 0.05). Hepatic venous pressure gradient was significantly higher in patients with ascites (15.1 (5) mm Hg, n = 15) or renal failure (14.4 (5.3) mm Hg, n = 16) than in those without (9.3 (3.4) mm Hg and 10.1 (4) mm Hg, respectively; p less than 0.05). Portal hypertension was associated with systemic vasodilation and a hyperkinetic circulatory state, with decreased arterial pressure, and peripheral resistance and increased cardiac output.

Acute Kidney Injury↗
PubMed1992

Limitations of laser-Doppler velocimetry and reflectance spectrophotometry in estimating gastric mucosal blood flow.

This study investigated the accuracy of laser-Doppler flowmetry (LDV) and reflectance spectrophotometry (RS) measurements as an index of blood flow in the gastric mucosa of the rat, in experimental conditions such as pharmacologically induced vasoconstriction, hypoxia, hyperoxia, and acute normovolemic anemia. Hydrogen gas clearance was used as a reference method. After vasopressin infusion, LDV signal and indexes of hemoglobin (IHb) and oxygen (ISO2) content in the gastric mucosa estimated by RS significantly decreased in parallel with the reduction of gastric mucosal blood flow (GMBF). Neither hypoxia (5% O2 administration) nor hyperoxia (100% O2) affected GMBF or LDV signal. However, both IHb and ISO2 significantly decreased or increased after hypoxia or hyperoxia, respectively. Acute normovolemic anemia induced a significant increase in GMBF, while LDV signal and ISO2 remained unchanged. IHb significantly decreased in linear relationship with the decrements in the hematocrit. It is concluded that 1) in pharmacologically induced GMBF changes, LDV and RS correlate with GMBF; 2) when changes in hemoglobin saturation are induced, LDV but not RS reflects GMBF; and 3) in acute normovolemic anemia, neither LDV nor RS reflects changes in GMBF.

Anemia↗
PubMed1992

Double-antibody sandwich enzyme-linked immunosorbent assay and immunoblot analysis used for control of caseous lymphadenitis in goats and sheep.

A double-antibody sandwich ELISA for detection of antibodies directed against the exotoxin of Corynebacterium pseudotuberculosis, the cause of caseous lymphadenitis (CL) in small ruminants, was developed. A concentrated exotoxin was used. For interpretation of ELISA results, these sera were tested: sequentially obtained sera of C pseudotuberculosis-inoculated goats and sheep that were monitored for 68 weeks; sequentially obtained sera from 80 goats of 3 flocks with CL; sera from 652 goats of 7 flocks without CL; sera from 160 sheep of 4 flocks without CL; and 2,265 caprine and 208 ovine sera submitted for diagnostic testing. Data regarding the infection status and history of 10,454 of the 23,302 animals were collected after testing; most of these were goats that had been part of a CL control program. Specificity and sensitivity of the ELISA were nearly 100%. Subsequently, 31,978 animals from which no data on infection status of flocks had been collected were then tested. It was concluded that the ELISA is a useful diagnostic test for CL eradication programs. Sera with doubtful or inconclusive ELISA results were examined by use of immunoblot analysis. Proteins from C pseudotuberculosis culture supernatant were separated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and blotted onto nitrocellulose. Six proteins with molecular mass of 68, 65, 39, 38, 31, and 29 kDa reacted with sera from goats and sheep with experimentally induced or naturally acquired infection. Immunoblot analysis was valuable in classifying sera with doubtful or inconclusive results by ELISA.

Abscess↗
PubMed1992

[Decrease in the incidence of epidural hematomas surgically treated during coma after a lucid interval. Is this an index of quality of care?].

The level of consciousness prior to surgery has been analyzed in a series of 64 patients suffering epidural hematoma (EDH) who underwent surgery during the period from July 1987 to June 1989. The percentage of cases which underwent surgery in coma after a lucid interval have been compared in different periods of time (1978-80, 1981-82, 1983-84 and July 1987 to June 1989). During the period from July 1987 to June 1989 surgery was performed on: 15 patients (23.5%) in coma from the moment of accident, 8 patients (12.5%) underwent surgery in coma but after a lucid interval and 41 patients (64.1%) were conscious. During the different periods of time the number of patients undergoing surgery in coma after a lucid interval were the following: 1979-80, 9 cases (26.5%); 1981-82, 17 cases (43.6%); 1983-84, 8 cases (20%) and during the last period, 1987-89, 7 cases (15.2%). The difference between the percentage of patients intervened in coma after a lucid interval in the previously referred periods of time was statistically significant (p 0.05).

Coma↗
PubMed1992

Pathophysiology of portal hypertension.

Portal hypertension is characterized by a pathologic increase in portal venous pressure that leads to the formation of an extensive network of portosystemic collaterals that divert a large fraction of portal blood to the systemic circulation, bypassing the liver. Experimental models have improved understanding of the pathophysiology of portal hypertension. It is now clear that an increased vascular resistance to portal blood flow is the initial factor responsible for the increase in portal pressure. This resistance is exerted along the hepatic and portal-collateral circulation and is in part modifiable by pharmacologic agents. In a latter stage, an increased portal venous blood inflow, promoted by splanchnic vasodilation, contributes to maintenance and aggravation of portal hypertension. Humoral vasodilatory agents play an important role in the splanchnic vasodilation. Several vasodilators are likely to be involved, including glucagon, prostacyclin, endotoxins, and nitric oxide. The splanchnic vasodilation is associated with a hyperkinetic systemic circulation, with reduced arterial pressure and peripheral resistance and increased cardiac output. The splanchnic circulation is probably the vascular territory in which the vasodilation is more pronounced. Therefore, splanchnic and systemic vasodilation probably share some pathophysiologic events. An expanded plasma volume is observed in all forms of portal hypertension. Expansion of plasma volume is due to renal sodium retention, which has been shown to precede the increase in cardiac output and can be prevented or reversed by sodium restriction and spironolactone. The expanded blood volume represents another mechanism that contributes to further increases in portal pressure.

Animals↗
PubMed1992

[Intraventricular meningiomas].

Eight cases of surgically intervened intraventricular meningiomas are presented. The patients were six males and 2 females with a mean age of 41.7 years (11-70). The length of symptoms was of several months in 6 (75%) of the cases. The most frequent symptoms observed were cephalea and alterations of the upper functions which were presented in six and four cases, respectively. Papilloedema and involvement of long pathways were the most usual findings observed in neurological examination. Diagnosis was made by computerized tomography and angiography in all the cases. Surgery using a transtemporal approach was carried out in six patients and in the other two a parietal-occipital route was used. Two patients were dead and other two presented bilateral amaurosis. The other patients had good postsurgery.

Adolescent↗
PubMed1991

Propranolol in prevention of recurrent bleeding from severe portal hypertensive gastropathy in cirrhosis.

The two main causes of gastrointestinal bleeding in cirrhosis are oesophageal varices and portal hypertensive gastropathy (PHG). Rebleeding from varices can be prevented by beta-blockers, but it is not clear whether these drugs effectively reduce rebleeding from PHG. 54 cirrhotic patients with acute or chronic bleeding from severe PHG took part in a randomised, controlled trial to investigate the efficacy of propranolol in prevention of rebleeding from PHG. 26 patients were randomised to receive propranolol daily at a dose that reduced the resting heart rate by 25% or to 55 bpm (20-160 mg twice daily), throughout mean follow-up of 21 (SD 11) months. 28 untreated controls were followed-up, with the same examinations, for 18 (13) months. The actuarial percentages of patients free of rebleeding from PHG were significantly higher in the propranolol-treated patients than in the untreated controls at 12 months (65% vs 38%; p less than 0.05) and at 30 months of follow-up (52% vs 7%; p less than 0.05). Propranolol-treated patients had fewer episodes of acute bleeding than controls (0.010 [0.004] vs 0.120 [0.040] per patient per month). Multivariate analysis showed that absence of propranolol treatment was the only predictive variable for rebleeding. Actuarial survival was slightly higher in the propranolol group than in the controls, but the difference was not significant. Thus, long-term propranolol treatment significantly reduces the frequency of rebleeding from severe PHG, and may improve the prognosis of cirrhotic patients with this disorder.

Actuarial Analysis↗
PubMed1991

Propranolol compared with propranolol plus isosorbide-5-mononitrate for portal hypertension in cirrhosis. A randomized controlled study.

OBJECTIVE: To investigate whether isosorbide-5-mononitrate (Is-5-Mn) given with propranolol reduces hepatic portal pressure more than does propranolol alone in patients with cirrhosis. DESIGN: A randomized controlled trial. PATIENTS: Fifty patients with cirrhosis and esophageal varices entered and 42 completed the study. INTERVENTION: Twenty-one patients received oral propranolol at increasing doses until their resting heart rate was reduced by 25%, and 21 patients received oral propranolol (on the same schedule) plus oral Is-5-Mn, 40 mg twice a day. MEASUREMENTS: Hepatic vein pressure gradient, liver function, and splanchnic and systemic hemodynamics before and after 3 months of continuous therapy. MAIN RESULTS: At 3 months, the hepatic venous pressure gradient decreased more (P less than 0.01) in patients given propranolol plus Is-5-Mn (19%, from 18.4 +/- 3.9 to 14.9 +/- 3.8 mm Hg; 95% CI, -2.4 to -4.5 mm Hg) than in those given propranolol alone (10%, from 18.2 +/- 3.5 to 16.3 +/- 3.1 mm Hg; CI, -1.1 to -2.7 mm Hg). The hepatic venous pressure gradient decreased by more than 20% of the baseline value in 10% of patients receiving propranolol, but in 50% of patients receiving combined therapy (P less than 0.02). There were statistically significant decreases in hepatic blood flow and the intrinsic clearance of indocyanine green after propranolol therapy, but not after combined therapy. The treatments caused similar reductions in azygos blood flow and cardiac output. CONCLUSIONS: The long-term combined administration of propranolol plus Is-5-Mn reduces portal pressure more than propranolol alone without adverse effects on hepatic perfusion and liver function. Whether this greater hemodynamic effect translates into better clinical efficacy should be determined in randomized controlled trials.

Aged↗
PubMed1991

Glucagon hinders the effects of somatostatin on portal hypertension. A study in rats with partial portal vein ligation.

Whether the decrease of portal venous inflow and portal pressure induced by somatostatin is related to the effects of somatostatin in inhibiting the secretion of glucagon and other vasodilatory peptides that are increased in portal hypertension was investigated in the current study. Splanchnic vascular resistance and splanchnic blood flow were determined using radioactive microspheres in rats with portal hypertension caused by partial portal vein ligation. Somatostatin infusion significantly decreased portal pressure (from 13.1 +/- 1.9 to 12.1 +/- 2.2 mm Hg; P less than 0.05). This was associated with a significant decrease in portal venous inflow caused by splanchnic vasoconstriction, as evidenced by increased splanchnic vascular resistance, and with a marked suppression of glucagon secretion. The simultaneous infusion of somatostatin and glucagon (2.8 ng/min, a dose that prevented any decrease in circulating glucagon levels) abolished all the hemodynamic effects of somatostatin. This effect seems to be specific because no hemodynamic changes were noted in portal hypertensive rats receiving only the glucagon infusion.

Animals↗
PubMed1991

Effects of molsidomine, a long acting venous dilator, on portal hypertension. A hemodynamic study in patients with cirrhosis.

The present study investigated the effects of molsidomine, a predominant venous dilator which, contrary to organic nitrates, does not produce pharmacological tolerance on splanchnic and systemic hemodynamics in patients with cirrhosis. Twenty-seven cirrhotic portal hypertensive patients were studied prior to and up to 2 h after the oral administration of 2 mg of molsidomine (n = 11), 4 mg of molsidomine (n = 8) or placebo (n = 8). Molsidomine caused a significant reduction in the hepatic venous pressure gradient. The mean decrease at 60 min was -6.8 +/- 9% after 2 mg (p less than 0.05) and -15.4 +/- 12% after 4 mg (p less than 0.01). The decrease in the hepatic venous pressure gradient was maintained at 120 min: -11% after 2 mg (p less than 0.05) and -19% with 4 mg (p less than 0.01). This was associated with mild changes in azygos blood flow and with a significant decrease in hepatic blood flow (-17%, p less than 0.05). There was a moderate reduction in mean arterial pressure (-12.6% after 2 mg and -13.2% after 4 mg, p less than 0.01), which was due to a reduction in cardiac output, without any significant fall in systemic vascular resistance. Placebo administration did not change systemic or hepatic hemodynamics. This study shows that molsidomine causes a significant and sustained reduction in portal pressure in patients with cirrhosis, suggesting the potential role of this agent in the treatment of portal hypertension.

Adult↗
PubMed1991

Portal pressure in patients with exudative ascites in the course of acute hepatitis B.

We describe three patients who developed ascites during the course of acute viral hepatitis B. Two of them had exudative ascites, with a high protein and cell content, and the other transudative ascites, with low protein and cell content. Both patients with exudative ascites had a benign clinical course, and their liver disease was milder than in the patient with transudative ascites, who had signs of severe liver failure and a submassive hepatic necrosis on liver biopsy. Moreover, the patient with transudative ascites had evidence of portal hypertension (as indicated by a hepatic vein pressure gradient of 12.5 mmHg, normal 1-6 mmHg), whereas patients with exudative ascites did not (hepatic vein pressure gradient of 5 and 5.5 mmHg, respectively). These data support our previous suggestion that "exudative" ascites during acute viral hepatitis B represents a self-limited immunopathetic sign that is not related to portal hypertension or severe hepatic disease.

Adult↗
PubMed1991

[Multicenter study of the Rosco-Neisseria system for the identification of pathogenic neisserias and Branhamella catarrhalis].

The commercial Rosco-Neisseria system was evaluated in the identification of 228 oxidase-positive Gram-negative diplococci and it was compared with conventional tests. The procedure detects gamma-glutamyl aminopeptidase, ONPG, tributyrin hydrolysis, and sensitivity to the disk of 10 micrograms of colistin. A correct identification was obtained in the 65 strains of Neisseria gonorrhoeae, the 33 of N. meningitidis, the 12 of N. lactamica, and the 56 of B. catarrhalis. The method was also able to discriminate 54 out of the 62 strains of nonpathogenic Neisseria. However, the 7 strains of Neisseria polysaccharea and one strain of N. subflava biovar perflava were erroneously identified as N. gonorrhoeae. None of the latter was superoxol positive in contrast with the 100% of cases of gonococcal strains. The Rosco-Neisseria system is simple and inexpensive but it should be applied on specimens that grow on selective media for gonococci (such as Thayer-Martin and others) and it should be complemented by superoxol test.

Bacterial Infections↗