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Biomedical subjects

J Rodés

Publications and source records attributed to J Rodés.

At least 397 records · Page 22Linked to original sources
PubMed1988

Somatostatin compared with cimetidine in the treatment of bleeding peptic ulcer without visible vessel.

In a randomized double-blind trial 100 patients with severe bleeding peptic ulcers were treated with an intravenous (i.v.) infusion of cimetidine or somatostatin. Only those patients in whom endoscopy performed within 6 h of admission showed non-arterial bleeding or signs of recent haemorrhage without a visible vessel entered the trial. The two treatment groups were well matched for age, sex, presence of underlying disease, prior ingestion of ulcerogenic drugs, tobacco habits, type of bleeding, haematocrit at admission, presence of hypovolaemic shock, source of bleeding and endoscopic findings. Four patients in each group were excluded after randomization. Further haemorrhage occurred in eight (17.3%) patients in the somatostatin group and in 10 (21.7%) in the cimetidine group, but the difference was not statistically significant. The number of surgical procedures, blood transfusion requirement, duration of hospitalization and mortality rates were similar in the two treatment groups. These results suggest that somatostatin does not improve the results obtained with cimetidine in patients with bleeding peptic ulcer, in whom the endoscopy discloses non-arterial bleeding or signs of recent haemorrhage without a visible vessel.

Aged↗
PubMed1988

Post-transfusional vs. sporadic non-A, non-B chronic hepatitis. A clinico-pathological and evolutive study.

The clinical, morphological and evolutive features of 60 patients with chronic hepatitis, presumably caused by non-A, non-B virus infection, have been retrospectively analyzed. In all the cases the disease began as an acute episode of viral hepatitis that was followed by persistently abnormal liver function tests. No patient had evidence of current or past hepatitis B virus infection and other known causes of chronic liver disease were excluded. Thirty patients had received blood transfusions in the recent past, five were drug addicts and the source of the infection was not identified in the remaining 25, in whom the disease was considered to be sporadic. Clinical or biochemical differences between patients with post-transfusional and sporadic non-A, non-B chronic hepatitis were not observed, but liver histology showed a higher proportion of patients with chronic persistent hepatitis in the sporadic (72%) than in the transfusional group (53%). On follow-up, sustained normalization of liver function tests was observed in 46% of the cases with sporadic hepatitis but only in 13% of the cases with post-transfusion hepatitis. These observations suggest that non-A, non-B chronic hepatitis is more severe in patients with transfusion-related infection than in sporadic cases.

Adult↗
PubMed1988

Effects of somatostatin on splanchnic hemodynamics and plasma glucagon in portal hypertensive rats.

The effects of somatostatin infusion on splanchnic and systemic hemodynamics and plasma glucagon levels were investigated in rats with portal hypertension. Forty-four male Sprague-Dawley rats were studied. Portal hypertension was induced in 26 rats by partial portal vein ligation (PVL). These rats were divided in two experimental groups to receive blindly 1) somatostatin (PVL-SMT, n = 13) at a dose of 25 micrograms/kg body wt during 30 min preceded by a bolus injection of 15 micrograms/kg body wt or 2) placebo (saline) (PVL-P, n = 13) infused at the same rate as in the previous group. The remaining 18 rats were used as normal controls and received somatostatin (n = 9) or saline infusion (n = 9). Regional blood flows and cardiac output were measured using radioactive microspheres. Arterial and portal pressures were also measured. In portal hypertensive rats somatostatin infusion produced significant reductions in the increased portal venous inflow, reductions in portal pressure, and significantly increased portal venous resistance. Reduction of portal venous inflow was due to splanchnic vasoconstriction, evidenced by increased splanchnic arteriolar resistance. No significant differences were observed in systemic hemodynamic parameters between PVL-SMT and PVL-P rats. Plasma glucagon levels were significantly reduced by somatostatin to levels similar to those observed in sham-operated rats. In sham-operated rats, somatostatin also caused significant reduction in portal venous inflow and plasma glucagon concentration, although these changes were of lesser magnitude than in portal hypertensive rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Prevention of pancreatic reactions by bolus somatostatin administration in patients undergoing endoscopic retrograde cholangio-pancreatography and endoscopic sphincterotomy.

Mild pancreatitis is a common complication of endoscopic retrograde cholangio-pancreatography (ERCP) and endoscopic sphincterotomy. Knowing that a bolus injection of natural somatostatin (SRIF) dramatically reduces pancreatic secretion, a study was conducted in 33 subjects undergoing invasive diagnostic procedures. A placebo (n = 16) or SRIF (n = 17; 4 micrograms/kg) were injected before cannulation. Enzymatic rise was observed in 16 (94%) subjects receiving placebo and in 8 (50%) injected previously with SRIF. In the former group 65% reported abdominal pain whereas only 19% had this complaint in the SRIF series. Results suggest that a bolus injection of SRIF may attenuate pancreatic irritation caused by diagnostic procedures or sphincterotomy.

Acute Disease↗
PubMed1988

Effect of atrial natriuretic peptide on arterial pressure and renal function in cirrhotic rats with ascites.

Glomerular filtration rate, urine volume, sodium excretion and mean arterial pressure were measured in 10 rats with Cl4C induced cirrhosis presenting sodium retention and ascites, and in 10 control rats before and during the iv administration of the 28 aminoacid rat alpha-Atrial Natriuretic Peptide (alpha-ANP) (a bolus of 1 microgram followed by a constant infusion of 33 ng/min). alpha-ANP induced a similar increase in glomerular filtration rate and filtered sodium load in both groups of rats. In contrast, the increase in urine volume and sodium excretion produced by alpha-ANP was significantly lower in cirrhotic rats (from 13.8 +/- 1.9 to 37.9 +/- 9.1 microliters/min., and from 0.5 +/- 0.1 to 3.3 +/- 1.0 microEq/min) than in control animals (from 14.6 +/- 1.3 to 102.5 +/- 17.7 microliters/min., p less than 0.005; and from 1.0 +/- 0.3 to 14.1 +/- 3.2 microEq/min., p less than 0.001). The results indicate that in rats with experimental cirrhosis and ascites there are blunted diuretic and natriuretic responses to alpha-ANP, probably as a consequence of the exaggerated tubular sodium reabsorption present in these animals.

Animals↗
PubMed1988

Diagnosis and evaluation of portal hypertension.

In the past recent years there have been several major innovations in the diagnosis and 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, specially 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. Endoscopic measurements of variceal pressure may help to understand the mechanism of variceal bleeding, and perhaps might permit to assess the risk of haemorrhage in the individual patient. In addition to the measurement of portal pressure, measurement of blood flow through the azygos vein has been the major innovation in the haemodynamic evaluation of portal hypertension. Azygos blood flow represents an index of blood flow through gastroesophageal collaterals and varices draining in the azygos vein. This technique has been very useful in the development of new forms of pharmacological therapy for portal hypertension.

Azygos Vein↗
PubMed1987

Temporal relationship between the impairment of free water excretion and antidiuretic hormone hypersecretion in rats with experimental cirrhosis.

To investigate the temporal relationship between the impairment of water excretion, sodium retention, and antidiuretic hormone hypersecretion in cirrhosis, free water excretion (estimated by the minimum urinary osmolality) and urinary antidiuretic hormone excretion (which correlates with the plasma levels of this hormone) were measured weekly after an oral water load in 18 rats with carbon tetrachloride-induced cirrhosis and in 20 control animals. The onset of ascites (as an index of sodium retention) in cirrhotic rats was estimated by sequential paracentesis. Thirteen cirrhotic animals developed an impairment of water excretion 2-5 wk after the onset of ascites. The urinary excretion of antidiuretic hormone in these animals, which was normal before the impairment of water excretion, increased markedly within the week in which this abnormality was first detected and remained high thereafter. The remaining 5 cirrhotic rats did not experience an impairment of free water excretion in spite of developing ascites. The urinary excretion of antidiuretic hormone in these animals was similar to that of control rats during the entire study. In all urine samples obtained from cirrhotic rats, there was a highly significant direct linear correlation between the urinary excretion of antidiuretic hormone and the minimum urinary osmolality. Our results show the following: in rats with carbon tetrachloride-induced cirrhosis, sodium retention preceded the impairment of water excretion; and in these animals, the defect in water metabolism correlated chronologically and quantitatively with antidiuretic hormone hypersecretion. These findings are consistent with the concept that antidiuretic hormone is a major determinant of the impaired water metabolism in cirrhosis.

Animals↗
PubMed1987

Effects of alpha-adrenergic stimulation and beta-adrenergic blockade on azygos blood flow and splanchnic haemodynamics in patients with cirrhosis.

The effects of beta-blockade with propranolol and of alpha-adrenergic stimulation with methoxamine, a powerful alpha-agonist, on azygos blood flow and on systemic and hepatic haemodynamics were investigated in 26 cirrhotic patients with portal hypertension. Beta-adrenergic blockade with propranolol (n = 12), evidenced by a significant reduction of heart rate (-17 +/- 1%, P less than 0.001) and cardiac index (-17 +/- 2%, P less than 0.001), caused a mild but significant decrease of hepatic venous pressure gradient (-10 +/- 2%, P less than 0.05) and a marked fall of azygos venous blood flow (-31 +/- 5%, P less than 0.05). Alpha-adrenergic stimulation with methoxamine (n = 14), manifested by a significant increase of mean arterial pressure (19 +/- 2%, P less than 0.001), mimicked the effects of propranolol on hepatic venous pressure gradient (-10 +/- 4%, P less than 0.05) and cardiac index (-11 +/- 2%, P less than 0.001). However, azygos blood flow was not significantly reduced by methoxamine (0.7 +/- 0.1 vs 0.6 +/- 0.1 l/min). On the contrary, hepatic blood flow was significantly reduced by methoxamine (-19 +/- 4%, P less than 0.01) but not by propranolol (-7 +/- 7%, ns). Similarly, in 8 patients who received methoxamine after being beta-blocked by propranolol, azygos blood flow, that was markedly reduced by beta-blockade, did not experience a further reduction but increased slightly by alpha-adrenergic stimulation, while hepatic blood flow, that was not reduced by propranolol, decreased significantly during the subsequent methoxamine infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Azygos Vein↗
PubMed1987

Portal hypertension in primary biliary cirrhosis. Relationship with histological features.

The prevalence and type of portal hypertension (PH) in primary biliary cirrhosis (PBC) and their relationship with liver lesions have been investigated in 32 patients with the disease. Portal hypertension was considered when oesophageal or gastric varices were observed by endoscopy and/or when hepatic venous pressure gradient measured by hepatic vein catheterization was greater than 6 mmHg. Within 3 days of endoscopy, a liver biopsy was performed for histological staging and semiquantitative grading (0 to 3+) of portal and sinusoidal fibrosis, portal inflammation, piecemeal necrosis, lobular necrosis, cholestasis, as well as the presence of granulomas and Mallory's hyaline. Twenty patients (62.5%) had portal hypertension, five of them showing presinusoidal PH (15.5%) and the remaining 15 (47%) with sinusoidal component. The four patients in stage IV had sinusoidal PH and the only patient in stage I had no PH. The prevalence of portal hypertension was similar in patients in stage II (57%) and stage III (55%), but presinusoidal PH was only observed in patients in stage II. Patients with PH showed significantly higher portal inflammation and piecemeal necrosis than patients without PH. By contrast, there were no differences in portal and sinusoidal fibrosis, nor in the other histologic features. These results indicate that portal hypertension is common in PBC and it may be present in the early stages of the disease. The fact that presinusoidal PH was only observed in patients in stage II suggests that portal hypertension is initially of presinusoidal type, and then as the disease progresses is joined by a sinusoidal component.

Adult↗