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Biomedical subjects

F Rivera

Publications and source records attributed to F Rivera.

At least 127 records · Page 7Linked to original sources

Circulating levels of endothelin in cirrhosis.

BACKGROUND: Current information concerning endothelin in cirrhosis is conflicting. Plasma endothelin concentration has been found to be increased in some studies and normal or reduced in others. The present study was aimed to investigate the plasma levels of endothelin in cirrhosis and to assess whether it is involved in the renal and hemodynamic disturbances and neurohumoral changes present in this condition. METHODS: Renal function, plasma renin activity, and plasma concentration of aldosterone, norepinephrine, antidiuretic hormone, atrial natriuretic factor, and endothelin were measured in 9 healthy subjects, 7 compensated cirrhotics, and 25 cirrhotics with ascites (10 with functional renal failure). RESULTS: Cirrhotics with ascites with and without functional renal failure showed higher endothelin levels (15.6 +/- 6.4 and 15.7 +/- 4.6 pg/mL, respectively; mean +/- SD) than compensated cirrhotics (6.4 +/- 1.8 pg/mL) and healthy subjects (3.4 +/- 1.0 pg/mL) (analysis of variance, F = 21.84; P < 0.001). These patients also showed higher plasma levels of renin, aldosterone, norepinephrine, antidiuretic hormone, and atrial natriuretic factor, although plasma endothelin levels only correlated significantly with plasma atrial natriuretic factor (r = 0.73, P < 0.001) and antidiuretic hormone concentrations (r = 0.59, P < 0.001). In 7 additional nonazotemic cirrhotics with ascites, plasma renin activity and the plasma concentration of aldosterone and endothelin were measured before and 24 hours after the intravenous administration of a saline solution of human serum albumin. Volume expansion markedly suppressed renin and aldosterone but not endothelin (21.03 +/- 7.34 vs. 23.97 +/- 14.29 pg/mL). CONCLUSIONS: Circulating plasma levels of endothelin are elevated in cirrhosis with ascites and do not decrease following plasma volume expansion.

Adult↗

Sex hormone receptors in hepatocellular carcinoma. Is there a rationale for hormonal treatment?

The present study assessed the tumor concentration of receptors for estrogens, progesterone and androgens in a series of Western patients with hepatocellular carcinoma. Receptors for estrogens and for progesterone were determined by enzyme immunoassay, while androgen receptors were determined by receptor binding assay. Receptors for progesterone were always absent. Estrogen receptors were detected in only 4 tumors, while in the remaining specimens estrogen receptor concentration was lower than 5 fmol/mg of protein. The concentration of receptors within the tumor was not related to the presence of receptor in the non-tumoral liver, which contained estrogen receptors in 12 cases, ranging between 5 and 27 fmol/mg of protein. In contrast, 14 of the 26 tumors contained androgen receptors at concentrations ranging between 2 and 211 fmol/mg of protein; these were not related to the characteristics of the underlying liver, which contained androgen receptors in 14 cases. The results suggest that the beneficial effects of tamoxifen on the survival of patients with hepatocellular carcinoma cannot be explained by the action of this drug on estrogen receptors and that anti-androgen therapy may have some benefit in patients with androgen-receptor-positive tumors.

Adult↗

Oral misoprostol or intravenous prostaglandin E2 do not improve renal function in patients with cirrhosis and ascites with hyponatremia or renal failure.

Prostaglandins play an important role in the maintenance of renal hemodynamics and water excretion in cirrhosis. To investigate whether the administration of prostaglandins improves renal function in cirrhotic patients with ascites, 16 patients with functional renal failure and/or dilutional hyponatremia were given oral misoprostol, a prostaglandin E1 analogue (200 micrograms/6 h for 4 days; n = 9) or intravenous prostaglandin E2 (0.5 microgram/min for 1 h followed by 1 microgram/min for another hour; n = 7). The administration of misoprostol did not induce significant changes in the glomerular filtration rate (59 +/- 11 vs. 54 +/- 11 ml/min), sodium excretion (4.0 +/- 1.3 vs. 4.1 +/- 2.1 microEq/min), and free water clearance (2.4 +/- 0.8 vs. 2.1 +/- 0.9 ml/min), nor did it improve the natriuretic response to an intravenous bolus of 40 mg of furosemide (486 +/- 124 vs. 406 +/- 88 microEq/min). Similarly, an infusion of prostaglandin E2 did not induce significant changes in the glomerular filtration rate (baseline: 33 +/- 6; 0.5 microgram/min: 31 +/- 5; 1 microgram/min: 31 +/- 6 ml/min) and sodium excretion (5.7 +/- 2.7; 3.2 +/- 1.4; and 1.5 +/- 0.7 microEq/min, respectively), whereas free water clearance decreased significantly (1.1 +/- 0.7; 0.5 +/- 0.5; and -0.1 +/- 0.2 ml/min, respectively, p < 0.05). These results indicate that oral misoprostol or the intravenous infusion of prostaglandin E2 do not improve renal function in cirrhosis with ascites.

Administration, Oral↗

CMV front-line chemotherapy in transitional bladder carcinoma.

BACKGROUND: Despite standard treatment, surgery and/or radiotherapy, most patients with muscle invasive bladder carcinoma die early of distant metastasis. CMV chemotherapy has demonstrated a high response rate with moderate toxicity in advanced bladder carcinoma. In an attempt to eradicate undetectable metastatic disease and to avoid cystectomies, 36 patients were given up-front CMV. MATERIALS AND METHODS: The patients were 34 males and 2 females with a median age of 62 years (45-75); performance status 0-1 (WHO) in 34 patients; histology: 34 transitional carcinomas and 2 anaplastic carcinomas (grade II: 8, grade III: 28). Clinical staging was T2-3a: 19 patients, T3b: 14 patients and T4: 3 patients. Nineteen patients had complete trans-urethral resections (TUR) at diagnosis. The multimodal protocol started with 3 CMV courses (cisplatin 100 mg/m2 i.v. d 1, methotrexate 30 mg/m2 i.v. d 1, 8 and vinblastine 4 mg/m2 i.v. d 1, 8 every 3 weeks). Patients who yielded clinical complete responses (cCR) by cystoscopy, TUR biopsies and imaging techniques were given 3 additional courses. Cystectomy was performed in non-cCR patients and as salvage treatment. RESULTS: Following 3 CMV cycles, 29 patients (81%) responded (20 cCR and 9 cPR) and 7 (19%) did not (NR). Currently, with a median follow-up of 23.5 months (13-59), 13 have died and 23 are alive, 12 of whom retain their bladders. The projected overall survival is 51% at 4.5 years. Grade 3-4 hematological toxicity was presented in 8% of the cycles. No toxic deaths were observed. CONCLUSION: The CMV regimen, after TUR, produces a high response rate with tolerable toxicity. Bladders could be preserved in half of the CR patients.

Aged↗

[Intelligence evaluation with short forms of WAIS for populations of low socioeconomic status].

A WAIS-S short form for the assessment of intelligence as a confounding variable is proposed. A number of 161 complete WAIS-S protocols, relating to women of lower-middle and low socioeconomic status were analysed. Six subtests (Social Comprehension, Similarities, Vocabulary, Block Design, Picture Completion and Object Assembly) were chosen using two criteria: specific functions evaluated by each subtest and correlation coefficients relating IQ to the subtests. Five WAIS-S short forms were evaluated: one consisting of six subtests and the others with different combinations of four of them. Data showed that they were all appropriate for the measurement of intelligence as a confounding variable; the correlation coefficients between short forms and total IQ ranged from 0.90 to 0.94. The standard errors of the short forms for the estimation of total IQ were of 3 or 4 points, and 3 to 7% of the subjects were wrongly classified. When maternal intelligence had to be measured in relation to infant development the short form that included Social Comprehension, Similarities, Block Design and Picture Completion seemed the most appropriate. Nevertheless when choosing a WAIS-S short form not only economy of time but also the specific relevant functions assessed in each subtest must be considered.

Adolescent↗

Regulation of islet amyloid polypeptide in human pancreatic islets.

This study investigated the effect of glucose on islet amyloid polypeptide secretion, content, and mRNA synthesis of human pancreatic islets. The release of islet amyloid polypeptide from fresh isolated islets in response to glucose was parallel to that of insulin. The islet amyloid polypeptide-to-insulin molar ratios in response to 5.5 and 16.7 mM glucose were 1:16 and 1:15 respectively. Islets were cultured for 1 and 7 days at two different glucose concentrations (5.5 and 16.7 mM). The islet amyloid polypeptide response to the 1-day culture was similar to that of the fresh islets; however, after the 7-day culture the islet amyloid polypeptide and insulin secretory responses to glucose were dissociated. The insulin response of islets to a high-glucose stimulus was significantly (P < 0.001) increased, whereas the islet amyloid polypeptide response of islets to the same stimulus was blunted. The IAPP content was greater than insulin content in a molar ratio (1:50 to 1:30) after long exposure of islets to concentrations of high glucose even though the increase was significant for both peptides (P < 0.005). Northern blot analysis of each cultured condition showed an increase of both mRNA IAPP and insulin signals after exposure of islets at 16.7 mM glucose, the maximum mRNA expression being after long exposure to high-glucose concentrations. Quantification of both signals by densitometry showed a greater increase for islet amyloid polypeptide than for insulin. These findings suggest that IAPP can be accumulated in beta-cells after long exposure of human islets to high-glucose concentrations, because glucose increases IAPP synthesis but not secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Actins↗

Impaired responsiveness to angiotensin II in experimental cirrhosis: role of nitric oxide.

Impaired vascular responsiveness to angiotensin II is a common feature in human cirrhosis with ascites. The aim of this study was to investigate whether vascular reactivity to angiotensin II is also decreased in rats with carbon tetrachloride-induced cirrhosis and ascites and to assess the role of endogenous nitric oxide in this abnormality. Increasing doses of angiotensin II (from 31 to 500 ng.kg-1.min-1) induced significantly smaller increases in total peripheral resistance in conscious cirrhotic rats with ascites (n = 8) than in control animals (n = 9) at each dose tested. A reduced response to angiotensin II was also observed in vitro in aortic rings of rats with cirrhosis and ascites compared with that in control aortic rings (maximal response: 104 +/- 16 mg vs. 204 +/- 18 mg; p < 0.001). This in vitro hyporesponsiveness to angiotensin II in aortic rings of cirrhotic rats with ascites was reversed on endothelium denudation or nitric oxide synthesis inhibition with N omega-nitro-L-arginine but was not influenced by cyclooxygenase inhibition with indomethacin. In conclusion, this study shows reduced vascular reactivity to angiotensin II in carbon tetrachloride-induced cirrhosis with ascites and indicates that this abnormality is mediated by nitric oxide.

Angiotensin II↗

Effect of dipyridamole on kidney function in cirrhosis.

Adenosine is a potent endogenous renal vasoconstrictor. To investigate the sensitivity of the renal circulation to adenosine in cirrhosis, we evaluated kidney function and vasoactive hormones in 20 patients with cirrhosis before and after administration of dipyridamole (0.4 mg/kg, intravenously), a drug that increases extracellular levels of adenosine. In patients with ascites and increased plasma renin activity (6.9 +/- 4.0 ng/ml.hr [mean +/- S.D.]) (n = 7), dipyridamole induced marked reductions in renal plasma flow (from 623 +/- 294 to 374 +/- 188 ml/min, p = 0.03), glomerular filtration rate (from 89 +/- 22 to 48 +/- 16 ml/min, p = 0.009), urine volume (from 7.1 +/- 2.1 to 1.5 +/- 1.1 ml/min, p = 0.0001), free water clearance (from 4.0 +/- 1.7 to 0.4 +/- 0.6 ml/min, p = 0.001) and sodium excretion (from 28 +/- 36 to 7 +/- 15 mu Eq/min, p = 0.05) in the absence of changes in arterial pressure, plasma renin activity and levels of aldosterone, norepinephrine and antidiuretic hormone. In patients without ascites (n = 5) and in patients with ascites and normal plasma renin activity (0.9 +/- 0.5 ng/ml.hr) (n = 8), renal plasma flow and glomerular filtration rate did not change significantly after dipyridamole administration, whereas excretion of sodium and free water was reduced. These results indicate that in cirrhotic patients with ascites and overactivity of the renin-angiotensin system, dipyridamole induces renal vasoconstriction in the absence of changes in systemic hemodynamics, suggesting that these patients are particularly sensitive to the renal vasoconstrictor effect of endogenous adenosine.

Ascites↗

Brachial and femoral artery blood flow in cirrhosis: relationship to kidney dysfunction.

Brachial artery and common femoral artery blood flows and cardiac output were measured with duplex-Doppler ultrasonography in 12 normal subjects, 12 patients with compensated cirrhosis and 35 patients with cirrhosis and ascites (8 with functional kidney failure). The aim of this study was to investigate whether arteriolar vasodilation in these vascular territories contributes to hyperdynamic circulation in cirrhosis. Cardiac output was significantly increased and systemic vascular resistance significantly reduced in the three groups of cirrhotic patients. We found no significant differences between normal subjects and compensated cirrhotic patients in brachial artery (55 +/- 7 vs. 57 +/- 7 ml/min) and femoral artery (353 +/- 20 vs. 310 +/- 25 ml/min) blood flow. Nonazotemic cirrhotic patients with ascites showed significantly lower (p < 0.05) brachial artery blood flow (40 +/- 3 ml/min) than healthy subjects and compensated patients. Femoral artery blood flow (327 +/- 25 ml/min), however, was not significantly different. Brachial artery (25 +/- 3 ml/min) and femoral artery (213 +/- 22 ml/min) blood flows were markedly reduced in the patients with kidney failure (p < 0.05 with respect to the other three groups). Glomerular filtration rate correlated directly with brachial (r = 0.74, p = 0.0001) and femoral (r = 0.52, p = 0.03) artery blood flow in the cirrhotic patients. These results indicate that the arteriolar vasodilation causing hyperdynamic circulation in cirrhosis does not take place in the brachial and femoral vascular territories.

Aged↗

Renal effects of acute isosorbide-5-mononitrate administration in cirrhosis.

The aim of this study was to assess the effects of an oral dose (20 mg) of isosorbide-5-mononitrate on systemic hemodynamics, kidney function, plasma renin activity and plasma aldosterone and atrial natriuretic peptide concentrations in 16 nonazotemic cirrhotic patients. Isosorbide-5-mononitrate significantly reduced cardiopulmonary pressures, cardiac output, peripheral vascular resistance, mean arterial pressure, renal plasma flow, glomerular filtration rate, free water clearance, sodium excretion and atrial natriuretic peptide concentration and significantly increased renin and aldosterone values. Cardiopulmonary pressures, atrial natriuretic peptide, cardiac output and mean arterial pressure decreased to a similar extent in patients with (n = 9) and without ascites (n = 7). In patients with ascites we noted marked increases in plasma renin activity (3.7 +/- 1.1 ng/ml/hr to 6.4 +/- 1.8 ng/ml/hr; p = 0.01) and aldosterone level (61.1 +/- 17.5 ng/dl to 108.4 +/- 36.1 ng/dl; p = 0.01). In contrast, in patients without ascites the elevation of plasma renin activity (0.5 +/- 0.16 ng/ml/hr to 0.95 +/- 0.27 ng/ml/hr; p = 0.02) and aldosterone level (5.9 +/- 1.3 ng/dl to 12.3 +/- 3.8 ng/dl; p = 0.02) was mild, and in no case did these parameters increase over the upper normal limit. Isosorbide-5-mononitrate produced a significantly greater reduction of glomerular filtration rate (-21.4% +/- 3.3% vs. -8.9% +/- 4.2%; p = 0.03) and free water clearance (-82.4% +/- 16.1% vs. -34.5% +/- 12.3%; p = 0.03) in patients with ascites than in those without.(ABSTRACT TRUNCATED AT 250 WORDS)

Aldosterone↗

Amoebological study of the atmosphere of San Luis Potosi, SLP, Mexico.

A one year round survey was conducted for isolation of free living amoebae (FLA) in the city of San Luis Potosi, (SLP), Mexico, which is placed in a desert environment. Samples were taken by modified impinger method and cultivated in laboratory conditions for FLA isolation following a week period of rehidration. 57 strains were isolated, 39% belonged to Acanthamoeba genus (which is important because it bears opportunistic pathogens that produce amoebic keratitis and granulomatous amoebic encephalitis in humans), 16% to Hartmannella, 9% to Vahlkampfia and the other proportion was divided among 6 other genera. The isolations were more abundant during dry season and the main genera were present in all four stands. The difference among them was the species variety which is discused as connected with abundance of organic wastes and lack of urbanization near the stations.

Air Microbiology↗

Monoclonal enzyme immunoassay measurement of estradiol and progesterone receptors in in vitro fertilization and spontaneous cycles.

So far, the few studies performed on endometrial steroid receptors in in vitro fertilization (IVF) cycles have been carried out by the dextran-coated charcoal (DCC) method. Despite widespread efforts to standardize the DCC assay method, assay results still vary and thus, data obtained in IVF cycles are controversial. In the present article, late luteal estradiol (E2) and progesterone (P) receptor (R) levels were measured by a new monoclonal enzyme immunoassay (EIA) method in endometrial samples obtained from 21 patients in an IVF program who received no embryo transfer (ET) after ovarian stimulation with follicle-stimulating hormone/human menopausal gonadotrophin/human chorionic gonadotrophin under pituitary suppression with buserelin. Plasma levels of E2, P and prolactin (PRL) were measured in three blood samples collected in the midluteal phase. Results were compared with those obtained in a control group of 21 spontaneous cycles. E2, P and PRL were significantly higher in stimulated than in spontaneous cycles. The level of E2R was decreased in endometrium in IVF stimulated cycles, but PR remained unchanged.

Adult↗

Pathogenesis of arterial hypotension in cirrhotic rats with ascites: role of endogenous nitric oxide.

Nitric oxide is a vasodilator tonically secreted by endothelial cells that is involved in the regulation of arteriolar tone. This study, which includes two protocols, was performed to investigate whether nitric oxide plays a role in the pathogenesis of arterial hypotension in cirrhosis with ascites. In protocol 1, the administration of increasing doses (25, 50, 250, 500 and 1,000 micrograms.kg-1.min-1) of the nitric oxide biosynthesis inhibitor N omega-nitro-L-arginine to 18 conscious rats with cirrhosis and ascites produced, at each dose tested, a significantly greater increase in arterial pressure than in 17 conscious control rats. At the lowest dose of N omega-nitro-L-arginine, arterial pressure significantly rose in cirrhotic rats but not in controls. In protocol 2, arterial pressure, estimated renal plasma flow, glomerular filtration rate and sodium excretion were measured in 12 cirrhotic rats with ascites and 10 control rats before and during the sequential infusion of previously selected doses of N omega-nitro-L-arginine (25, 50 and 250 micrograms.kg-1.min-1). Changes in arterial pressure reproduced those observed in protocol 1. In control rats, N omega-nitro-L-arginine caused a decrease in estimated renal plasma flow without affecting glomerular filtration rate or sodium excretion. In contrast, N omega-nitro-L-arginine administration to cirrhotic animals did not produce any appreciable renal vasoconstrictor effect, and it increased glomerular filtration rate and sodium excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Lymphocyte beta 2-adrenoceptors and plasma catecholamines in patients with cirrhosis.

The hemodynamic response to propranolol in patients with cirrhosis is heterogeneous. In some patients, there is an expected decrease in portal pressure, whereas in others, portal pressure fails to decrease despite adequate beta-blockade. It has been suggested that this lack of response could be related to down-regulation of beta 2-adrenoceptors, promoted by the increased adrenergic activity frequently found in decompensated cirrhosis. The present study investigated this hypothesis by measuring the density and affinity of lymphocyte beta 2-adrenoceptors (L-beta 2-AR), an established index of beta 2-adrenoceptors in target organs, and the plasma levels of norepinephrine and epinephrine in a group of 32 patients with cirrhosis and portal hypertension. The portal pressure response to propranolol administration (0.1 mg/kg + 2 mg/h) was also investigated (n = 27). Patients with cirrhosis had increased norepinephrine levels (605 +/- 360 vs. 224 +/- 110 pg/mL in controls; P less than 0.001), but plasma epinephrine level was not increased (136 +/- 72 vs. 111 +/- 22 pg/mL in controls; NS). There were no differences between cirrhotic patients and controls in the density of L-beta 2-AR (1398 +/- 489 vs. 1278 +/- 356 receptors/cell; NS). Portal pressure decreased greater than 10% in 12 patients (responders) and less than 10% in the remaining 15 (nonresponders). Contrary to previous suggestions, there were no significant differences between responders and nonresponders in relation to the density of L-beta 2-AR (1362 +/- 527 vs. 1487 +/- 419 receptors/cell; NS), to the affinity of these receptors (0.15 +/- 0.27 vs. 0.13 +/- 0.12 nmol/L; NS), to the plasma levels of norepinephrine (661 +/- 508 vs. 621 +/- 256 pg/mL; NS), and to plasma epinephrine concentration (141 +/- 90 vs. 140 +/- 75 pg/mL; NS). These results show that the response of portal pressure to propranolol administration is neither related to the density and affinity of L-beta 2-AR nor to the plasma levels of norepinephrine and epinephrine. Thus, the determination of these parameters cannot substitute measurements of portal pressure to identify those patients with an adequate portal pressure response to propranolol treatment.

Aged↗

Mineralocorticoid escape in patients with compensated cirrhosis and portal hypertension.

Failure to escape from mineralocorticoids in compensated cirrhosis is considered a major argument supporting the overflow theory of ascites. To assess the frequency and mechanism of mineralocorticoid escape in cirrhosis, 9-alpha-fluorohydrocortisone (0.6 mg/day) was administered to 19 patients with compensated cirrhosis, portal hypertension, and no history of ascites who were able to maintain sodium balance on a 250 mmol Na+ diet. Fifteen patients (78.9%) escaped from mineralocorticoids, while 4 patients (21.1%) did not escape and developed ascites. Patients who did not escape had significantly higher cardiac index (4.97 +/- 0.42 vs 3.46 +/- 0.21 L.min-1.m-2) and lower peripheral vascular resistance (485.9 +/- 37.5 vs. 665.8 +/- 32.9 dyne.s.cm-5/m2) than those who escaped. Hepatic venous pressure gradient was not significantly different. The escape phenomenon was associated with a significant increase in mean arterial pressure, creatinine clearance, and atrial natriuretic factor and suppression of plasma renin activity. All of these parameters showed minimal or no changes in patients who did not escape. These results indicate that failure to escape from mineralocorticoids is uncommon in patients with compensated cirrhosis, is related to an inadequate expansion of effective plasma volume due to the accumulation of ascites, and occurs in patients with marked peripheral arteriolar vasodilation.

Adult↗