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Biomedical subjects

F Rivera

Publications and source records attributed to F Rivera.

At least 199 records · Page 11Linked to original sources
PubMed1986

Pathogenic and free-living protozoa cultured from the nasopharyngeal and oral regions of dental patients: II.

Protozoa of the nose, mouth, and pharynx of 30 randomly chosen male caries patients at an odontological clinic of the National Autonomous University of Mexico, in Mexico City, were surveyed by culture from swabs. Culture tubes from swabs were observed every other day for 5 weeks. Pathogens found included Entamoeba histolytica, Naegleria fowleri, Acanthamoeba castellanii, A. culbertsoni, A. polyphaga, and Giardia lamblia. Such isolations of pathogens suggest that patients may be healthy carriers of cysts and trophic forms of protozoa responsible for several human diseases. Amoebae responsible for primary amoebic meningoencephalitis were well represented in the samples. Small pathogenic free-living amoebae have not been isolated before from healthy males in Mexico. Many species of free-living cyst-forming protozoa and some commensals without cysts were also cultured from swabs.

Adult↗
PubMed1986

Urinary excretion of 6-keto-prostaglandin F1 alpha, thromboxane B2 and prostaglandin E2 in cirrhosis with ascites. Relationship to functional renal failure (hepatorenal syndrome).

The aim of the study was to investigate the urinary excretion of 6-keto-PGF1 alpha (a stable metabolite of PGI2), thromboxane B2 (TxB2; a stable metabolite of TxA2), and PGE2 in 18 normal subjects, 49 cirrhotics with ascites without renal failure (GFR = 90 +/- 4 ml/min, means +/- S.E.M.) and 20 cirrhotics with functional renal failure (FRF) (GFR = 36 +/- 3). The study was made after 5 days on a 50 mEq sodium diet and without diuretics. Plasma renin activity (PRA), plasma norepinephrine concentration (NE) and plasma antidiuretic hormone concentration (ADH) were also measured. Cirrhotics without FRF showed a significantly higher urinary excretion of 6-keto-PGF1 alpha, TxB2 and PGE, (15.9 +/- 1.7 ng/h, 3.0 +/- 0.3 ng/h, and 6.2 +/- 1.0 ng/h) than did normal subjects (9.2 +/- 0.9, 1.3 +/- 0.1 and 2.3 +/- 0.4). On the contrary, the urinary excretion of these prostaglandins was normal or reduced in patients with FRF (5.3 +/- 0.8, 1.3 +/- 0.2 and 1.9 +/- 0.4). PRA, NE and ADH were significantly increased in cirrhotics with FRF (15.2 +/- 3.9 ng/ml/h, 1026 +/- 149 pg/ml and 4.1 +/- 0.3 pg/ml) and in patients without FRF (8.0 +/- 1.4, 667 +/- 67 and 3.9 +/- 0.3) as compared to normal controls (1.3 +/- 0.2, 275 +/- 46 and 2.4 +/- 0.2). These results suggest that renal hemodynamics in cirrhosis depends upon a critical equilibrium between the activity of endogenous vasoconstrictor systems and the renal production of the vasodilator prostaglandins PGI2 and PGE2. In addition, they do not support FRF in cirrhosis being related to an increased renal production of the vasoconstrictor prostaglandin TxA2.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Atrial natriuretic factor: reduced cardiac content in cirrhotic rats with ascites.

The present study was designed to investigate whether cirrhosis with ascites is associated with altered tissue content of atrial natriuretic factor. Atrial extracts from 14 cirrhotic rats with ascites and increased plasma renin activity (PRA) (14.4 +/- 4.6 ng X ml-1 X h-1) and aldosterone concentration (148.3 +/- 17.3 ng/dl) and from 10 control rats (PRA, 3 +/- 0.5 ng X ml-1 X h-1; aldosterone, 34.7 +/- 3.7 ng/dl) were intravenously injected into anesthetized normovolemic rats. Only one extract was assayed in each bioassay rat. Atrial extracts from control rats increased diuresis and natriuresis 513 +/- 91 and 3,029 +/- 752%, respectively (means +/- SE). In contrast, atrial extracts from cirrhotic rats increased urine volume 199 +/- 49% (P less than 0.001) and sodium excretion 546 +/- 132% (P less than 0.001). These results strongly suggest that atrial content of atrial natriuretic factor is reduced in cirrhotic rats as compared with control animals.

Animals↗
PubMed1986

Mechanism of inhibition of human testicular steroidogenesis by oral ketoconazole.

To determine the antisteroidogenic effect of ketoconazole (KTZ) in the human testis, we measured the plasma delta 5-pregnenolone, delta 5-17 alpha-hydroxypregnenolone, dehydroepiandrosterone (DHEA), progesterone, 17 alpha-hydroxyprogesterone, androstenedione (A), and testosterone (T) concentrations in three men with previously untreated metastatic prostate cancer at various time intervals for 24 h before and 48 h after the administration of 200 mg oral KTZ every 8 h. The adrenal glands of these three patients were suppressed (as measured by the plasma cortisol levels) by the administration of 1.0 mg dexamethasone daily for 7 days before and during the study. After six doses of KTZ, bilateral orchiectomy was performed, and the intratesticular concentration of the aforementioned seven steroids and the intratesticular activities of the 17 alpha-hydroxylase, 17,20-desmolase, and 17 beta-hydroxysteroid dehydrogenase enzymes in the delta 4-steroidogenic pathway were determined. These seven intratesticular steroids and three intratesticular enzyme activities were compared to those in five men with previously untreated prostate cancer who underwent orchiectomy as primary treatment for their disease. Plasma A, DHEA, and T all significantly decreased during KTZ therapy. There was no significant change in the other four steroids in the plasma. In the testis, delta 5-pregnenolone, delta 5-17 alpha-hydroxypregnenolone, and delta 4-17 alpha-hydroxyprogesterone were all significantly elevated, whereas intratesticular DHEA, A, and T were significantly decreased in the three KTZ-treated patients compared to levels in the five non-KTZ-treated patients. Measurement of the enzyme activities demonstrated a significant reduction in both 17 alpha-hydroxylase and 17,20-desmolase, but no change in 17 beta-hydroxysteroid dehydrogenase, in the KTZ-treated patients compared to the levels in the non-KTZ-treated patients. We conclude that oral KTZ decreases testicular T production by inhibiting the 17,20-desmolase and also the 17 alpha-hydroxylase steps in both the delta 4- and delta 5-T biosynthetic pathways.

Administration, Oral↗
PubMed1986

Neurohormonal responses to antihypertensive treatment with captopril or hydrochlorothiazide.

In order to assess the neurohormonal responses to oral administration of two drugs with different antihypertensive mechanisms, and their implications for long-term efficacy, we studied the changes in plasma renin activity, aldosterone, catecholamines and blood pressure after two cross-over periods of treatment with captopril and hydrochlorothiazide for three months in 14 patients with moderate essential hypertension. Similar levels of plasma renin activity were achieved with both but plasma levels of noradrenaline and aldosterone rose with hydrochlorothiazide (P less than 0.005 and P less than 0.05). Dopamine levels decreased with captopril. Six patients on hydrochlorothiazide had potassium levels under 3.5 mmol/l. Captopril and hydrochlorothiazide were effective in controlling blood pressure in 78% and 50% of the patients respectively, but in cases where noradrenaline was significantly increased after treatment, the effect on diastolic blood pressure was less (P less than 0.05). These data suggest that captopril is highly effective for blood pressure control and that the neurohormonal responses to the drug probably provide additional benefits for long-term therapy in hypertension.

Adult↗
PubMed1986

[Technics for the study of the renal excretion of free water in normal rats and those with experimental liver cirrhosis].

Different techniques to measure free water excretion in rats, administered an oral water overload and with measurement of its ability to excrete it into the urine have been studied. When 30 or 50 ml/kg b.wt. were administered and the urine excreted in 3 h was collected, a decrease on the urinary osmolality (UOSM) was observed with respect to the baseline UOSM, which was similar in both overloads, although the percentage of the overload excreted was significantly greater with 50 ml/kg. However, the UOSM obtained was hypertonic as compared to plasma osmolality (POSM) indicating that this determination was not useful to study free water excretion. In a further study it was investigated if there was any period of time in which all the animals excreted hypotonic urine. However, results indicated that the period for excreting a maximally diluted urine was very variable in time. The best technique to study free water excretion in these animals was the collection of each spontaneously voided urine independently, to measure the minimal UOSM. When a 50 ml/kg water load was administered and the minimal UOSM was determined it was observed to be lower than POSM in all the animals indicating that this technique was useful to study this derangement in these animals.

Animals↗
PubMed1986

[Determination of arginine-vasopressin in small volumes of rat plasma].

A radioimmunoassay to determine arginine-vasopressin concentration in rat plasma is described. This method was a modification from a previously described technique from which the incubation volume was reduced. It allows us to use only 300 microliter of plasma, 1/4 of the original volume, without any impairment to the sensitivity. The intra- and inter-assay coefficients of variation are 11% and 13% respectively. The accuracy ranges between 90 and 99%. To investigate the influence of sampling blood conditions on arginine-vasopressin levels, five groups of Sprague-Dawley rats are analyzed: Group I, decapitation; Group II, ether anaesthesia and cardiac puncture; Group III, ether anaesthesia and decapitation; Group IV, ketamine anaesthesia and cardiac puncture; Group V, ketamine anaesthesia and decapitation. Arginine-vasopressin levels in Group V (2.2 +/- 0.8 pg/ml) are significantly lower than those from the other four groups and similar to those obtained by other authors using a chronic catheter.

Animals↗
PubMed1985

Renal hemodynamic abnormalities in patients with short term insulin-dependent diabetes mellitus: role of renal prostaglandins.

To determine if renal functional alterations in diabetes mellitus could be related to disturbances of vasoactive systems, renal plasma flow (RPF), glomerular filtration rate (GFR), PRA (basal and stimulated), plasma catecholamine levels, and urinary excretion of prostaglandin E2 (PGE2), 6-keto-PGF1 alpha, and kallikrein were determined in 21 patients with insulin-dependent diabetes mellitus (IDDM) of short duration and 15 normal subjects. In 7 additional patients with IDDM and in 4 normal subjects, the effect of lysine acetylsalicylate (LAS; 450 mg, iv) on GFR and RPF was studied. Patients with IDDM had higher RPF and GFR than normal subjects. Plasma norepinephrine and basal and stimulated PRA were significantly lower in IDDM than in the control group [161 +/- 82 (+/- SD) vs. 243 +/- 114 pg/ml, 0.19 +/- 0.20 vs. 1.15 +/- 0.33 ng/ml X h, and 0.93 +/- 0.82 vs. 2.8 +/- 1.73 ng/ml X h, respectively). No significant differences were found in the urinary excretion of PGE2, 6-keto-PGF1 alpha, and kallikrein in the two groups. LAS administration significantly reduced RPF (from 641 +/- 72 to 535 +/- 38 ml/min X 1.73 m2) and GFR (from 168 +/- 25 to 150 +/- 18 ml/min X 1.73 m2) in patients with IDDM, but not in normal subjects. In IDDM patients, there was a close direct correlation between the percent decrease in RPF and GFR induced by LAS and the baseline values of these parameters. The results suggest that in IDDM, there may be an imbalance between the degree of activation of the renin-angiotensin and sympathetic nervous systems and the renal production of PGs. The observation that LAS administration reduced RPF and GFR in these patients suggests that renal PGs are involved in the renal hyperperfusion of IDDM.

Adult↗
PubMed1985

Somatostatin and counterregulatory hormone responses to hypoglycaemia in diabetics with and without autonomic neuropathy.

Blood glucose, somatostatin and counterregulatory hormone responses to an i.v. bolus of insulin were studied in insulin-dependent diabetics with different degrees of autonomic neuropathy, after 24 hours of optimised control with an artificial pancreas. There was no plasma catecholamine response in patients with a sympathetic autonomic neuropathy. A normal somatostatin response to hypoglycemia was absent in patients with autonomic neuropathy. Glucagon did not respond in diabetics, independently of the degree of neuropathy. In all diabetics, cortisol and GH were stimulated. Absence of warning symptoms was observed in patients with catecholamine deficiency. Despite different hormone behaviour, blood glucose fall and recovery were similar in all diabetic groups. It is concluded that the glucagon response to insulin hypoglycaemia is reduced in all type 1 longstanding diabetics, whereas catecholamine and somatostatin responses are only abolished in those with autonomic neuropathy. Patients with sympathetic neuropathy would be considered at increased risk severe hypoglycaemia.

Adult↗
PubMed1985

[Effect of the method of blood extraction on plasma levels of renin in the Wistar rat].

To investigate the influence of blood extraction conditions on the renin-angiotensin system in rats, plasma renin activity (PRA) and plasma renin concentration (PRC) were measured in blood samples obtained by different methods. PRA and PRC in samples obtained by chronic catheterization, cardiac puncture without anesthesia, and decapitation immediately following light ether anesthesia were not significantly different from those obtained by simple decapitation (control group). In contrast, PRA and PRC in samples obtained by cardiac puncture and cavernous sinus puncture after light ether anesthesia were significantly (p less than 0.01) higher than those obtained in the control group. There was a significant direct correlationship between PRA and PRC in all samples studied (r = 0.87, p less than 0.001). The present results suggest that light ether anesthesia increases renin levels, except when blood samples are taken by decapitation, and that chronic catheterization and cardiac puncture are the choice blood extraction methods to evaluate the renin-angiotensin system in rats.

Anesthesia, General↗
PubMed1984

Pathogenic and free-living protozoa cultured from the nasopharyngeal and oral regions of dental patients.

Protozoa of nose, mouth, and pharynx of 30 randomly chosen female caries patients at an odontological clinic of the National Autonomous University of Mexico, were surveyed by culture from swabs. Culture tubes of swabs from each patient were observed every other day during 5 weeks. Pathogenic protozoa found included Entamoeba histolytica Schaudinn, 1903; Naegleria fowleri Carter, 1970; Acanthamoeba castelanii Douglas, 1930; Acanthamoeba culbertsoni Singh & Das, 1970; and Balantidium coli (Malmsten, 1857) Stein, 1862. This isolation of pathogens suggests that healthy patients may be healthy carriers of cysts of protozoa, mainly amoebae, responsible for several diseases, including primary amoebic meningoencephalitis. Small pathogenic free-living amoebae have not been isolated before from females in Mexico. Many species of free-living protozoa were also cultured from swabs from the patients.

Adult↗
PubMed1984

Evidence that renal prostaglandins are involved in renal water metabolism in cirrhosis.

Plasma antidiuretic hormone (ADH) and urinary prostaglandin E2 excretion (UPGE2V) were measured in basal conditions, after water restriction, and after water-loading in 10 normal subjects (free water clearance after the water load, CH2O, 9.6 +/- 0.8 ml/min) and in 27 patients with cirrhosis and ascites (13 with a positive CH2O: 3.6 +/- 0.5; 14 with a negative CH2O: -0.37 +/- 0.007). Plasma ADH and UPGE2V were significantly increased in patients with a positive CH2O as compared with normal subjects. Patients with a negative CH2O showed a significantly higher plasma ADH and a lower UPGE2V and GFR than did normal subjects and patients with the positive CH2O. In 18 additional subjects (6 normal and 12 with cirrhosis, ascites, and a positive CH2O) submitted to a sustained water overload, the i.v. administration of 450 mg of lysine acetylsalicylate (LAS) induced a marked reduction of UPGE2V, but it had no effect on plasma ADH. LAS did not alter GFR and CH2O in normal subjects; however, it reduced CH2O in all the 12 patients (from 5.1 +/- 0.4 to 0.6 +/- 0.3) and the GFR in only 6 of these patients. These results suggest (a) that renal PGE2 plays an important role in the maintenance of water excretion in cirrhosis with ascites, and (b) that impaired ability to dilute the urine in cirrhosis may be a consequence of the simultaneous occurrence of impaired renal hemodynamics, nonostomic hypersecretion of ADH, and reduced renal production of PGE2.

Arginine Vasopressin↗
PubMed1984

Studies on the mechanisms of somatostatin release after insulin induced hypoglycaemia in man.

Insulin-induced hypoglycaemia, which stimulates gastric acid secretion, is associated with an increase in circulating somatostatin levels in man. In order to assess the mechanisms involved in this rise, six normal volunteers connected to a Biostator for continuous glucose monitoring were studied, on three separate occasions. On each occasion after basal blood sampling, 0.15 i.u./kg body weight of insulin was administered i.v. and further samples were obtained intermittently over 150 min. On one occasion, dextrose was infused by the Biostator to prevent hypoglycaemia, while on the other two, a constant infusion of either normal saline or the specific H2 antagonist cimetidine was administered. Insulin plus dextrose caused no significant changes in circulating somatostatin levels, whereas insulin plus saline was associated with a marked, sustained and significant rise in all subjects; insulin plus cimetidine also produced a rise but it was delayed; the area under the curve was significantly (P less than 0.05) greater with insulin plus saline than with insulin plus cimetidine. These results show that in man insulin itself does not stimulate somatostatin secretion directly, but indirectly via hypoglycaemia. Further, the inhibition of gastric acid secretion with cimetidine reduces somatostatin release during insulin-induced hypoglycaemia. This suggests that gastric acid may mediate somatostatin secretion associated with insulin-induced hypoglycaemia.

Adult↗
PubMed1984

Role of spontaneous portal-systemic shunting in hyperinsulinism of cirrhosis.

The possible contribution of hepatocellular damage and portal-systemic shunting to hyperinsulinism in cirrhosis was studied in 23 cirrhotics, 8 of whom had a surgical portacaval shunt, and 16 controls by measuring insulin and the connecting peptide (C-peptide) concentrations in simultaneous samples of peripheral arterial and hepatic venous blood. The fractional hepatic insulin extraction (0.48 +/- 0.06, mean +/- SE) was normal in cirrhosis. The hepatic insulin elimination rate was directly related to arterial insulin levels (r = 0.91, P less than 0.001) even at very high circulating levels. Extrahepatic insulin metabolism was measured across the kidney and lower limb. There were no significant differences between cirrhotics and control subjects in relation to renal (0.25 +/- 0.05 vs. 0.23 +/- 0.04) and lower limb insulin extraction (0.14 +/- 0.07 vs. 0.19 +/- 0.04). While in the control group hepatic venous insulin (0.143 +/- 0.018 pmol/ml) markedly exceeded the peripheral insulin concentration (0.083 +/- 0.009 pmol/ml, P less than 0.01), the contrary was found in cirrhotics with end-to-side portacaval shunt in whom all the pancreatic venous effluent is shunted to the systemic circulation (hepatic venous insulin, 0.130 +/- 0.028 pmol/ml; peripheral, 0.234 +/- 0.037 pmol/ml; P less than 0.01). Portal-hypertensive cirrhotics without a surgical portacaval shunt also had hepatic venous insulin levels (0.132 +/- 0.029 pmol/ml) below peripheral arterial insulin concentrations (0.205 +/- 0.041 pmol/ml, P less than 0.01). The study suggests that hyperinsulinism in cirrhosis is not the result of an intrinsic defect of hepatic insulin metabolism but of the spontaneous shunting of portal blood to the systemic circulation.

C-Peptide↗