[Lymphocutaneous sporotrichosis: report of a case].
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Adult↗
Biomedical subjects
C López
Publications and source records attributed to C López.
Effect of V1-vasopressin receptor blockade on arterial pressure in conscious rats with cirrhosis and ascites.
Angiotensin II blockade with saralasin in human cirrhosis with ascites is associated with a significant reduction in arterial pressure, indicating that endogenous angiotensin II plays an important role in the maintenance of systemic hemodynamics in this condition. The aim of the current study was to investigate whether vasopressin also contributes to the maintenance of arterial pressure in cirrhosis with ascites. The study was performed using three groups of cirrhotic rats with ascites and three groups of control animals. The administration of d(CH2)5Tyr(Me)AVP, a selective antagonist of the vascular effect of vasopressin, to 10 cirrhotic rats induced a significant reduction in mean arterial pressure (from 94 +/- 4 to 85 +/- 4 mm Hg; P less than 0.001) and a significant increase in plasma renin activity (from 24.3 +/- 4.9 to 34.3 +/- 5.9 ng/mL.h; P less than 0.02) and plasma norepinephrine concentration (from 1474 +/- 133 to 2433 +/- 253 pg/mL; P less than 0.01). Similar results were observed following saralasin administration in a second group of 5 cirrhotic rats [mean arterial pressure decreased from 97 +/- 4 to 85 +/- 5 mm Hg (P less than 0.0001); and plasma renin activity and norepinephrine concentration increased from 18.4 +/- 5.8 to 40.3 +/- 5.7 ng/mL.h (P less than 0.02) and from 1383 +/- 70 to 2312 +/- 334 pg/mL (P less than 0.05), respectively]. The simultaneous blockade of angiotensin II and vasopressin in a third group of cirrhotic rats resulted in a significantly greater reduction of mean arterial pressure (from 97 +/- 6 to 74 +/- 6 mm Hg; P less than 0.05). No changes in arterial pressure were observed in the three groups of control rats. These findings indicate that endogenous vasopressin is as important as angiotensin II in the maintenance of arterial pressure in cirrhotic rats with ascites and support the contention that arterial hypotension is the initial event leading to the stimulation of the renin-angiotensin system and vasopressin in this animal model of cirrhosis.
Angiotensin II↗
Immunocytochemical detection of 5'-bromodeoxyuridine in fluoro-gold-labeled neurons: a simple technique to combine retrograde axonal tracing and neurogenetic characterization of neurons.
To characterize the axonal projections of 5'-bromodeoxyuridine (BrdU)-labeled neurons, we have combined retrograde tracer injection of Fluoro-Gold with the immunocytochemical detection of BrdU. Pregnant mice were labeled with pulses of BrdU at embryonic days E12, E13, E14, or E16. Young adult offspring were perfused with 4% paraformaldehyde 2 days after receiving a Fluoro-Gold injection into the cerebral cortex, thalamus, or hippocampus. Brain sections were processed for immunocytochemical visualization of BrdU using the peroxidase-anti-peroxidase method and a diaminobenzidine-nickel ammonium sulfate (DAB-Ni) reaction, and finally observed on a microscope equipped with brightfield and fluorescence optics. Both BrdU-immunoreactive nuclei and retrogradely labeled Fluoro-Gold-positive cells were detected. Double-labeled neurons were recognized by the presence of fluorescent particles in the cytoplasm and a black immunoreactive nucleus. Since both labelings occurred in different cell compartments, Fluoro-Gold granules were not obscured by the DAB-Ni precipitate. The method shown here permits a correlation of the neurogenesis of subsets of neurons identified by their BrdU content with the specific target into which such cells project.
Animals↗
Research note: ability of fenthion to increase gizzard erosion in broiler chicks.
Fenthion, an irreversible cholinesterase inhibitor, was used to study the role of the cholinergic system on the development of gizzard erosion. Fenthion increases the gizzard erosion score in a dose-dependent manner and this effect became significant at levels higher than .1 ppm (p less than .05). An inverse relationship between plasma cholinesterase activity and pesticide concentration was also observed at doses higher than 1 ppm (P less than .05). These results show the necessity to evaluate organophosphate pesticide levels during the selection of fish meals in poultry.
Animals↗
[Pneumococcal meningitis. 6-year review].
We have reviewed 29 episodes of pneumococcal meningitis seen in a 6-year period (1983-1988) in 11 pediatric patients and 16 adults. An underlying disease or condition was present in 81.5% of cases, in 55.5% there was an anatomical defect, either congenital, acquired or traumatic in origin. Gram stain of CSF was positive in 86% of cases, and latex test was positive in the 22 CSF samples analyzed with this technique. MIC for penicillin ranges from 1 to 2 mcg/ml in 51.7% of cases. These isolates were also resistant to tetracycline (100%), trimethoprim-sulfamethoxazole (100%) and chloramphenicol (87%). All strains isolated were sensitive to vancomycin, rifampin and cefotaxime. Of all 14 episodes due to penicillin-sensitive strains, 10 cases were treated with this drug and in 4 cases, third generation cephalosporins were prescribed. All cases showed good clinical response. Of all 15 episodes due to penicillin-resistant strains, vancomycin was used first in 10 cases, cefotaxime in three, moxalactam in one and ampicillin plus chloramphenicol in another. Treatment failures (one in cefotaxime and one in moxalactam group) were solved with vancomycin. Of all 12 patients treated with vancomycin, clinical and microbiological cure was achieved in 10 cases. Two additional patients died, one with sterile CSF after 45 days of admission and one few hours after admission. Our data give support to vancomycin as a useful therapeutic option in the treatment of pneumococcal meningitis due to penicillin-resistant strains.
Adolescent↗
Temporal relationship between the decrease in arterial pressure and sodium retention in conscious spontaneously hypertensive rats with carbon tetrachloride-induced cirrhosis.
It has been proposed that the initial event of sodium retention in cirrhosis is a peripheral arteriolar vasodilation causing underfilling of the arterial vascular compartment and stimulation of the renin-aldosterone and sympathetic nervous systems. To test this hypothesis, systolic blood pressure, sodium balance and urinary excretion of sodium and aldosterone were sequentially measured in 13 conscious spontaneously hypertensive rats submitted to a cirrhosis induction program with carbon tetrachloride and phenobarbital and in 14 control hypertensive animals. No significant differences were found between control and cirrhotic rats in any of the measured parameters during the first 7 wk of the study. The eighth week sodium retention developed in cirrhotic rats as indicated by a positive sodium balance and a marked decrease of sodium excretion. At the same time a significant reduction in systolic blood pressure and a great increase in urinary excretion of aldosterone were detected. These changes were more marked the ninth week of the study. In cirrhotic rats there was a highly significant direct correlation between systolic blood pressure and urinary sodium excretion. Postmortem examination showed a histological picture of cirrhosis in all animals given carbon tetrachloride and ascites in six of them. These results indicate that the onset of hyperaldosteronism and sodium retention in conscious spontaneously hypertensive rats with carbon tetrachloride-induced cirrhosis is chronologically related to a significant decrease in arterial pressure, thus supporting the "peripheral arterial vasodilation hypothesis" of ascites.
Aldosterone↗
Phenanthrylalkanoic acids, IV: Syntheses and antiinflammatory activity of 2-, 3-, and 9-phenanthryl- and 9-chloro-3-phenanthryl derivatives of propanoic acid.
The phenanthrylethanols 2a-d were obtained by reduction of the acetyl derivatives 1a-d and converted, through the phenanthrylethyl halides 3a-d and 4b, into the nitriles 5a-d, whose acid hydrolysis afforded the acids of the title, 6a-d. The antiinflammatory activity of these acids was measured on the carrageenin-induced edema and found as 1/3 (6a), 1/43 (6b), 1/5 (6c), and 1/7 (6d) of that of fenbufen.
Animals↗
Natriuretic hormone activity in the urine of cirrhotic patients.
The ability of urine extracts to inhibit sodium and potassium-activated ATPase, cross-react with antidigoxin antibodies and induce natriuresis in rats was investigated in 10 healthy subjects, 10 cirrhotic patients without ascites (compensated cirrhotics), 27 nonazotemic cirrhotic patients with ascites and 10 cirrhotic patients with ascites and functional renal failure to assess whether reduced activity of natriuretic hormone contributes to sodium retention in cirrhosis. No significant differences were seen between healthy subjects and compensated cirrhotic patients in any of these parameters (sodium and potassium-activated ATPase inhibition = 178.5 +/- 19.8 vs. 247.4 +/- 48.7 nmol equivalent of ouabain/day; digoxinlike activity = 43.9 +/- 6.1 vs. 48.0 +/- 5.6 ng equivalent of digoxin/day; natriuretic activity = 0.36 +/- 0.15 vs. 0.63 +/- 0.27 mumol/min). Cirrhotic patients with ascites with and without functional renal failure showed significantly higher values of sodium and potassium-activated ATPase inhibition (708.1 +/- 94.0 and 529.2 +/- 53.9 nmol equivalent of ouabain/day, respectively), digoxinlike activity (136.9 +/- 7.2 and 116.3 +/- 7.9 ng equivalent of digoxin/day) and natriuretic activity (1.78 +/- 0.48 and 1.93 +/- 0.37 mumol/min) than healthy subjects and compensated cirrhotic patients. We saw no significant differences between these two groups of cirrhotic patients with ascites with respect to these parameters. In the cirrhotic patients studied, sodium and potassium-activated ATPase inhibition and antidigoxin antibodies directly correlated with the degree of impairment of hepatic and renal function, plasma renin activity and plasma levels of aldosterone and norepinephrine.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Urinary excretion of endogenous digitalis-like natriuretic substances in healthy subjects. Effect of sodium load.
In the current study digoxin-like immunoreactivity (DLIA), Na-K-ATPase inhibition and natriuretic activity of urinary extracts from 10 healthy volunteers following a low and a high-sodium intake, respectively, were measured. Detectable urinary DLIA (46.1 +/- 5.6 ng eq digoxin/day), Na-K-ATPase inhibition (182.9 +/- 22.7 nmol eq oub/day) and natriuretic activity (UNaV: 0.38 +/- 0.11 microEq/min) were observed during the low-sodium diet period in all subjects. High-sodium diet was associated with a significant increase in DLIA (87.9 +/- 9.2 ng eq digoxin/day, p less than 0.001) which parallelled changes in Na-K-ATPase inhibition (359.8 +/- 51.9 nmol eq oub/day, p less than 0.005) and natriuretic activity (UNaV: 1.33 +/- 0.3 microEq/min, p less than 0.025). These results support the contention that DLIA is related to NH.
Adult↗
N3-arylspiroimidazolidine-2,4-diones N3-arylspiroimidazolidine-2-thio-4-ones and 4-hydroxy derivatives. Synthesis and anthelmintic activity.
The synthesis of new N3-arylciclohexanespiroimidazolidine-2,4-diones, N3-arylciclohexanespiroimidazolidine-2-tio-4-ones and the 4-hydroxy derivatives is described and their structures discussed on the basis of I.R. and 1H-N.R.M. data. The anthelmintic activity of these compounds was tested.
Animals↗
[Changes in various hematologic parameters following treatment with zinc acetate].
The effect of different doses of zinc acetate (1,000 and 3,000 ppm) on several haematological values was studied on Wistar rats. Decreased haematocrit, mean corpuscular volume and white cell counts were appreciated, along with increased red cell counts. The leucocyte differential count was also modified, an important reduction of the percentage of neutrophils and monocytes being registered.
Acetates↗
Phenanthrylalkanoic acids, III: Syntheses and biological activities of 4-phenanthryl derivatives.
Reformatsky reactions between 2,3-dihydro-4(1H)-phenanthrenone (5) and ethyl alpha-bromoacetate or propanoate yield several unsaturated esters which, upon aromatization followed by saponification, lead to the 4-phenanthrylacetic (1) and 2-(4-phenanthryl)propanoic (2) acids. The analgesic and anti-inflammatory properties of 1 and 2 were measured and compared with those of Fenbufen.
Animals↗
Blockade of the hydroosmotic effect of vasopressin normalizes water excretion in cirrhotic rats.
Water retention in cirrhosis has classically been considered to be due to a low distal fluid delivery secondary to increased proximal sodium reabsorption. However, recent studies showing high plasma vasopressin levels in patients and rats with cirrhosis, ascites, and dilutional hyponatremia suggest that a nonosmotic vasopressin hypersecretion could be an alternative mechanism. To investigate the role of vasopressin in water retention in cirrhosis, the renal ability to excrete a water load (50 ml/kg body wt), as estimated by the minimum urinary osmolality and the percentage of the water load excreted during 3 h, was assessed in 10 control rats and in 20 cirrhotic rats with ascites and impaired water excretion and high urinary excretion of vasopressin. Twenty-four hours later, the same procedure was repeated in cirrhotic rats 20 min after the subcutaneous injection (30 micrograms/kg body wt) of d(CH2)5Tyr(Et) VAVP, an antagonist of the hydroosmotic effects of vasopressin (10 rats), or the vehicle (10 rats). Treatment with the vasopressin antagonist normalized water excretion in 9 of the 10 rats. No significant changes in renal water metabolism were observed in the group of rats given the vehicle. These results indicate that vasopressin hypersecretion is the predominant mechanism of the impairment in water excretion in rats with experimental cirrhosis and ascites.
Animals↗
Role of altered systemic hemodynamics in the blunted renal response to atrial natriuretic peptide in rats with cirrhosis and ascites.
The natriuretic effect of pharmacological doses of atrial natriuretic peptide (ANP) is markedly reduced in cirrhosis with ascites. The current study, which includes two protocols, was carried out to investigate whether this phenomenon is related to the altered systemic hemodynamics present in cirrhosis. In protocol A, the administration of ANP (2.5 micrograms.kg-1 as a bolus followed by a constant infusion of 0.1 microgram.kg-1.min-1) to 10 rats with carbon tetrachloride-induced cirrhosis and ascites produced a significantly lower increase in diuresis (13.4 +/- 1.3 microliters/min) and natriuresis (2.3 +/- 0.3 mu Equiv/min) than in 10 control rats (56.3 +/- 1.4 microliters/min and 8.7 +/- 0.5 mu Equiv/min, respectively), indicating a renal resistance to the effect of ANP in this experimental model of cirrhosis. The reduction of arterial pressure induced by ANP was similar in both groups. However, since baseline mean arterial pressure was significantly lower in cirrhotic rats, the degree of hypotension during ANP infusion was also greater in this group of animals (82 +/- 3 vs. 109 +/- 2 mmHg). The aim of protocol B was to assess whether normalization of arterial pressure in cirrhotic rats increases the renal response to ANP. This protocol includes two groups of 10 rats with cirrhosis and ascites infused with a glucose solution containing norepinephrine (CT-NE rats) or angiotensin II (CT-AII rats) at doses to normalize arterial pressure and an additional control group of 10 cirrhotic rats with ascites receiving only glucose solution (CT rats). Angiotensin II, but not norepinephrine or glucose solution administration, was associated with a significant increase in urine volume and sodium excretion. During ANP infusion, CT rats showed a blunted diuretic and natriuretic response. In contrast, the ANP-induced increase in urine volume and sodium excretion observed in CT-NE (53.6 +/- 10.4 microliters/min and 9.3 +/- 2.2 mu Equiv/min) and CT-AII rats (98.3 +/- 11.6 microliters/min and 15.5 +/- 2.9 mu Equiv/m), was similar or even greater than that showed by the healthy rats of protocol A. The degree of hypotension during ANP administration was also similar (CT-NE, 104 +/- 2; CT-AII, 108 +/- 5 mmHg). These results suggest that the blunted response to pharmacological doses of ANP in cirrhosis with ascites is related to altered systemic hemodynamics of cirrhosis, which further deteriorates during the infusion of the peptide.
Angiotensin II↗
Phenanthrylalkanoic acids, II: Syntheses and antiinflammatory activity of 2-, 3- and 9-phenanthryl- and 9-chloro-3-phenanthrylacetic acids.
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Acetates↗
Endothelial cell growth factor and ionophore A23187 stimulation of production of inositol phosphates in porcine aorta endothelial cells.
The existence of a bovine brain-derived endothelial cell growth factor has recently been reported, but its mode of action is unknown. We show that the endothelial cell growth factor is a potent stimulant of inositol monophosphate release in porcine aorta endothelial cells. Although the activation of phospholipase C by this factor does not appear to be dependent on Ca2+, the Ca2+ ionophore A23187 stimulates release of inositol phosphates. It is suggested that the inositol 1,4,5-trisphosphate 3-kinase/5-phosphomonoesterase pathway could account for the ionophore-induced changes in inositol 1,3,4-triphosphate.
Animals↗
An assessment of single doses of 8 mg sustained-release molsidomine using serial exercise tests.
The effectiveness and duration of the anti-anginal action of two sustained-release preparations, molsidomine (8 mg) and isosorbide dinitrate (20 mg), were assessed by means of serial exercise tests in 12 patients with angina of effort. The tests, which were limited by the symptoms, were carried out on three consecutive days using the Bruce protocol. Each patient was tested four times each day: the first test was performed before treatment and the others were carried out 1, 4 and 8 h after administration of the drug or placebo. One hour after administration of molsidomine, the appearance of signs of ischaemia in the ECG were considerably delayed and they were reduced in magnitude. Furthermore, the length of time during which the patients were free of angina increased. After 4 h both drugs significantly delayed the onset of angina and depression of the ST segment by 1 mm. The conclusion is that at the doses used both drugs prolong the length of time in which there is no angina, but that they have no significant effect at 8 h.
Aged↗
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↗