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E Novoa

Publications and source records attributed to E Novoa.

At least 19 recordsLinked to original sources

Effect of dopamine on platelet activating factor induced-pulmonary edema in isolated and perfused rabbit lungs.

The effect of dopamine over pulmonary edema induced by PAF was studied. Thirty preparations of rabbit lungs were used: six control preparations (CP), six PAF preparations (PP) in which we injected a dose of 1 microg/kg of rabbit weight and eighteen dopamine preparations (DAP) divided in three groups of six pretreated with a dose of 1-5 (dopaminergic range), 10-20 (Beta range) and 20-30 ug/kg/min (Alpha range) of dopamine, respectively for 30 min, followed by an injection of PAF as in the PP. DAP at Beta and Alpha-adrenergic range decreased pulmonary artery pressure (Pap) as compared to CP, with values of 11.66 (CI 95%: 10.83-12.48), 11.66 (CI 95%: 9.87-13.44) versus 17.12 (CI 95%: 16.12-18.11) cm of water, respectively. DAP in Beta and Alpha-adrenergic range prevented Pap increment as compared to PP, with values of 17.16 (CI 95%: 16.37-17.94), 17.5 (CI 95%: 14.93-20.06) versus 84 cm of water (CI 95%: 71.41-96.58), respectively. Dopamine, at its three ranges inhibited the augmentation of the fluid filtration rate observed in PP with values of 1.01 (CI 95%: 0.77-1.24), 0.03 (CI 95%: 0.01-0.04) and 0.02 g/min (CI 95%: -0.0004-0.03) versus 2.13 g/min (CI 95%: 1.56-2.69), respectively. We concluded that dopamine has a vasodilator effect on Pap and exerts an inhibiting action over PAF effects in pulmonary circulation. Such effects seem to be mainly mediated by Beta-receptors, rather than by dopaminergic receptors.

Animals↗

Effect of hydrocortisone on platelet activating factor induced lung edema in isolated rabbit lungs.

The effect of hydrocortisone on platelet activating factor (PAF)-induced pulmonary edema is studied. Thirty four isolated and perfused rabbit lung preparations were used: eight control preparations, eight PAF preparations with two doses of PAF called low dose (LD = 0.5 microg/kg of rabbit weight) and high dose (HD = 1 microg/kg of rabbit weight). Eighteen preparations divided in three groups of six were pretreated with doses of 20, 200 and 2000 mg of hydrocortisone and later given the same doses of PAF as described above. Hydrocortisone significantly decreased (P < 0.05) the effect of PAF LD over the pulmonary arterial pressure (Ppa) in the 200 and 2000 mg groups (58 and 89% decrease, respectively) and it significantly decreased (P < 0.05) the effect of PAF HD over Ppa in all hydrocortisone pretreated groups (48, 70 and 96% decrease, respectively). Fluid filtration rate (FFR) increases mediated by PAF HD were significantly inhibited (P < 0.05) in the 200 and 2000 mg groups (64 and 96% decrease, respectively). We conclude that hydrocortisone inhibits the effect of PAF over the pulmonary circulation.

Animals↗

[Detection of parvovirus B19 in patients of the Zulia State blood bank with different hematological alterations].

PURPOSE: To assess the seroprevalence of IgG and IgM specific for parvovirus B19 (B19) and its association with aplastic crisis developing in patients with different haematological disorders. PATIENTS AND METHODS: Fifty-three serum samples were evaluated, 24 from patients with aplastic crisis and 29 from others without such crises, all of them suffering from different haematological diseases diagnosed at the University Hospital of Maracaibo and the Zulia State Blood Bank, in Venezuela; 15 samples from healthy blood donors were examined as well. Indirect immunofluorescence technique was used in the study. Lymphocyte subsets were quantified in 10 of the patients with aplastic crisis by means of cytofluorometry. Serum proteins were assessed by electrophoresis in all samples. The statistical analysis was performed according to Student's t test and chi square, by applying the statix 4.0 and SAS programmes. RESULTS: Positive IgG was found in 20 of the 24 patients with aplastic crisis (83.3%), 20 of the 29 without crisis (68.9%) and 7 of the 15 healthy controls (46.6%). Positive IgM was found only in 2 of the 24 patients with aplastic crisis (8.3%). Both the patients without aplastic crises and the control groups were negative for PB19 IgM. The average CD4 and CD8 T lymphocyte count and the CD4-CD8 index in the patients studied were 454 CD4 cells/microL, 1,006 CD8 cells/microL and 0.5%, significantly different from the control group, whose figures were 860 CD4 cells/microL, 546 CD8 cells/microL and 1.6%. The average B lymphocyte count of the patients (628 cells/microL) was higher than that of the control group (349 cells/microL). The average NK cell count in the patient was 174 cells/microL, slightly below the control group (221 cells/microL). Mild beta-globulin decrease was found in the electrophoretic study of the serum proteins of the patients, along with significant increase of the total protein and the gammaglobulin fraction with regard to the control group. CONCLUSIONS: Higher PB19 IgG seropositivity was seen in the patients with aplastic crisis with respect to the control group, suggesting wider exposition to the virus among them with regard to the healthy population. Specific PB19 IgM was detected in 2 patients with immunodeficiency and aplastic crisis. A significant decrease of the CD4 and CD8 T-lymphocyte subsets, along with decreased CD4-CD8 quotient, were found in the aplastic crisis group, and an impairment of the immune response to the viral challenge can be inferred form this. The alterations of the serum proteins, together with the increased B lymphocytes, might suggest a polyclonal activation of these cells. The absence of other known lymphotropic viruses in most of the patients studied (50) show that the alterations found here are related to recent or past B19 infection.

Anemia, Aplastic↗

Mechanism of enhancement of renal (Na(+)+K+) ATPase activity following chronic ethanol exposure.

A method was devised to determine the nature of the mechanism of the increase in renal (Na(+)+K+)-ATPase in rats fed dilute ethanol for ten weeks. Antiserum to (Na(+)+K+)-ATPase obtained from rabbits was added to microsomal fractions of kidney and the activities of (Na(+)+K+)-ATPase and Mg2+ ATPase were determined. The addition of antiserum resulted in a same pattern of dose-related inhibition of (Na(+)+K+)-ATPase activity in control and ethanol-fed rats, whereas Mg(2+)-ATPase was not affected by the antiserum. These results suggest that the mechanism of ethanol-induced enhancement of renal (Na(+)+K+)-ATPase activity could be explained through an increase in the number of catalytic units.

Analysis of Variance↗

Is the renal (Na + K)-ATPase modulated by intracellular messengers?

The basic cellular mechanisms involved in the regulation of (Na + K)-ATPase are discussed. Various ligands seem to be responsible for the short-term modulation of this enzyme activity (intracellular messengers). Cytosolic Ca2+ has a key role in mediating changes induced by hormones or receptor agonist; but, in turn, intracellular Ca(2+)-dependent proteins like calmodulin, calnaktin or others, are also needed for these changes. Phosphorylation of effector proteins, following the activation of PKC, PKA or CaM-kinase II, may result in changes of (Na + K)-ATPase activity either by a direct effect on the catalytic subunit or by modulating the Na(+)-H+ exchanger thereby resulting in an effect on intracellular sodium, whose concentration is known to be rate-limiting for the enzyme activity. Despite the ubiquity of (Na + K)-ATPase in various organs and tissues, its response to modulators partly depends on the heterogeneity of the alpha-subunit that give rise to the existence of different isoforms. The relative abundance of alpha 1, alpha 2, alpha 3 or other isoforms is tissue-specific and represents another way of regulation among different cell types. While these cellular mechanisms occur in various cell types the kidney shows an opposite response respect to other tissues such as liver or brain. The functional relevance of the mechanisms of acute adaptation of (Na + K)-ATPase, discussed in this review, is becoming increasingly recognized for the renal enzyme, what may contribute to stimulate new approaches to the study of the short-term regulation of the pump activity in molecular terms.

Animals↗

Renal handling of electrolytes and (Na + K)-ATPase activity after unilateral nephrectomy during long-term ethanol feeding.

The effect of long-term ethanol feeding on the activity of (Na + K)-ATPase in cortex and outer medulla and fractional excretion of electrolytes in remnant kidney of adult rats after unilateral nephrectomy were studied. Wistar adult rats were fed 20% (v/v) aqueous ethanol solution as sole drinking fluid for 8-10 weeks. Right kidney was removed under ether anaesthesia. The animals were subjected to an acute NaCl loading by means of a continuous infusion given 2, 7 and 14 days after nephrectomy. Renal handling of electrolytes was estimated from fractional excretion of sodium and potassium. After the infusion the animals were killed and (Na + K)-ATPase and Mg2+-ATPase activities were measured in the cortex and outer medulla of the remnant kidney. Two days after nephrectomy both groups showed a gradual increase of renal (Na + K)-ATPase activity reaching 60 percent at day 14. Mg2+-ATPase activity did not change with respect to basal values. Compared to basal values the fractional excretion of sodium after nephrectomy, dropped in both groups but more significantly in the ethanol-fed rats than in the control group. Fractional excretion of potassium did not change in the control group after nephrectomy while the ethanol-fed group displayed a significative decrease at days 7 and 14. According to our results the rise in renal (Na + K)-ATPase activity is consistent with the renal sodium retention found in ethanol-fed rats.

Adaptation, Physiological↗

Changes in platelet aggregation caused by glyburide in diabetic patients.

The effect of glyburide on platelet aggregation was investigated in 31 patients with maturity-onset diabetes. Platelet aggregation in platelet-rich plasma was measured before and one hour after the patients had ingested 5 mg of glyburide. The drug caused a significant decrease in platelet aggregation as determined by changes in the amplitude and slope of the curve.

Adult↗

Familial spastic ataxia associated with Ehlers-Danlos syndrome with platelet dysfunction.

Four members of a family with consanguineous relationships, the proband and his three children (2 sons and 1 daughter) are affected with Familial Spastic Ataxia and with Ehlers-Danlos' Syndrome with platelet aggregation dysfunction. In the four cases, this exceptional association appears remarkably homogeneous both in clinical and laboratory studies. The two syndromes are of dominant-autosomic transmission and probably originated in a new mutation which presumably maintained a genetic linkage. Spastic ataxia is characterized by a precocious onset and a slow evolution. The first-born son shows a dominant pyramidal syndrome with mild ataxia suggesting that it is a transitional form of familial spastic paraplegia. The Ehlers-Danlos syndrome pertains to form II or "mitis" with moderate skin hyperelasticity and joint hypermobility. The abnormal platelet aggregation curves have the same profile in all the patients. The first-born son also presents a mitral valve prolapsus as we may find either in Ehlers-Danlos syndrome or in spastic ataxia. The neurophysiological, tomographical, histological, ultrastructural and biochemical studies attempt to accomplish a better definition of these associated nosological entities.

Adolescent↗