PubMed Health⌕ Search

Biomedical subjects

A Coca

Publications and source records attributed to A Coca.

At least 91 records · Page 5Linked to original sources
PubMed1990

[Toxic megacolon and intestinal perforation caused by Salmonella enteritidis].

Two cases of colitis due to Salmonella enteriditis which later developed a toxic megacolon with intestinal perforation are presented and the probable pathogenesis is discussed. This exceptional clinical course which has not been previously described forces to perform a differential diagnosis with chronic intestinal inflammatory disease which must be based on microbiologic, serologic and/or histologic criteria. Moreover, the authors warn about the unsuitability of using anticholigernic drugs in gastroenteritis since they could be related to the ethiopathogenical basis of the disease's unfavorable course in the described patients.

Adult↗
PubMed1990

[Prevalence, forms of clinical presentation and treatment of arterial hypertension at an emergency unit].

In order to determine the prevalence of arterial hypertension and clinical presentation of the hypertensive crisis, as well as the need and efficacy of treatment, 3626 patients who were seen at an Emergency care Unit during a period of 37 randomly chosen days in a total time period of three months, have been studied. Two hundred and fifty one patients presented arterial hypertension, defined as a systolic arterial pressure above 160 mmHg and/or diastolic above 95 mmHG, which represents 6,92% of medical emergencies and 1.79% of total emergencies. Only 104 patients (2.86%) seeked help for some pathology related to hypertension, of whom 49 (19.5% of hypertense patients) presented as a hypertensive emergency, being the acute lung edema and unstable angina the most frequently encountered emergencies. Nifedipine was the most frequently used drug in both groups and managed to control pressure levels in almost 90% of patients with a hypertensive emergency in a mean time of less than one hour.

Adult↗
PubMed1989

Abnormal erythrocyte sodium leak in a subset of essential hypertensive patients.

We measured the ouabain- and bumetanide-resistant Na+ efflux in Mg2+-sucrose medium (passive Na+ leak) in erythrocytes from 30 normotensive controls and 72 essential hypertensive patients. The mean values (+/- SEM) of the rate constant of Na+ leak (kpNa) were not significantly different between normotensives and hypertensives. Nevertheless, using the 95% confidence limits of the kpNa (in 10(-3).h-1) in the normotensive group as a cut-off point, 7 (9.7%) essential hypertensives exhibited increased values (58.96 +/- 10.12) when compared with the other 65 patients (23.86 +/- 0.74). revealing increased passive Na+ permeability in the former (leak "+" hypertensives). Na+ fluxes depending on the Na+-K+ pump, outward Na+-K+ cotransport, and Na+-Li+ countertransport were also measured in fresh erythrocytes from the same 72 patients. Three of them (4.2%) exhibited decreased values of ouabain-sensitive Na+ efflux and 6 (8.3%) of bumetanide-sensitive Na+ efflux, while 8 patients (11.1%) showed increased values of Li+-stimulated Na+ efflux and, finally, 48 patients (59.7%) did not present any evident abnormality in these Na+ transport systems. No differences were observed between leak "+" hypertensives and the remaining 65 patients when both basal erythrocyte Na+ content and clinical parameters of hypertension were compared. However, Na+ efflux depending on the outward Na+-K+ cotransport was significantly higher in the leak "+" hypertensive subset (299.43 +/- 43.18 vs 181.52 +/- 10.76 mumol.(l cells.h)-1; P = 0.0078), suggesting a compensatory phenomenon. Enhancement of Na+ permeability detected in 3% to 16% of essential hypertensives may be implicated in the pathogenesis of primary hypertension.

Adult↗
PubMed1989

Clinical profiles and erythrocyte Na+ transport abnormalities of four major types of primary hypertension in Spain.

The interaction of three different Na+ transport systems (Na+-K+ pump, Na+-K+ cotransport and Na+-Li+ countertransport), with internal Na+ and the passive Na+ leaks, were measured in erythrocytes from 72 Spanish, essential hypertensive patients and 30 normotensive controls. According to the observed abnormalities in Na+ transport pathways, 93.1% of the patients were classified into the following subsets: 12 (16.7%) exhibited a decreased apparent affinity of Na+-K+ pump for internal Na+ (Pump "-" hypertensives); 20 (27.7%) showed a decreased apparent affinity of Na+-K+ cotransport for internal Na+ (Co "-" hypertensives); 27 (37.5%) showed an accelerated Na+-Li+ countertransport (Counter "+" hypertensives); and 5 (6.9%) exhibited an increased rate constant of passive Na+ leaks (Leak "+" hypertensives). Finally, 5 patients (6.9%) did not show any abnormality in their Na+ transport systems and 3 exhibited more than one. Moreover, distinctive clinical features were recognize in Co "-" and Counter "+" subsets. Blood pressure values were lower in the former and, conversely, Counter "+" hypertensives showed a higher prevalence of moderate or severe hypertension (65.5% vs. 32.6%; P = 0.0059) and higher values of stimulated plasma renin activity (1.63 +/- 0.52 vs. 0.81 +/- 0.15; P = 0.0443). Our results confirm the heterogeneity of Na+ transport abnormalities in essential hypertension and suggest that these subsets of hypertensives could represent clinical entities.

Adult↗
PubMed1989

Disturbances of transmembranous sodium transport systems induced by ethanol in human erythrocytes. An approach to the pressor effect of alcohol.

Several epidemiological and clinical studies have established a clear association between alcohol consumption and hypertension. The mechanism of the pressor effect of ethanol is not well understood. We studied the in vitro effects of increasing amounts of ethanol on different Na+ transport systems from human erythrocytes. Ethanol at concentrations higher than 32 mmol/L stimulated ouabain-sensitive Na+ efflux, the Na+ efflux depending on the Na+:Li+ countertransport and Na+ leak. At the same concentrations, ethanol inhibited bumetanide-sensitive Na+ efflux. We conclude that, with the exception of Na+-K+ pump, alcohol-induced alterations and those observed in erythrocytes from essential hypertensives may overlap. Therefore, alcohol consumption could potentiate those genetic abnormalities of Na+ transport and contribute to the pathogenesis of essential hypertension.

Antiporters↗
PubMed1989

Outward Na+-K+-Cl- cotransport function in erythrocytes from essential hypertensives.

We have performed a kinetic analysis of the interaction of the outward Na+-K+-Cl- cotransport system with intra-cellular Na+ in erythrocytes from 30 normotensive controls and 72 patients with essential hypertension. Neither maximal rate of ouabain-resistant, bumetanide-sensitive sodium efflux (Vmax) nor intracellular Na+ content required for half-maximal stimulation (K50%) were significantly different between normotensives and hypertensives. Nevertheless, using 95% confidence limits of the K50% in the normotensive group as a cut-off point, 21 (29.17%) essential hypertensive patients exhibited values above the upper normal limit of 20.11 mmol/l cells, revealing a decreased apparent affinity of outward Na+-K+-Cl- cotransport for internal Na+ ('Co-' hypertensives). The Vmax of Na+-K+-Cl- cotransport exhibited a great variability among hypertensives but 'Co-' patients tended to have increased values of this parameter when compared with the remaining essential hypertensives (959 +/- 84 vs 652 +/- 39 mumol/l cells/h, P = 0.0024). Mean BP values were significantly lower in the 'Co-' subset (121.4 +/- 1.6 mmHg), compared with the remaining 51 hypertensive patients (126.4 +/- 1.3 mmHg, P = 0.0297). We conclude that an abnormal function of outward Na+-K+-Cl- cotransport is present in 19% to 40% of Spanish patients with essential hypertension and this abnormality may be implicated in the mechanisms of hypertension.

Adult↗
PubMed1988

Na+-Li+ countertransport in essential hypertension.

Several studies on Na+-Li+ countertransport have reported higher rates in essential hypertensive than in normotensives, with a distribution pattern which is dependent on racial and ethnic background. However, it is not well established whether this abnormality in Na+ transport is associated with an abnormal clinical setting. In the present study we have performed a kinetic analysis of the interaction of the Na+-Li+ countertransport system with internal Na+ in erythrocytes from a sample of 72 essential hypertensives and 30 normotensive controls. A significant increase in mean values of the maximal rate of Li+-stimulated Na+ efflux (Vmax; 375.1 +/- 23.8 versus 213.7 +/- 8.5 mumol/l cells per h; mean +/- s.e.m.; Mann-Whitney test: U = 500; P less than 0.0001), as well as in the apparent affinity constant for internal Na+ (KNa; 10.03 +/- 0.08 versus 6 +/- 0.4 mmol/l cells; Mann-Whitney test: U = 718; P less than 0.0079), were observed in essential hypertensives with respect to normotensives. Using the 95% confidence interval of Vmax in normotensives as the normal range, 29 (40.3%) of the essential hypertensives exhibited values above the normal upper limit. The maximal rate (Vmax) and the internal Na+ content required for half-maximal stimulation (K50%) of Na+-K+ ATPase and outward Na+-K+ cotransport, and the rate constant of Na+ leak (KPNa) in this subset were similar to the values observed in the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Abnormal Na+-K+ ATPase kinetics in a subset of essential hypertensive patients.

We have performed a kinetic analysis of the interaction of Na+-K+ ATPase with internal Na+ in erythrocytes of 30 normotensive controls and 72 essential hypertensive patients. Neither the maximal rate of ouabain-sensitive sodium efflux (Vmax) nor the internal Na+ content required for half-maximal stimulation (K50%) were significantly different between normotensive and hypertensive patients. Nevertheless, using the 95% confidence limits of the K50% in the normotensive group as a cut-off point, 13 (18.06%) essential hypertensive patients exhibited increased values of this parameter (29.16 +/- 4.31 mmol l-1 cells) revealing decreased affinity of Na+-K+ ATPase for internal Na+ (Pump-hypertensives). The Vmax was also higher in the Pump '-' subset (14.08 +/- 4.85 mmol (1 cells h)-1 vs. 6.92 +/- 1.80; P = 0.0002) and 10 of these 13 hypertensives exhibited a Vmax above the upper end limit of 10.5 mmol (1 cells h)-1, suggesting a compensatory effect. No differences were observed between the Pump '-' subset and the remaining 59 hypertensives without Na+-K+ pump abnormality when basal erythrocyte Na+ content and clinical parameters of hypertension were examined. Decreased apparent affinity of Na+-K+ pump for internal Na+ present in 9-27% of essential hypertensives may be implicated in pathogenetic mechanisms of hypertension.

Adult↗
PubMed1988

Disturbances in Na+ transport systems induced by ethanol in human red blood cells.

The effects of ethanol on fluxes catalyzed by four Na+ transport systems (ouabain-sensitive Na+, K+ pump, bumetanide-sensitive Na+, K+ cotransport system, Na+:Li+- countertransport and anion carrier) and on Na+ and K+ leaks were investigated in human red blood cells. Ethanol concentrations higher than 32 mM were required in order to significantly modify erythrocyte Na+ transport function. The observed changes can be summarized as follows: (a) stimulation of Na+ efflux through the Na+, K+ pump (by 21-32% at 160-400 mM) and Na+:Li+ countertransport (by 34-59% at 160-400 mM); (b) inhibition of outward Na+, K+ cotransport (by 23-34% at 160-400 mM) and LiCO3- influx through the anion carrier (by 17-21% at 64-400 mM); and (c) increase in Na+ and K+ leaks (by 13-16% at 64-400 mM). The effects of ethanol on the Na+,K+ pump and Na+,K+ cotransport system resulted from changes in maximal rates of Na+ efflux (increased and decreased, respectively) without any significant effect on the apparent affinities for internal Na+. Erythrocytes preincubated for 1 hr with 160 mM ethanol, washed and further incubated in flux media, recovered a normal Na+ transport function. In conclusion, high concentrations of ethanol induced reversible perturbations of fluxes catalyzed by erythrocyte Na+ transport systems. The observed effects may reflect disturbances in Na+ transport function associated with severe intoxication.

Biological Transport, Active↗