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Biomedical subjects

J Alvarez

Publications and source records attributed to J Alvarez.

At least 235 records · Page 13Linked to original sources
PubMed1992

Hemodynamic effects of prostaglandin E1 and isoproterenol early after cardiac operations for mitral stenosis.

Patients with mitral stenosis and some degree of right ventricular failure may benefit from inotropic or pulmonary vasodilator drugs in the early postoperative period. Thirty patients undergoing an operation for mitral stenosis were randomized into three groups. In group I (n = 10), isoproterenol (5 micrograms/kg/min) was started in the immediate postoperative period. In group P (n = 10), prostaglandin E1 (0.08 microgram/kg/min) was given, and in group C, the control group (n = 10), no drugs were used. After the operation and before drug therapy was begun, basal measurements of cardiac index, mean pulmonary arterial and mean arterial pressures, and pulmonary vascular resistance were taken. Measurements were repeated at 6, 12, and 24 hours. Mean measurements of cardiac index (basal up to 24 hours) were as follows: 1.39 +/- 0.3, 1.92 +/- 0.4, 2.4 +/- 0.5, and 2.34 +/- 0.3 L/min/m2 for group C; 1.54 +/- 0.5, 2.64 +/- 0.4, 2.68 +/- 0.7, and 2.2 +/- 0.6 L/min/m2 for group I, and 1.57 +/- 0.3, 2.2 +/- 0.6, 2.72 +/- 0.7, and 2.27 +/- 0.4 L/min/m2 for group P (p less than 0.05 between groups C and I at 6 and 12 hours). Mean pulmonary artery pressures were as follows: 19.5 +/- 3.2, 24.8 +/- 7, 27.7 +/- 7.3 and 28.8 +/- 5.7 mm Hg in group C; 21.4 +/- 8.7, 25.7 +/- 7.2, 26.4 +/- 7, and 29.4 +/- 8.6 mm Hg in group I, and 19.1 +/- 4, 19.2 +/- 3, 20.4 +/- 6, and 20.7 +/- 5 mm Hg in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). Mean pulmonary vascular resistances were as follows: 3.9 +/- 2.4, 3.9 +/- 1, 3.36 +/- 2, and 3.2 +/- 1.4 Wood units in group C; 4.84 +/- 4, 3.37 +/- 2.2, 3.69 +/- 3, and 4.69 +/- 4.1 Wood units in group I, and 3.29 +/- 1.3, 1.71 +/- 0.5, 1.61 +/- 0.5, and 1.96 +/- 0.8 Wood units in group P (p less than 0.05, group P versus groups C and I at 6, 12, and 24 hours). There was no difference in mean systemic arterial pressure among the three groups. Our results indicate that patients subjected to mitral valve operations have a low cardiac index. Isoproterenol increases cardiac index but has little effect on pulmonary resistance. At low doses, prostaglandin E1 effectively decreases pulmonary vascular resistance without altering systemic arterial pressure or heart rate.

Alprostadil↗
PubMed1992

The axonal microtubular density is higher than normal in fibres innervating spastic muscles.

In infants with spastic disorders and with congenital dysplasia of the hip (CDH), the microtubular content of nonmedullated and myelinated fibres of the anterior obturator nerves was studied with the electron microscope. In CDH infants, the microtubular content of nonmedullated and myelinated fibres was similar to values reported for experimental animals. In spastic patients, the microtubular content of nonmedullated fibres was similar to that found in CDH patients while the microtubular densities of 3- and 10-microns myelinated fibres were 37.5 and 16.7 microtubules/micron2, respectively, or 100% and 43% greater than corresponding values of CDH patients. We propose that the high firing rate determines the abnormally high microtubular content of myelinated axons supplying spastic muscles.

Axons↗
PubMed1991

Agonist-induced Ca2+ influx into human platelets is secondary to the emptying of intracellular Ca2+ stores.

We have studied the relation between the filling state of the intracellular Ca2+ stores and the plasma-membrane permeability to Mn2+, used here as a Ca2+ surrogate for Ca2+ channels. Emptying of the intracellular Ca2+ stores either by incubation in Ca(2+)-free medium or by treatment with low concentrations of the Ca2+ ionophore ionomycin accelerated the influx of Mn2+. Refilling of the Ca2+ stores by incubation in Ca(2+)-containing medium restores low Mn2+ permeability. This Ca(2+)-store-regulated permeability was inhibited by Ni2+ and by cytochrome P-450 inhibitors. Stimulation of platelets with thrombin produced Ca2+ release from the intracellular stores, which was followed, after a temperature-dependent lag (2 s at 37 degrees C; 5 s at 18 degrees C), by an acceleration of Mn2+ influx. Cytochrome P-450 inhibitors prevented the thrombin-induced Mn2+ influx, with little effect on the Ca2+ mobilization from the intracellular stores. Ki values were similar to those estimated for inhibition of the store-regulated permeability in non-stimulated platelets. Similar results were found in platelets stimulated by platelet-activating factor or by ADP. We propose that agonist-induced Ca2+ (Mn2+) influx in platelets is secondary to the emptying of the intracellular Ca2+ stores. The activation of the plasma-membrane Ca2+ (Mn2+) pathway may take place by a mechanism involving microsomal cytochrome P-450, similar to that described previously in thymocytes [Alvarez, Montero & García-Sancho (1991) Biochem. J. 274, 193-197] and neutrophils [Montero, Alvarez & García-Sancho (1991) Biochem. J. 277, 73-79].

Adenosine Diphosphate↗
PubMed1991

Recognition of osteopontin and related peptides by an alpha v beta 3 integrin stimulates immediate cell signals in osteoclasts.

We have investigated the nature of immediate cell signals produced by occupancy of the chicken osteoclast alpha v beta 3 integrin. Synthetic osteopontin and peptides from the osteopontin and bone sialoprotein sequences containing Arg-Gly-Asp stimulated immediate reductions in osteoclast cytosolic Ca2+. The changes in cytosolic Ca2+ required the Arg-Gly-Asp sequence and were blocked by a monoclonal antibody to the alpha v beta 3 integrin, LM609. Osteoclast stimulation by the proteins through the integrin did not require immobilization since soluble peptides produced changes in cytosolic Ca2+ and inhibited osteoclast binding to bone particles and bone resorption. The decrease in cytosolic Ca2+ stimulated by osteopontin and related peptides appeared to be due to activation of a plasma membrane Ca(2+)-ATPase by calmodulin. Thus, the data suggest that ligand binding to the osteoclast alpha v beta 3 integrin results in calmodulin-dependent reduction in cytosolic Ca2+ which participates in regulation of osteoclast function.

Amino Acid Sequence↗
PubMed1991

Agonist-induced Ca2+ influx in human neutrophils is secondary to the emptying of intracellular calcium stores.

Emptying of the intracellular calcium stores of human neutrophils, by prolonged incubation in Ca(2+)-free medium, by treatment with low concentrations of the Ca2+ inophore ionomycin, or by activation with cell agonists, increased the plasma-membrane permeability to Ca2+ and Mn2+. The chemotactic peptide formylmethionyl-leucyl-phenylalanine and the natural agonists platelet-activating factor and leukotriene B4 released different amounts of calcium from the stores and induced Ca2+ (Mn2+) uptake, the rate of which correlated inversely with the amount of calcium left in the stores. The increased Mn2+ uptake induced by these agonists was persistent in cells incubated in Ca(2+)-free medium, but returned to basal levels in cells incubated in Ca(2+)-containing medium, with the same time course as the refilling of the calcium stores. The calcium-stores-regulated Mn2+ influx, including that induced by agonists, was prevented by cytochrome P-450 inhibitors. We propose that agonist-induced Ca2+ (Mn2+) influx in human neutrophils is secondary to the emptying of the intracellular stores which, in turn, activates plasma-membrane Ca2+ channels by a mechanism involving microsomal cytochrome P-450, similar to that described previously in thymocytes [Alvarez, Montero & Garcia-Sancho (1991) Biochem. J. 274, 193-197].

Calcium↗
PubMed1991

Cytochrome P-450 may link intracellular Ca2+ stores with plasma membrane Ca2+ influx.

We have studied the mechanism of the regulation of plasma membrane Ca2+ permeability by the degree of filling of the intracellular Ca2+ stores. Using Mn2+ as a Ca2+ surrogate for plasma membrane Ca2+ channels, we found that Mn2+ uptake by rat thymocytes is inversely related to the degree of filling of the intracellular Ca2+ stores. This store-dependent plasma membrane permeability is inhibited by oxygen scavenging, CO, imidazole antimycotics and other cytochrome P-450 inhibitors. The pattern of inhibition is similar to that reported previously for the inhibition of microsomal cytochrome P-450-mediated aryl hydrocarbon hydroxylase activity of lymphocytes. Several calmodulin antagonists, both phenothiazinic (trifluoperazine, fluphenazine and chlorpromazine) and dibenzodiazepinic (clozapine), accelerate Mn2+ uptake by cells with Ca2(+)-filled stores, and this effect is prevented by imidazole antimycotics. Our results suggest that cytochrome P-450 may be the link between the stores and the plasma membrane Ca2+ pathway. We propose a model in which this cytochrome, sited at the stores, stimulates plasma membrane Ca2+ influx. This stimulatory effect is, in turn, prevented by the presence of Ca2+ inside the stores, possibly via a calmodulin-dependent mechanism.

Animals↗
PubMed1991

Choledocholithiasis in acute gallstone pancreatitis. Incidence and clinical significance.

A prospective study of choledocholithiasis was performed using 110 patients with presumptive diagnoses of acute gallstone pancreatitis. The incidence of migrating and persistent bile duct stones was determined using stool screening and intraoperative cholangiography, and the clinical significance of continued stone obstruction of the papilla was investigated using ultrasound assessment of migration time and a second evaluation of prognostic signs. Pancreatic inflammation was confirmed at surgery in 51 patients, of whom only 27 had stones in the stools (n = 22) or the bile duct (n = 5), suggesting that choledocholithiasis may not be the sole triggering factor of acute gallstone pancreatitis. Neither delayed migration nor persistent stone obstruction of the papilla promoted pancreatic inflammation.

Acute Disease↗
PubMed1991

Minimal change nephrotic syndrome associated with Hodgkin's lymphoma.

This report documents the occurrence of minimal-change nephropathy in four patients with Hodgkin's disease. In two cases the onset of the nephrotic syndrome antedated the recognition of lymphoma by 4 and 7 years respectively, while in the other two the nephrotic syndrome manifested 5.5 years and 13 months respectively after lymphoma. In all cases, the nephrotic syndrome resolved when therapy was effective in treating active Hodgkin's disease. The significance of minimal-change nephropathy in association with Hodgkin's disease is discussed. It may be that abnormalities in T-cell function lead to minimal-change nephropathy in some patients with certain forms of Hodgkin's disease.

Adult↗
PubMed1991

Effects of variation in sodium intake on cystinuria.

This study was designed to characterize the effect of urinary sodium excretion on amino acid excretion in cystinuria. We studied three homozygous patients with cystinuria at various levels of sodium intake ranging between 50 and 230 mmol/day. A reduction in sodium intake produced a marked decrease in rates of urinary cysteine excretion. The low-sodium diet also reduced the excretion of lysine but had no significant effect on the excretion of ornithine or arginine. We conclude that a dietary restriction of sodium may reduce the urinary excretion of cystine and can provide a simple and safe long-term approach to the treatment of cystinuria.

Administration, Oral↗
PubMed1991

Axonal microtubules: comparative anatomy in vertebrates, including man.

The microtubular density was assessed with the electron microscope in 3 microns myelinated fibers, myelin excluded, of 11 species from the following classes: Osteichthyes, Amphibia, Reptilia, Aves, and Mammalia. The average for all species was 20.6 microtubules/microns 2. Dispersion of values was restricted as shown by a coefficient of variation of 15.8. The microtubular content of nonmedullated axons was assessed in trout, lizard, finch, and man. In the four species, the number of microtubules increased with the cross sectional area of the axon. In trout, lizard and finch, the microtubular density decreased from over 100 microtubules/microns 2 in fibers smaller than 0.1 micron 2 to about 30 in 1 micron 2 fibers; in axons of equal size, the packing of microtubules of nonmedullated was similar between them, and with reported values for peripheral axons of cat and rat. In man, the microtubular density of nonmedullated fibers exhibited only a mild decrease with the axonal size. In the finch, myelinated and nonmedullated axons overlapped in the range 0.23-0.60 micron 2 and both groups exhibited similar microtubular densities. We conclude that the packing of microtubules of the vertebrate peripheral axon is a feature largely conserved during evolution.

Animals↗
PubMed1990

Uptake of Ca2+ and refilling of intracellular Ca2+ stores in Ehrlich-ascites-tumour cells and in rat thymocytes.

We have studied the uptake of Ca2+ and its redistribution between the cytoplasm and the intracellular stores in Ehrlich-ascites-tumour cells and rat thymocytes previously depleted of Ca2+ by incubation in Ca2(+)-free medium. Measurements included changes of the cytoplasmic Ca2+ concentration ([Ca2+]i), uptake of 45Ca2+ and uptake of Mn2+, a Ca2+ surrogate for Ca2+ channels. Refilling of the Ca2+ stores in thymocytes was very fast (half-filling time: 4 s at 37 degrees C) and very sensitive to temperature (10 times slower at 20 degrees C). It was always preceded by increase of [Ca2+]i. In the Ehrlich cell, both refilling and increase of [Ca2+]i were about one order of magnitude slower. The increase of [Ca2+]i and the refilling of the intracellular stores were both almost completely blocked by Ni2+ in thymocytes, but only partially in the Ehrlich cell. The rates of 45Ca2+ and Mn2+ uptake varied consistently with temperature and the kind of cell. These results suggest that the intracellular stores are refilled by Ca2+ taken up from the cytoplasm. We also find that filling of the Ca2+ stores decreases by about 90% the rate of Mn2+ uptake in thymocytes. This is direct evidence of modulation of the plasma-membrane Ca2+ entry by the degree of filling of the intracellular stores. This modulation occurs in the absence of agonists, suggesting some kind of signalling between the intracellular stores and the Ca2+ entry pathways of the plasma membrane.

Aminoquinolines↗