Search PubMed⌕ Search

Biomedical subjects

P Soler

Publications and source records attributed to P Soler.

117 records · Page 7Linked to original sources
PubMedDate not supplied

[Mitral valve disease in infants. Anatomical and functional evaluation by echocardiography].

To describe the incidence of mitral valve abnormalities among infants aged 0 to 24 months, their anatomic features, site of lesion, severity and associated heart defects, the records of 3,583 such patients submitted for bi-dimensional ultrasound and pulsed Doppler cardiac studies by presumptive heart disease were analyzed. Mitral valve abnormalities were thus detected in 88 of these cases, and were also documented by clinical examination (n: 88), heart catheterization and angiocardiography (n: 11), surgery (n: 17) and necropsy (n: 2). Seventy five cases had additional heart disease, most commonly aortic stenosis (27%), aortic coarctaction (26%) and ventricular septal defects (43%). Papillary muscle deformities at the subvalvar mitral apparatus were considered to be the most frequent mechanism for congenital mitral stenosis (100%), and annulus dilatation was the most frequent cause of mitral insufficiency (49%). Relative incidences of mitral valve stenosis and insufficiency among the whole studied sample were 0.5% and 1.48% respectively. There was a rough correlation between Doppler transmital gradient or regurgitation jet area and the corresponding mitral valve abnormality. This kind of noninvasively obtained data about mitral architecture and function seems to be a very useful and sensitive guide to define and manage this patients.

Cardiomyopathies↗
PubMedDate not supplied

[Serum digoxin in children treated with beta methyl digoxin].

Concentrations of serum digoxin were measured by the polarized immunofluorescence Abbot TDx11 method in 59 samples from 53 children under treatment with mean beta methyl digoxin doses of 8.9 +/- 2.0 micrograms.kg.day. The therapeutic range for serum digoxin concentration was estimated to be 0.9 to 2.25 ng/ml. Simultaneous Na, K and creatine serum concentrations were measured. In 36 samples mean serum digoxin level was 1.52 +/- 0.45 ng/ml -within therapeutic range- and in only one of these cases clinical evidence of toxicity was apparent. In 15 samples digoxin level was above the therapeutic range and 11 patients of this group (73%) showed clinical signs of toxicity, consisting in arrythmias (six cases: supraventricular in 5 patients, ventricular in one child) and gastrointestinal symptoms (eight patients). Six patients with digoxin levels over therapeutic range and signs of digitalis toxicity had coincidental acute renal failure, which in 4 cases was subclinical--in 2 of these late it was pre-renal- and, in spite of this, all were inadvertently given the usual dosage of beta methyl digoxin. Almost invariably there was clinical evidence of toxicity when digoxin serum levels were above 2.4 ng/ml, so established maximal therapeutic level at 2.25 ng/ml seems adequate. Signs of digitalis toxicity must be looked on systematically in children treated with such drugs. In the critically ill or in children with acute renal failure it is necessary to monitor serum digoxin concentration. Among the clinical signs of toxicity, gastrointestinal symptoms are more frequent in children. An oral dose from 7 to 10 micrograms.kg.day of beta methyl digoxin in recommended.

Acute Kidney Injury↗
PubMedDate not supplied

Delayed lymphoid lung infiltration induced by cyclophosphamide in rats.

The pulmonary toxicity of antineoplastic drugs may be either direct or mediated by hypersensitivity. The aim of this study was to determine whether the mechanism by which cyclophosphamide (CY) damages the lung is direct and immediate or is the result of delayed immune toxicity. Pulmonary and immune changes following intraperitoneal injection of either CY (50 mg/kg) or NaCl (0.9%) in rats were assessed repeatedly over a period of 31 days by semi-quantitative histological studies, by measuring the pulmonary water/body weight ratio, dry lung weight/body weight ratio, heart weight and by assessing the transfer of [125I]-albumin in lung tissue. Lung damage was delayed and greatest at 11 (D11) and 14 (D14) days after CY injection. The pulmonary lesions were: (i) an infiltration of lymphocytes, plasma cells and histiocytes surrounding blood vessels and small airways, (ii) an alveolitis composed of macrophages, lymphocytes, a few neutrophils and a lymphoid infiltration of alveolar septa. Pulmonary water/body weight and dry lung weight/body weight ratios also increased and peaked at D11-D14 in CY-treated rats. No significant increase in [125I]-albumin in lung tissue or in heart weight was observed. It can be concluded that the mechanism by which CY induces a lymphoid lung infiltration is not direct and immediate but is the result of a delayed immune toxicity.

Animals↗
PubMedDate not supplied

Nitric oxide effects on lung structure and blood oxygen affinity in rats.

Two month-old Wistar rats were exposed continuously for six weeks, either to 2.0 +/- 0.1 ppm nitric oxide (NO) mixed homogeneously with air for tests, or to ambient air for controls. Oxyhemoglobin dissociation curve (ODC), erythrocytic variables, methemoglobin (MetHb) concentration and lung structure, particularly through electron microscopy studies, were investigated each week of exposure. The hemoglobin affinity for oxygen was not modified, probably as a result of both pH and 2,3-diphosphoglycerate (2,3-DPG) stability. Moreover MetHb formation was not found in treated rats. The few ultrastructural alterations found under electron microscopy may not prove NO-induced since they were found similarly in both groups. Slight emphysematous changes were found only in 1 micrometer-thick sections of lungs from NO-treated rats.

Adenosine Triphosphate↗