Biomedical subjects

M L dos Santos

Publications and source records attributed to M L dos Santos.

At least 19 recordsLinked to original sources

PubMed1992

Cross-sectional and evolutive studies of schistosomiasis mansoni in untreated and mass treated endemic areas in the southeast and northeast of Brazil.

Cross-sectional and evolutive studies on schistosomiasis mansoni were carried out before and after mass treatment in the endemic areas of Capitão Andrade and Padre Paraiso, state of Minas Gerais, Riachuelo, state of Sergipe, Alhandra, state of Paraiba, and Aliança, Alegre and Coroatá, lowland of the state of Maranhão, Brazil, in the last eighteen years. The studies included clinical and fecal examination by the Kato-Katz quantitative technique, skin test for Schistosoma mansoni infection, evaluation of man-water contact and other epidemiological investigations such as infection rate and dynamic of the snail population. Results showed: (1) Higher prevalence of S. mansoni infection, greater egg load elimination and higher and earlier morbidity of the chronic forms of the disease in the southeast areas of Capitão Andrade and Padre Paraiso; (2) The incidence of hepatosplenic form is higher in some family clusters, in whites and mulattos in all the endemic areas but develop earlier in the southeast; (3) The prevalence and morbidity of schistosomiasis are decreasing both in the mass treated northeast and in the untreated southeast areas; (4) The mass treatment reduces rapidly the prevalence of the infection and the morbidity of the disease but can not control it because of the frequent reinfections due to the intensity of man-water contact.

Adolescent↗

PubMed1991

[The effect of nifedipine on hemodynamics and gas exchange in dogs with experimental acute respiratory insufficiency].

PURPOSE: Evaluate the action of nifedipine, a calcium channel blocking agent, on the hemodynamics and gas exchange experimental acute respiratory failure. METHODS: Lung injury was provoked in sixteen mongrel dogs with intratracheal instillation of hydrochloric acid (HC1) (0.1N; pH = 2.0; 2.0 ml/kg body weight). As steady state was achieved after HC1 instillation (maintenance of a stable arterial PO2), saline 1 ml (six dogs) or nifedipine (ten dogs) 30 micrograms/kg for body weight were intravenously injected. The hemodynamic variables and gas exchange parameters were analyzed before HC1, after HC1 and 10 and 30 minutes after nifedipine or saline. RESULTS: The intratracheal instillation of HC1 provoked significant drop of PaO2, of systemic oxygen transport index (ITO2S), and increase of venous admixture (QVA/Q). Nifedipine provoked significant reduction of the mean systemic arterial pressure (Pas), and of the systemic (IRVS) and pulmonary vascular resistance index (IRVP), with significant increase of cardiac (IC) and systolic index (IS), with no changes ot the mean arterial pulmonary (Pap) and capillary pressures (Pcap). After nifedipine there was a significant increase of PaO2, PvO2, and ITO2S, with no significant variations of QVA/Q and alveolar arterial O2 difference (P(A-a)O2). CONCLUSION: Nifedipine promoted systemic vasodilation, and probably by increasing the venous return and/or by a reflex mechanism, the cardiac output increased, augmenting the ITO2S. The IRVP decreased in the nifedipine group, with no significant alterations of Pap and Pcap, probably consequent to the systemic vasodilation provoked by the drug. The arterial PO2 augmented in the nifedipine group, as a consequence of mixed venous PO2 increase, since no changes occurred in QVA/Q, P(A-a)O2, inspired fraction of O2 and alveolar ventilation.

Acute Disease↗

PubMed1989

[The role of angiotensin-converting enzyme inhibitor (captopril) on the mechanism of hypoxic pulmonary vasoconstriction. Experimental study in dogs].

In order to evaluate the action of an angiotensin converting enzyme inhibitor (Captopril) on the pulmonary hypoxic vasoconstriction, twenty one mongrel dogs were studied in two groups: group I with hypoxia, group II with normoxia. The dogs were anesthetized, intubated, and had their femoral vein and artery cannulated for blood-gas sampling and pressure records. They were mechanically ventilated with hypoxic gas mixtures (12.3% O2-87.7% N2)--group I and room air group II, at random. In both groups we measured, before and after administration of captopril 3 mg/kg intravenously, gas exchange and hemodynamic variables, as well as plasmatic levels of renin and angiotensin converting enzymes (ACE). Our results showed that the group I dogs decreased the systemic and pulmonary vascular resistances with small changes in pulmonary arterial pressures and no significant variations of pulmonary systemic resistances ratio. There were no significant variations of the same variables in the group II dogs. The gas exchange has not changed in either group of animals. In the group I dogs Captopril provoked systemic and pulmonary vasodilatation, with no gasometric and ventilation/perfusion ratio changes. In our experimental model we could not conclude that Captopril inhibited the hypoxic pulmonary vasoconstriction and/or that the angiotensin II had some action on the hypoxic pulmonary vasoconstriction mechanism, but there are some evidences favoring that hypothesis.

Analysis of Variance↗

PubMed1989

[Effects of captopril on hemodynamics, gas exchange and exercise capacity in patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease].

Captopril, a potent inhibitor of angiotensin converting enzyme, was tested in patients with COPD (means forced expired volume in the first second--FEV1 = 0.73 l) and pulmonary hypertension (PAP = 41.3 mmHg). In the first phase of the experiment, patients underwent and incremental exercise test to the limit of tolerance. These were double blind, randomized, cross-over studies, where the patients received oral placebo (Pl) or captopril (Cp) 25 mg, on different days. In a second phase, the patients were submitted to hemodynamic and gasometric studies in the supine position, before placebo, the 60 min after and immediately after exercise (cycling-like leg movements). After 30 min of rest the same protocol was repeated with oral administration of 25 mg of captopril. In the metabolic evaluation (cycloergometry) captopril increased significantly exercise tolerance (means VO2-uptake at maximal exercise: CP = 0.81 vs Pl = 0.73 1/min), associated with a slower heart rate and higher O2-pulse at maximal exercise. In the hemodynamic study, when the effects of Cp and Pl were compared, the mean values of pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were similar at rest, but significantly lower during exercise, after captopril (means PAP Cp = 41.3 vs Pl = 51.2 mmHg; XPVR Cp = 278 vs Pl = 392 dyn. sec. cm5). There were similar systemic hemodynamic effects after Cp, but these were more intense in the pulmonary circulation (lower PVR/SVR ratio post-Cp in relation to post-Pl, during exercise). The cardiac index, systemic O2 transport and arterial and mixed venous blood gases were similar at rest and during exercise, with Pl or Cp.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1986