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Biomedical subjects

L Valdes

Publications and source records attributed to L Valdes.

At least 19 recordsLinked to original sources
PubMed1999

Maintenance of blood pressure control and left ventricular performance with small doses of enalapril.

Enalopril treatment (20 mg every 12 hours) of 24 patients with essential hypertension and left ventricular (LV) hypertrophy established normal blood pressure (BP) after 8 weeks, and after 7 years had reduced LV mass index by 39% from 148 +/- 34 to 90 +/- 16 g/m2, and had normalized LV structure and function and QT dispersion. Stepwise reduction of the enalapril dosage from 40 to 30, 20, 10, and 5 mg/day during the eighth year caused no significant changes in BP, LV structure, LV systolic function, or QT dispersion, which all likewise remained unaltered during a further year of the 5-mg/day regimen. We conclude that for hypertensive patients in whom prolonged treatment with standard doses of enalapril has normalized BP, LV structure and function, and QT dispersion, significantly smaller doses are sufficient to maintain these cardiovascular achievements.

Adult↗
PubMed1999

[Severe lactic acidosis disease disclosing milk-protein intolerance to cows' milk].

UNLABELLED: The age of discovery and initial symptoms of cow milk allergy can vary. Lactic acidosis is exceptionally associated to this allergy. CASE REPORT: A 32-day-old girl was admitted for a severe malaise with metabolic acidosis and hyperlactacidemia. There were no neonatal or family problems; breastfeeding was stopped on the 25th day. Fever was noted on the 29th day and her mother reported behavior anomalies followed by a severe malaise with unconsciousness between the 29th and 32nd day. At admission, the infant showed a severe neurological distress, hypotonia and lethargy. Infection and neurological imaging were normal. A compensated metabolic acidosis with hyperlactacidemia (5.96 mmol/L) was noted. There was no argument for esophageal reflux nor vagal hypertony; mitochondrial cytopathy was also excluded. After a 24 hours fast, the clinical state gradually improved and normalized at h48. The infant was discharged with a milk protein hydrolysate formula. Her mother attempted to reintroduce cow milk on the 59th and 64th day, but this was immediately followed by allergic manifestations which supported the diagnosis of cow milk allergy. CONCLUSION: Neurological distress and hyperlactacidemia exceptionally reveal this type of intolerance. The mechanism of hyperlactacidemia remains unclear; it is possibly the consequence of severe changes of the intestinal mucosa, an exclusive glycolytic tissue.

Acidosis, Lactic↗
PubMed1997

Utility of tumour markers in the diagnosis of neoplastic pleural effusion.

Approximately 20% of pleural effusions are caused by neoplastic processes. Although cytology is the most specific routine diagnostic procedure, its sensitivity of 50-60% is insufficient, and thus diagnosis is usually carried out by more invasive techniques such as pleural biopsy, thoracoscopy or thoracotomy. The object of this study is to evaluate the use of determining some tumour markers in pleural fluid obtained by thoracocentesis for diagnosis of neoplastic pleural effusion. Patients (271) with pleural effusions were classified in five groups: I: neoplasms n = 88; II: tuberculosis n = 63; III: parapneumonics n = 53; IV: miscellaneous exudates n = 39 and V: transudates n = 28. The tumour markers studied were: carcinoembryonic antigen (CEA), CA 125, squamous cell carcinoma antigen (SCC), and neuron specific enolase (NSE). The tumour makers had the following diagnostic efficiencies for neoplastic origin of the pleural effusion: CEA 76% (sensitivity 31%, specificity 93%); CA 125 66% (70% and 61%); SCC 65% (48% and 80%) and NSE 53% (30% and 89%). The diagnostic efficiencies for pulmonary neoplastic origins were 68% for NSE (sensitivity 83%, specificity 53%); 65% for SCC (54% and 75%); 63% for CEA (80% and 48%) and 61% for CA 125 (79% and 42%). We believe that the routine testing of tumour markers in pleural fluid obtained by thoracocentesis would greatly increase diagnostic effectiveness and could avoid the practice of more aggressive diagnostic techniques on the patient.

Antigens, Neoplasm↗
PubMed1997

[Syncope with long QT interval in a 39 day-old infant treated with cisapride].

UNLABELLED: Cardiotoxicity of cisapride may increase when this drug is associated with ranitidine. CASE REPORT: A 37-day old term infant, treated with cisapride (1.2 mg/kg/d) and ranitidine for regurgitations, was hospitalized for malaise. A prolonged QT interval (with isolate ventricular extrasystoles), noted at admission, disappeared rapidly after cisapride withdrawal. Linkage to cisapride was probable, promoted by high dosage and cisapride metabolism inhibition by ranitidine, but its plasma concentration was not measured. CONCLUSION: This case report stresses the problem of cisapride dosage in infants and the question of an interaction between cisapride and ranitidine.

Anti-Ulcer Agents↗
PubMed1997

Early captopril treatment reduces plasma endothelin concentrations in the acute and subacute phases of myocardial infarction: a pilot study.

It has been reported that endothelin-1 (ET-1) increases in acute myocardial infarction (AMI). Experimental studies showed that captopril administration reduces ET-1 secretion. In addition, it was reported that the increased ET-1 levels are a negative prognostic index. The study sought to verify whether captopril can reduce plasma ET levels in the acute and subacute phases of reperfused anterior AMI. Forty-five patients, hospitalized for suspected anterior AMI within 4 h from the onset of symptoms, suitable for thrombolysis (first episode), Killip class I-2, were randomized (double blind) into two groups: group A (23; seven women/16 men) received captopril (as first dose) 2-4 h after starting thrombolysis (the dose was then increased up to 25 mg every 8 h). Group B (22; five women/17 men) received placebo after thrombolysis. All the patients met the reperfusion criteria. The two groups were similar with regard to age, sex, CK peak, ejection fraction, end-systolic volume and risk factors. Plasma ET levels were measured at entry, and 2, 12, 24, 48, and 72 h after starting thrombolysis. Mean concentrations of ET +/- SD: Group A basal, 1.50 +/- 0.67; at 2h, 2.31 +/- 1.24; 12 h, 1.84 +/- 1.45; 24 h, 1.30 +/- 0.72; 48 h, o.95 +/- 0.50; 72 h, 0.60 +/- 0.15 fmol/ml; p < 0.001. Group B basal, 1.58 +/- 0.83; at 2 h, 2.38 +/- 1.35; 12 h, 2.33 +/- 1.71; 24 h, 1.80 +/- 1.41; 48h, 1.46 +/- 0.88; 72 h, 0.93 +/- 0.44 fmol/ml; p < 0.001. Difference between the two groups was significant at the beginning of the test (between 2 and 12 h, p[=]0.002). After that, the values of the plasma endothelin decreased in parallel, p < 0.001. Our data suggest that captopril affects plasma ET levels in the acute and subacute phases of AMI. Moreover, these results provide additional evidence for a beneficial effect of early captopril treatment.

Adult↗
PubMed1996

Muscle length changes during swimming in scup: sonomicrometry verifies the anatomical high-speed cine technique.

Recent attempts to determine how fish muscles are used to power swimming have employed the work loop technique (driving isolated muscles using their in vivo strain and stimulation pattern). These muscle strains have in turn been determined from the anatomical high-speed cine technique. In this study, we used an independent technique, sonomicrometry, to attempt to verify these strain measurements and the conclusions based on them. We found that the strain records measured from sonomicrometry and the anatomical-cine techniques were very similar. The ratio of the strain measured from sonomicrometry to that from the anatomical-cine technique was remarkably close to unity (1.046 +/- 0.013, mean +/- S.E.M., N = 15, for transducers placed on the muscle surface and corrected for muscle depth, and 0.921 +/- 0.028, N = 8, in cases where the transducers were inserted to the average depth of the red muscle). These measurements also showed that red muscle shortening occurs simultaneously with local backbone curvature, unlike previous results which suggested that white muscle shortening during the escape response occurs prior to the change in local backbone curvature.

Animals↗
PubMed1993

Effects of captopril on myocardial protection during cardioplegia.

UNLABELLED: The study aimed at checking effects exerted by captopril (C) on human myocardial ACE system as well as the role played by tissue ACE inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aorto-coronary-by-pass (CABG). Fifty-four patients with coronary artery disease affecting 3 vessels having suffered from acute myocardial infarction anterior (AMI-ant), homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo (P). A total of 4 mg/l Captopril was mixed into the cardioplegic solution with blood according to the method of Buckberg (Buckberg GD. J Thorac Cardiovasc Surg 1987; 93: 127-139). Eight samples (blood/perfusate) were obtained from each patients and norepinephrine (NE), epinephrine (E) were assayed using an HPLC technique. Angiotensin I was assayed by RIA. CK was also assayed (units/ml). Blood/perfusate samples were taken during CABG: (1) pre-pump; (2) pump sample; (3) pump preclamping; (4) coronary sinus; (5) coronary sinus sample during reperfusion; (6) coronary sinus during warm reperfusion; (7) after clamping sample; (8) after decanulation; RESULTS: Captopril group (29 patients): angiotensin I: (1) 8.15; (2) 7.0; (3) 7.31; (4) 8.45; (5) 8.93; (6) 8.73; (7) 9.07; (8) 9.40; versus placebo: (1) 7.09, (2) 7.43; (3) 7.80; (4) 9.31; (5) 9.01; (6) 8.35; (7) 8.85; (8) 8.07 ng/ml, probability, not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin I↗
PubMed1992

Captopril and glutathione before thrombolysis in acute myocardial infarction: a pilot study.

This study is aimed at checking whether treatment with glutathione (GL) and captopril (CA) before thrombolysis can further improve the protective effects of ACE-inhibitors in cases with anterior acute myocardial infarction (AMI). Ninety-eight double blind randomized patients (86 men and 12 women) showing symptoms of AMI anterior and undergoing thrombolytic treatment were admitted to our study and subdivided into 4 groups. Group A (25 pts) received thrombolytic treatment only, Group B (23 pts) received 3 g GL intravenously 15 min before thrombolysis and for 2 h thereafter, Group C (26 pts) received 6.25 mg CA orally 15 min before starting thrombolytic treatment, Group D (24 pts) received 3 g GL intravenously before thrombolysis and for 2 h thereafter, and captopril as well like group C. On the third day after AMI onset groups A and B received CA also. In all groups, the doses of CA were gradually increased according to blood pressure values. The following features were considered: a) the occurrence of early (within the first 2 h after thrombolysis) ventricular hyperkinetic arrhythmias; b) CK peak; c) the normalization time of CK peak (NT); d) the occurrence of late ventricular hyperkinetic arrhythmias (VHA) in the predischarge Holter test (Lown's class 2); e) ejection fraction (EF) being measured in 60 pts undergoing haemodynamic test. The results were an follows: Group A: VHA early 13/25, CK peak 1982 +/- 282; NT 71 +/- 2 h; Late VHA 8/25; EF 53.5 +/- 2.5% (16 pts). Group B: VHA early 11/23; CK peak 1917 +/- 242 U/l; NT 69 +/- 3 h; late VHA 7/23; EF 54.5 +/- 5.4% (14 pts). Group C: VHA early 4/26; CK peak 1671 +/- 266 U/l; NT 58 +/- 3 h; late VHA 5/26; EF 55.5 +/- 3% (16 pts). Group D: VHA early 3/24; CK peak 1463 +/- 201; NT 56 +/- 4 h; late VHA 5/24; EF 57.6 +/- 4% (14 pts).

Aged↗
PubMed1992

[Effect of captopril on human myocardial ACE-inhibition: neurohumoral variations during coronary sinus cardioplegia. Cardioprotective effect during aortocoronary bypass].

UNLABELLED: The present study is aimed at checking effects exerted by captopril on human myocardial ACE system (ACE-T) as well as the role played by tissue ACE-inhibition in reducing reperfusion damage. A human experimental model was used during cardioplegia due to aortocoronary bypass graft (CABG): 54 patients with coronary artery disease affecting 3 vessels having suffered from acute anterior myocardial infarction, homogeneous as far as ejection fraction (35-55%), number of grafts (3), clamping time, age and sex, were randomised in a double blind experiment, and were given captopril or placebo: 4 mg/l captopril were mixed into the cardioplegic solution with blood according to Buckberg, 8 blood samples were obtained from each patient and norepinephrine, epinephrine were assayed using an HPLC technique. Angiotensin 1 was assayed by RIA. CK was assayed as well (U/L). Blood samples were taken during CABG: pre-pump sample; pump sample; pump preclamping sample; coronary sinus sample; warm reperfusion sample; coronary sinus during warm reperfusion; after clamping sample; after cannulation. RESULTS: captopril group (29 patients): angiotensin 1:8.15; 6.9; 7.45; 8.66; 8.93; 8.70; 9.07; 9.40 versus placebo: 7.09; 7.43; 7.80; 9.31; 9.01; 8.35; 8.85; 8.07 mcg (all NS). Noradrenaline: captopril group: 359; 404; 329; 282; 263; 216; 310; 337 versus placebo: 439; 520; 499; 469; 526; 566; 501; 443 pg (p < 0.001). CK, captopril group: 79.9; 95.1; 100.8; 94.3; 104.2; 94.7; 108.4; 108 versus placebo: 76.2; 120.2; 135.5; 203; 225; 272; 247; 228.7 U/L (p < 0.01). Epinephrine values showed no significant difference between the 2 groups. Norepinephrine and CK decrease as well as angiotensin I increase in treated patients as compared to controls suggest some effect exerted by captopril ACE-T and its capability of reducing reperfusion damage and recommend its use for heart protection during CABG.

Aged↗
PubMed1987

Hemodynamics, prolactin and catecholamine levels during hemorrhagic shock in dogs pretreated with a prolactin inhibitor (bromocriptine).

Bromocriptin, a dopaminomimetic drug, causing inhibition of prolactin secretion, was used in experiments on haemorrhagic shock in dogs. 5 dogs were treated with bromocriptine (0.4 mg.day-1) for two days; a further 5 dogs were used as control animals. 30% of the blood volume was drawn from each dog. Mean arterial blood pressure, heart rate, central venous pressure, acid-base status, prolactin, GH and catecholamine levels were checked before blood letting and monitored until 1 hour after blood letting. Animals treated with bromocriptine showed a significant decrease of the mean arterial blood pressure and of the prolactin rate and a significant increase of catecholamine levels. Control animals, instead, showed a significant increase of the prolactine and catecholamine rates. The results obtained suggest that bromocriptine can constitute an additional hypotensive factor in subjects with acute haemorrhage. A considerable amount of research work previously carried out has shown a close correlation between stress and hyper-prolactinemia. The increase of prolactinemia and the effects of bromocriptine on this hormone during surgical stress is particularly interesting due to its possible implications (Lanza V. et coll., 1983). In previous experiments involving animals it was found that Prolactin exerts positive chronotropic and hypertensive effects (Horrobin D.F., 1977) whilst bromocriptine is a potent agonist of D2 dopaminergic receptors (Thorner M.O. et coll., 1980). Dopamine was found to be particularly useful in the clinical treatment of shock thus suggesting an involvement of peripheral D2 receptors. On the basis of these observations we have considered it worthwhile to investigate the haemodynamic effects of bromocriptine in haemorrhagic shock.

Animals↗
PubMed1987

[A case of botulism in a 11-month-old infant].

We report a case of botulism in a 11 month-old infant. Hypotonia complicated by progressive bulbar paralysis revealed the disease. Botulism B toxin was present in serum on the 8th day of the disease. On the occasion of this case report the clinical, diagnostic, epidemiological and pathophysiologic aspects of infant botulism are reviewed. The relationship between sudden infant death and botulism is discussed.

Botulism↗
PubMed1986

[Multifocal tuberculosis in a 15-year-old child].

We report the case of a 15 year-old boy, presenting with juxta-articular swellings and lacunar skeletal lesions associated with prolonged fever and cachexia. Among the multiple bacteriological samplings, only the trans-osseous puncture of a tibial lacunar lesions, yielded Bacillus tuberculosis. With triple anti-tuberculous chemotherapy, fever and juxta-articular swellings disappeared. However, several articular ankyloses persist, which might need a surgical correction.

Adolescent↗