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S Velasco

Publications and source records attributed to S Velasco.

54 records · Page 3Linked to original sources
PubMed1991

[Ischemic cardiopathy in women].

Life expectancy in western women is 8 years larger compared to men. This is due to the higher incidence of ischemic heart disease in men at least before reaching 45 years of age. This may also be due to differences in blood lipoprotein levels, differences in smoking habits, use of hormonal contraceptives, plasma iron levels, parity and other risk factors also found in men. After menopause the difference in the incidence of ischemic heart disease progressively decreases, basically because of a decrease in estrogen secretion. However, the role of estrogen supplement treatment in this group of women in the prevention of ischemic heart disease has not yet been clearly defined. The objectives of this study are to review the risk factors involved in the development of ischemic heart disease in women, the changes brought about by menopause and the possible beneficial effects of supplemental estrogens in the postmenopausal period.

Coronary Disease↗
PubMed1989

Olsalazine versus placebo in the treatment of mild to moderate ulcerative colitis: a randomised double blind trial.

The effect of olsalazine, an analogue of sulphasalazine, consisting of two molecules 5-aminosalicylic acid linked by an azobond has been investigated for the treatment of ulcerative colitis. In a randomised double blind trial we compared 2 g olsalazine with placebo for four weeks. Of the 105 patients, with mild to moderate ulcerative colitis, entered in the trial 52 received olsalazine, and 53 placebo. Treatment had to be terminated prematurely because of untoward effects of olsalazine (mainly diarrhoea) in three patients and treatment failure--that is, increased rectal bleeding in four patients (olsalazine group: one placebo group: three). After four weeks' treatment, a statistically significant improvement in the endoscopic findings in rectum and a positive trend in the reduction of rectal mucus and blood discharge was observed in the patients treated with olsalazine. No statistically significant difference was found for other factors, including stool frequency, consistency, urge to defecate, abdominal pain, and biopsy findings. A comparison between these clinical and endoscopic parameters at study entry and those at study completion (within drug evaluation) showed significant improvement in six of 10 parameters during treatment with olsalazine and in two of 10 during placebo treatment. This difference suggests the significant effect of olsalazine. We conclude that 2 g olsalazine was tolerated as well as placebo, apart from causing diarrhoea in some patients and was slightly superior to placebo during four weeks' treatment of mild to moderate ulcerative colitis. A study with 3 or 4 g olsalazine per day may show a more definite effect.

Adolescent↗
PubMed1988

Modulation of acetyl-CoA:1-alkyl-2-lyso-sn-glycero-3-phosphocholine (lyso-PAF) acetyltransferase in human polymorphonuclears. The role of cyclic AMP-dependent and phospholipid sensitive, calcium-dependent protein kinases.

In order to characterize the mechanism of activation of the enzyme 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine:acetyl-CoA acetyltransferase (EC 2.3.1.67) which is the limiting step in the regulation of the synthesis of the potent inflammatory mediator 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine; homogenates from human polymorphonuclear leukocytes were incubated in the presence of the catalytic subunit of cyclic AMP-dependent protein kinase and in the presence of a partially purified phospholipid sensitive, calcium-dependent protein kinase (PrKC). The first kinase was found to enhance up to 3-fold acetyltransferase activity in a dose- and time-dependent manner. In homogenates from PMN previously stimulated with complement-coated zymosan particles, the decay of acetyltransferase activity was partially prevented by the addition of soybean trypsin inhibitor and almost completely inhibited when the homogenates were supplemented with inhibitors of alkaline phosphatase such as 50 mM KF and 100 microM paranitrophenylphosphate. Under these conditions it was possible to initiate the decay of acetyltransferase activity by adding an excess of alkaline phosphatase. Preincubation of PMN with 12-O-tetradecanoylphorbol-13-acetate previous or simultaneously to the addition of ionophore A23187 reduced the increase in acetyltransferase produced by ionophore A23187, whereas the generation of superoxide anions was enhanced. Addition of partially purified PrKC to homogenates from ionophore A23187-stimulated PMN, reduced acetyltransferase activity by 63%, whereas only a 16% inhibition was observed on homogenates from resting PMN. These data indicate the modulation of acetyltransferase activity in human polymorphonuclear leukocytes by a phosphorylation-dephosphorylation mechanism linked to cyclic AMP-dependent protein kinase. Phospholipid sensitive, calcium-dependent protein kinase seems not to be involved in the mechanism of activation, but, most probably, in the generation of negative activation signals.

Acetyltransferases↗
PubMed1988

Biosynthesis of platelet-activating factor in human polymorphonuclear leukocytes. Involvement of the cholinephosphotransferase pathway in response to the phorbol esters.

The generation of platelet-activating factor (PAF) in response to complement-coated zymosan particles, ionophore A23187 and 12-O-tetradecanoylphorbol 13-acetate (TPA) was studied in human polymorphonuclear leukocytes (PMN). TPA was an active stimulator of PAF biosynthesis but showed a time course more protracted than that observed in response to other secretagogues. TPA was not found to activate acetyl-CoA:lyso-PAF acetyltransferase activity nor to significantly enhance the incorporation of either [3H] lyso-PAF or [3H]acetate into a lipid fraction co-migrating as PAF. To assess whether TPA could be a secretagogue that promotes the biosynthesis of PAF through the dithiothreitol-insensitive cholinephosphotransferase pathway, this enzymic activity was assayed in homogenates from PMN preincubated in the presence of several secretagogues. None of the agonists was found to enhance this enzyme activity. However, TPA did enhance the incorporation of [methyl-3H]choline and both alkyl- and acetyl-labeled 1-O-hexadecyl-2-acetyl-sn-glycerol into a lipid fraction co-migrating with PAF. This incorporation showed a time course parallel to that of the generation of PAF in response to TPA. Incubation of [methyl-3H]choline-labeled cells in the presence of 1-O-hexadecyl-2-acetyl-sn-glycerol caused an enhanced incorporation of the label into the fraction co-migrating as PAF, and this incorporation was synergistically enhanced by TPA. Pulse-chase experiments with choline showed that TPA caused an early accumulation of choline into phosphatidylcholine and PAF rather than into CDP-choline. The present data indicate that TPA is the only agonist that could initiate the biosynthesis of PAF in human PMN through the cholinephosphotransferase pathway and that this process of biosynthesis is regulated at an enzyme step other than dithiothreitol-insensitive cholinephosphotransferase.

Acetyltransferases↗
PubMed1988

Olsalazine in the treatment of mild to moderate ulcerative colitis: a randomized, placebo-controlled, double-blind, clinical trial.

Olsalazine, 2 g/day, was compared with placebo in 126 patients with mild or moderate ulcerative colitis. Evaluation after 4 weeks revealed a significant improvement in endoscopic findings in the rectum and sigmoid colon and in the clinical parameters rectal mucus and blood discharge, whereas no significant difference was found between olsalazine and placebo groups in clinical parameters, such as stool frequency and consistency, urge to defecate, abdominal pain and biopsy findings. It is concluded that olsalazine, 2 g/day, is tolerated as well as placebo except that it caused diarrhoea in some patients.

Aminosalicylic Acids↗
PubMed1986

Partial purification and characterization of 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine:acetyl-CoA acetyltransferase from rat spleen.

The enzyme 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine: acetyl-CoA acetyltransferase (EC 2.3.1.67) was purified from rat spleen approx. 1500-fold in 1.6% yield. The specific activity of the purified enzyme was 0.317 +/- 0.089 mumol/min per mg of protein (mean +/- S.D., n = 6). The Km for the substrate acetyl-CoA was 137 +/- 13 microM and the pH optimum was about 8. Incubation of the purified enzyme was 1-O-[3H]octadecyl-2-lyso-sn-glycero-3-phosphocholine followed by electrophoresis resulted in the incorporation of radioactivity into a protein of Mr 29,000. The enzyme was most active towards 1-O-alkyl-2-lyso-sn-glycero-3-phosphocholine as substrate, 1-palmitoyl-2-lyso-glycero-3-phosphocholine being a poor substrate. In addition, the enzyme preferred acetyl-CoA to palmitoyl-CoA or oleoyl-CoA as substrate.

Acetyltransferases↗
PubMed1985

Modulation of lyso-platelet activating factor: acetyl-CoA acetyltransferase from rat splenic microsomes. The role of cyclic AMP-dependent protein kinase.

Incubation of rat splenic microsomes with the catalytic subunit of cyclic AMP-dependent protein kinase in the presence of Mg-ATP stimulated 2-3-fold lyso-platelet-activating factor: acetyltransferase activity. This activation was due to an increase in the Vmax of the acetylation reaction, whereas the Km for acetyl-CoA was not affected. The ATP derivative, AMPPNP, could not replace ATP and preincubation of the microsomes with the heat-stable inhibitor of protein kinase prevented the activation by Mg-ATP obtained in the presence of the protein kinase. Activation of the acetylation reaction by the protein kinase was reversible. Evidence is provided that the reversal of activation is due to dephosphorylation of the enzyme. These data provide evidence that in vitro lyso-platelet-activating factor: acetyltransferase from splenic microsomes is regulated by phosphorylation.

Acetyltransferases↗
PubMedDate not supplied

[Contraceptives and ischemic cardiopathy].

The incidence of myocardial infarction is higher in women that use oral contraceptives. The most important pathophysiologic mechanisms are: a) modification of coronary risk factors: the pill produces an elevation of both serum cholesterol and trygliceride levels, increase of blood pressure and decompensation of diabetes mellitus; b) blood coagulation disorders: oral contraceptives increase platelet aggregation and fibrinogen blood levels, therefore they have a considerable thrombogenic capacity. At this moment there are several update publications concerning this matter; however most of the mechanisms involved in the increase of coronary heart disease in this specific group still remain unclear.

Arteriosclerosis↗
PubMedDate not supplied

[Update on coronary syndrome X].

Syndrome X is not a well-defined clinical entity. Patients included are those with typical effort angina with angiographically normal coronary arteries and with no evidence of other causes of chest pain. The pathophysiologic mechanisms involved in this syndrome could be a reduced vasodilatory capacity. The prognosis is usually good, but a subgroup of patients with left bundle brunch block in the ECG may develop a dilated cardiomyopathy. To present it lacks a full effective treatment.

Algorithms↗
PubMedDate not supplied

[Dysautonomic syncope. Diagnosis and treatment].

Inappropriate activation or disbalance of vasomotor reflexes may have a close relationship with the pathogenesis of disautonomic syndromes, a frequent underlying cause of recurrent syncope. A combined approach of meticulous historical data, physical examination and selected laboratory procedures may delineate the most common causes of recurrent syncope. Tests of autonomic function may be particularly helpful in the diagnosis of this entity. They include some non-invasive maneuvers such as stimulation of carotid sinus, Valsalva maneuver or tilt-table test. Therapy for this syndrome includes pharmacologic agents, surgical and radiotherapeutic maneuvers and atrioventricular sequential pacing. In this work we will present an overall formulation of the diagnostic evaluation and a therapy approach of the patient presenting with this complaint.

Carotid Sinus↗
PubMedDate not supplied

[Current use of anti-hemostatics in ischemic cardiopathy].

Antihemostatic drugs are widely used in the treatment and prevention of ischemic heart disease. Fibrinolytic agents are prescribed in the early phase of acute myocardial infarction, to reduce its size and improve survival. Their use in unstable angina is still controversial. Anticoagulants have substantial benefit in myocardial infarction, unstable angina and primary prevention of coronary disease. Finally, antiplatelet agents are used in stable and unstable angina, myocardial infarction and high risk patients.

Angina, Unstable↗
PubMedDate not supplied

[Applications of nuclear magnetic resonance in the diagnosis of cardiopathies].

Applications of nuclear magnetic resonance imaging in cardiovascular diagnosis. The role of magnetic resonance imaging in the evaluation of cardiovascular system is still evolving. Nevertheless, this technique is of great promise for cardiac patient management in the near future. Magnetic resonance imaging provides a high contrast between the blood pool and myocardial function that has been shown to be effective for the evaluation of a wide variety of anatomic abnormalities as well as to assess cardiac contractile function or myocardial perfusion. Moreover, magnetic resonance spectroscopy has provided a new research tool for the evaluation of myocardial metabolism. Such performances indicate the potential of magnetic resonance techniques to establish the link between myocardial function and metabolism. In this presentation we will review the current status of magnetic resonance imaging for the diagnosis and evaluation of a wide variety of cardiovascular diseases and discuss its future potential.

Aortic Diseases↗