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Biomedical subjects

J Merino

Publications and source records attributed to J Merino.

At least 163 records · Page 9Linked to original sources
PubMed1980

Malondialdehyde formation in rat platelet-rich plasma. I.A kinetic approach.

Malondialdehyde (MDA) is a stable produce of arachidonic acid metabolism, catalyzed by the enzyme cyclo-oxygenase. The experimental conditions for measuring the kinetics of MDA formation in rat citrated platelet-rich plasma were defined. Platelets were stimulated with either arachidonic acid, the substrate of MDA, or thrombin, an enzyme which induces release of free arachidonic acid from platelet membrane phospholipids. MDA formation was almost linear for a limited period of time (between 0 and 2 min with arachidonic acid and between 1 and 3 min with thrombin) and was concentration-dependent with saturation kinetics. The hyperbolic curves obtained could be recast in linear plots (according to Woolf transformation S/V versus S) when arachidonic acid was used. With thrombin, in contrast, the highest concentration at which no MDA production could be detected (3 NIH u/ml) had to be subtracted from each concentration of the enzyme used to obtain Woolf plots. The apparent Km value of arachidonic acid was 0.49 /+- 0.09 mM and Vmax was 1.44 /+- 0.06 nmoles MDA/1.4 Z 10(9) platelets/min. The corresponding values in experiments with thrombin were 6.5 /+- 1.5 NIH u/ml and 0.233 /+- 0.012 nmoles MDA/1.4 X 10(9) platelets/min.

Animals↗
PubMed1980

Malondialdehyde formation in rat platelet-rich plasma. II. Modification of the reaction kinetics by aspirin and indomethacin in vitro.

The type of inhibition and the relative potency of aspirin and indomethacin on rat platelet malondialdehyde (MDA) formation were investigated in an in vitro system. Both drugs inhibited the production of MDA after platelet stimulation with either thrombin (10 or 25 NIH u/ml) or sodium arachidonate (0.5-2.25 mM). Inhibition by both drugs was concentration-dependent, was partially removed when platelet-rich plasma was diluted with platelet-poor plasma, was much stronger when either drug was preincubated with platelets for 10 minutes than for 1 minute and was apparently competitive when analysed by Dixon plots (1/V versus inhibitor concentrations). It is suggested that both aspirin and indomethacin may inhibit in vitro cyclo-oxygenase activity in citrated platelet-rich plasma by a similar, if not identical, partially reversible mechanism, not involving - in a first step - covalent binding of either drug to enzyme. A scheme of the interaction of both drugs with cyclo-oxygenase is presented which also takes into account the irreversible acetylation of the enzyme occurring after longer incubation times with aspirin.

Animals↗
PubMed1980

Arachidonic acid-induced malondialdehyde formation in rat platelets. Kinetic aspects and inhibition by acetylsalicylic acid and indomethacin.

Malondialdehyde (MDA) is a stable product of arachidonic acid metabolism, catalyzed by the enzyme cyclo-oxygenase. The experimental conditions for measuring the kinetic of MDA formation in rat platelet-rich plasma were defined. In platelets stimulated with arachidonic acid MDA formation was almost linear for a limited period of time (between 0 and 2 min) and was concentration-dependent with saturation kinetics. The hyperbolic curves obtained were recast in a linear plot (according to transformation S/V versus S) and straight lines fitting all experimental points were obtained. The apparent Km value of arachidonic acid was 0.49 +/- 0.09 mM and Vmax 1.44 +/- 0.06 nmoles MDA/1.4 x 10(9) platelets/min. The apparent type of inhibition and the relative potency of acetylsalicylic acid and indomethacin on MDA formation were also investigated. Inhibition by both drugs was concentration-dependent, and was much stronger when either drug was preincubated with platelets for 10 min than for 1 min. Analysis of the data by Dixon plots (1/V versus inhibitor concentrations) revealed an apparently competitive type of inhibition. It is suggested that both acetylsalicylic acid and indomethacin inhibit cyclo-oxygenase in platelet-rich plasma by a similar mechanism, not involving covalent binding of either drug to the enzyme.

Animals↗
PubMed1979

Sex-hormone-binding globulin in the plasma of normal men and patients with benign prostatic hypertrophy.

Sex-hormone-binding globulin (SHBG) was measured in the plasma of normal men aged 30--50 yr, normal men 50--70 yr of age, and men 50--70 yr of age suffering from benign prostatic hypertrophy (BPH). The level of binding proteins in normal "young" men decreased approximately 45% in normal "older" men. A 100% rise was observed in BPH patients as compared to normal older men. This increase seemed to be related to a rise in SHBG and also to the appearance of binding species of smaller molecular weight than that of SHBG.

Adult↗
PubMed1977

Computed tomography of tumors of the pineal region.

Eight pathologically proven cases of pineal region tumors examined by computed tomography (CT) were found upon reviewing 11,000 consecutive CT studies at the Massachusetts General Hospital. The CT scan findings of the eight cases are described and related to a pathological classification of pineal tumors.

Adolescent↗
PubMed1976

[Platelet anti-aggregating activity of furosemide (author's transl)].

The effect of furosemide on platelet aggregation, factor 3 availability, and response to hypotonic stress has been studied. Furosemide greatly inhibits platelet aggregation, with ADP, epinephrine, collagen, ristocetin, thrombin and serotonin. The use of heparin as anticoagulant does not alter this effect. Furosemide action is not conducted through calcium chelation. Platelet factor 3 availability is not modified by furosemide. There is a direct correlation between furosemide concentration and inhibition in the second phase of platelet response to hypotonic stress. The possibility of a disorder furosemide induced on the platelet metabolism, is suggested.

Adult↗