Effects of balloon occlusion during percutaneous coronary intervention on circulating Ischemia Modified Albumin and transmyocardial lactate extraction.
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Angioplasty, Balloon, Coronary↗
Biomedical subjects
R Calvino
Publications and source records attributed to R Calvino.
Ion interaction reagent reversed-phase high-performance liquid chromatography determination of anti-tuberculosis drugs and metabolites in biological fluids.
New methods of ion interaction reagent (IIR) RP-HPLC are presented for the determination of anti-tuberculosis drugs and their metabolites, singly or in multi-component mixtures, in biological fluids. The following analytes are considered: isoniazid, ethionamide, pyrazinamide, morphazinamide, p-aminosalicylic acid, nicotinic and isonicotinic acids. Aqueous solutions of three different ion interaction reagents are alternatively or comparatively used as the mobile phases, namely: (A) 5.00 mM octylamine at pH 3.00 for o-phosphoric acid, (B) 5.00 mM octylamine at pH 8.00 for o-phosphoric acid, and (C) 5.00 mM 1,6 diaminohexane at pH 6.00 for o-phosphoric acid. The response linearity between peak area and analyte concentration is verified for all the analytes in the concentration range within the determination limits and 2.00 mg/l. Detection limits are always lower than 82 microg/l for standard solutions; in the analysis of samples of rat serum, rat plasma and human serum, the matrix effect is negligible, the detection limits are always lower than 94 microg/l and the average recovery yield is always greater than 96%.
Aminosalicylic Acid↗
Effect of oral aminophylline in patients with angina and normal coronary arteriograms (cardiac syndrome X).
BACKGROUND: Patients with syndrome X (exertional angina, positive exercise test, normal coronary arteriogram) have an altered perception of cardiac pain. This symptom may arise from increased sensitivity to adenosine. Previous studies suggest that intravenous aminophylline (an adenosine receptor blocker) improves exercise tolerance in patients with this disorder. OBJECTIVE: To examine the efficacy of oral aminophylline in syndrome X. METHODS: 13 patients (11 women and two men, mean (SD) 54 (6) years) with syndrome X were studied. Patients were randomised in a double blind crossover study to receive either oral aminophylline or placebo for three weeks. All patients underwent symptom limited exercise testing and ambulatory electrocardiography at the end of each three week period. RESULTS: 10 patients completed the study. The time to angina during exercise testing in patients who were given aminophylline was longer than for the placebo group (mean (SD) 632 (202) seconds v 522 (264) seconds, P = 0.004). Peak exercise ST depression did not differ significantly between patients who received aminophylline and those administered placebo (mean (SD) -1.9 (0.7) mm v -1.5 (0.8) mm). Six patients taking aminophylline reported a reduction in the total number of episodes of chest pain during the three weeks, but the frequency and duration of ST segment depression during Holter monitoring was unchanged. CONCLUSION: Oral aminophylline has a favourable effect on exercise induced chest pain threshold in patients with syndrome X. The disparate effects on symptoms and ST segment changes are intriguing and further study is warranted.
Administration, Oral↗
Angiotensin-converting enzyme insertion/deletion polymorphism and restenosis after coronary angioplasty in unstable angina pectoris.
We studied the relation between angiotensin-converting enzyme insertion/deletion gene polymorphism and restenosis in Caucasian patients who underwent coronary angioplasty for management of unstable angina pectoris. Our results indicate that, in contrast to previous reports in Japanese patients, no association exists between angiotensin-converting enzyme gene polymorphism and the development of restenosis in Caucasian patients with acute coronary syndromes.)
Aged↗
Activation of endothelial guanylate cyclase inhibits cellular reactivity.
The study shows that endothelial cells from human umbilical veins have a soluble guanylate cyclase which can be activated by sodium nitroprusside (SNP), SIN-1 (3-morpholinosydnonimine) and S35b (4-methyl-3-phenylsulfonylfuroxan). Cells which were pretreated with these compounds showed an inhibition of thrombin-induced arachidonic acid release, PGI2 formation, PAF synthesis and PMNL adhesion. Endothelial guanylate cyclase can also be activated by nitric oxide (NO) which is generated in endothelial cells upon stimulation with thrombin or ionomycin. It is suggested that endogenously produced NO might control cell activation and endothelial function through a cGMP-dependent mechanism.
Arachidonic Acid↗
S35b, a new phenylsulfonylfuroxan compound, inhibits thrombin-induced synthesis of platelet-activating factor and prostacyclin in human endothelial cells.
Endothelial cells (EC) produce platelet activating factor (PAF) and prostacyclin (PGI2) in response to inflammatory agents such as thrombin. Upon cell stimulation a calcium-dependent phospholipase A2 (PLA2) is activated which hydrolyzes a membrane phospholipid to yield 1-0-alkyl-2-lyso-sn-glycero-3-phospho-choline (lyso-PAF) and free arachidonic acid. Lyso-PAF is in turn converted into PAF by a specific acetyltransferase and arachidonic acid is metabolized via cyclic endoperoxides to PGI2. In the present study we report that S35b (4-methyl-3-phenylsulfonylfuroxan), a new phenyl-sulfonylfuroxan compound with potent antiaggregatory effect, inhibits thrombin-induced PAF synthesis and acetyltransferase activation as well as PGI2 production in human umbilical vein endothelial cells (HUVEC) in a concentration-dependent way. Additionally, we show that S35b stimulates the production of cyclic GMP (cGMP) in HUVEC in a concentration- and time-dependent manner. At high concentration, S35b potentiates the cAMP increase induced by iloprost or forskolin without having a significant influence on cAMP level itself. Potentiation of cAMP increase during agonist-induced EC stimulation seems not to be important for the effect of S35b on cellular function as the compound is active in inhibiting PAF production when endothelial cells are pretreated with indomethacin to block PGI2 synthesis. The increase of cGMP evoked by S35b may account for the effect on endothelial cell function.
1-Methyl-3-isobutylxanthine↗
Pharmacochemistry of the furoxan ring: recent developments.
In the present work recent results obtained in the pharmacochemistry of the furoxan system are reported. In particular, after a brief description of the salient points of the furoxan chemistry, the synthesis and the properties of a series of Nifedipine and Prazosin analogues, containing this heterocyclic system, are described. Since we observed that a few furoxan derivatives are able to elicit both a dose-dependent rise in platelet cGMP levels and to promote a dose-dependent inhibition of AA-induced [Ca++] rise, and that many substituted furoxans show potent vasodilating and antiaggregatory activity, the possibility of using the furoxan system as a lead in the design of new vasodilators is also discussed.
Animals↗
4-Methyl-3-(arylsulfonyl)furoxans: a new class of potent inhibitors of platelet aggregation.
A series of 4-methyl-3-(arylthio)furoxans were synthesized by oxidation of 1-(arylthio)-2-methylglyoxymes with dinitrogen tetroxide. Reduction with trimethyl phosphite of the furoxan derivatives afforded the corresponding furazans, while oxidation with an equimolar amount of 30% hydrogen peroxide in acetic acid or with an excess of 81% hydrogen peroxide in trifluoroacetic acid afforded the corresponding arylsulfinyl and arylsulfonyl analogues, respectively. All the furoxan and furazan derivatives showed activity as inhibitors of platelet aggregation. 4-Methyl-3-(arylsulfonyl)furoxans were the most potent derivatives of the series. 4-Methyl-3-(phenylsulfonyl)furoxan (10a), one of the most active derivatives, inhibits the AA-induced increase of cytosolic free Ca2+ and production of malondialdehyde. A primary action of the compound on cyclooxygenase is excluded, as a stable epoxymethano analogue of prostaglandin H2 does not reverse the inhibitory effect of 10a. This compound produces a significant increase in cGMP which is likely to cause inhibition at an early stage of the platelet activation pathway.
Arachidonic Acid↗
Characterization of a new compound, S35b, as a guanylate cyclase activator in human platelets.
The effects of S35b (4-methyl-3-phenyl sulfonylfuroxan), a new phenyl sulfonylfuroxan compound, were investigated on human platelets activated by different agonists. Platelet aggregation evoked by arachidonic acid (AA), collagen, ADP and thrombin was inhibited by the drug in a dose-dependent manner. S35b inhibited the AA-induced increase of cytosolic free Ca2+ ([Ca2+]i) and production of malondialdehyde. A primary action of the compound on cyclooxygenase is unlikely since: (1) U-46619 (15s-hydroxy-11,9-[epoxymethano]-prosta-5Z,13E-dienoic acid, a stable epoxymethano analog of prostaglandin H2) could not reverse the inhibitory effect of S35b on AA-induced aggregation and [Ca2+]i increase; (2) U-46619-induced aggregation and [Ca2+]i rise were inhibited by S35b; and (3) at high collagen concentrations platelet aggregation (which is unresponsive to aspirin under such conditions) was blocked by S35b as well. Thus the drug action is likely to be exerted at an early step of the platelet activation pathway. The elevation in the platelet cGMP level evoked by S35b in a time- and concentration-dependent manner can account for the inhibitory effect: increased cGMP levels could interfere, for instance, with G protein-phospholipase C coupling and subsequent phosphoinositide hydrolysis.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Potential histamine H2-receptor antagonists: analogues of classical antagonists containing 4-substituted-3-aminofurazan moieties.
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Animals↗
In vitro cytotoxic activity of aryl and heteroaryl-ONN-azoxycyanides.
Some aryl-N(O) = N-X and heteroaryl-N(O) = N-CN compounds were synthetized and tested against a culture of HeLa cells. The results obtained show that the - N(O) = N beta CN function, a new cytostatic group, is useful in the design of potential antitumoral compounds.
Antineoplastic Agents↗
Antimicrobial activity of heteroarylazoxycyanides and heteroarylazoxysulphones.
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Anti-Bacterial Agents↗
Chemical and biological studies on calvatic acid and its analogs.
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Animals↗
Potential histamine H2-receptor antagonists: ranitidine analogues containing "semicarbazono equivalent" groups.
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Animals↗
Syntheses, structures and antimicrobial properties of some halogenofuroxans and related furazans.
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Anti-Bacterial Agents↗
[Furazan sulfanilamides].
Synthesis and antibacterial activity against Escherichia coli of a series of furazan sulfanilamides are reported. A structural activity relationship for these derivatives is also briefly discussed.
Anti-Bacterial Agents↗
[Study of some derivatives of the benzotriazole nucleus].
The syntheses of 1-(beta-dimethylaminoethoxy)benzotriazole, 1-(gamma-dimethylaminopropoxy)benzotriazole and of their N-oxide isomers 3-(beta-dimethylaminoethyl)benzotriazole 1-oxide and 3-(gamma-dimethylaminopropyl)benzotriazole 1-oxide are reported. The structure of these compounds has been confirmed by N.M.R. spectroscopy; the structures of the N-oxide derivatives was also elucidated by chemical reduction to the parent benzotriazoles. The two benzotriazoles were also tested for antiinflammatory activity in the rat, and for analgesic and depressant activity on the CNS of the mouse.
Animals↗
[Synthesis and preliminary pharmacological characteristics of various derivatives of 1,2,5-oxadiazole (furazan)].
The synthesis, the chemical properties, the acute toxicity, the action of frog flexor reflex of 4-methylfurazan-3-N-methylcarboxamide (II), 4-methylfurazan-3-N-isopropylcarboxamide (III), 3-methyl-4-morpholinocarbonylfurazan (IV), 3-methyl-4-pyrrolidinocarbonylfurazan (V), 3-amino-4-methylfurazan (VI), 3-acetylamino-4-methylfurazan (VII), are reported. LD50 decrease in the following order: (VI), (II), (IV), (III), (VII), (V). All compounds, except (VII), depressed frog flexor reflexes.
Animals↗