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M Vos

Publications and source records attributed to M Vos.

At least 37 records · Page 2Linked to original sources
PubMed1993

Magnesium and the heart: antiarrhythmic therapy with magnesium.

Magnesium is an essential transmembrane and intracellular modulator of the electrical activity of cardiac cells. This review provides an up-to-date consideration of the cellular and clinical electrophysiological role of magnesium. This ubiquitous element seems to be important from both the theoretical and clinical point of view, because magnesium salts (MgSO4, MgCl2) administered intravenously are particularly effective in those arrhythmias in which the mechanism involves early or delayed after depolarization-induced triggered activity. The authors share the view that I.V. magnesium is the drug of choice in "torsade de pointes" ventricular tachycardia accompanying acquired long QT/QTU syndrome. It is complementary therapeutic agent in digitalis-induced tachycardias. Further studies are needed to elucidate magnesium's mode of action and efficacy in other types of clinical tachyarrhythmias.

Animals↗
PubMed1993

Biochemical characterization of peptide alpha-amidation enzyme activities of human neuroendocrine lung cancer cell lines.

Peptide alpha-amidation is a posttranslational modification of approximately half of all endocrine and neuroendocrine peptide hormones, including several hormones with mitogenic effects for tumor cells, and is typically essential for complete hormonal bioactivity. alpha-Amidated peptide hormones have been reported to be autocrine growth factors for small cell lung cancer cells. We report here that a variety of human lung tumor cell lines express both enzymes required for the two-step conversion of inactive glycine-extended peptides into their active COOH-terminal alpha-amide analogues. Human tumor cell peptidylglycine alpha-amidation enzymes are present in multiple molecular forms. Both proteins are metalloenzymes which are present at highest concentrations in secretory granules in neuroendocrine cell lines. The expression of these enzymes is positively correlated with expression of other markers of the neuroendocrine phenotype, such as DOPA decarboxylase. Peptidylglycine alpha-amidating enzyme-specific activities are approximately 50-fold higher in extracts of endocrine cell lines (lung small cell and carcinoid) than of nonendocrine lines. Biochemical characterization of the peptidylglycine alpha-amidating enzymes will enable development of tools for detection of endocrine processes in the early stages of neoplasia and for interruption of autocrine stimulation pathways in tumor cells.

Amidine-Lyases↗
PubMed1992

Antiarrhythmic drug treatment: need for continuous vigilance.

Any physician treating cardiac arrhythmias should be aware of a possible worsening of the arrhythmia (so-called arrhythmogenesis) after the start of antiarrhythmic drug treatment. To facilitate the recognition of that complication the type and possible mechanisms of arrhythmogenesis are reviewed. Recognition also requires an understanding of (a) the time of appearance of arrhythmogenic effects after different drugs, (b) the value of non-invasive and invasive tests, and (c) the profile of the patient most likely to develop this problem. Guidelines are given to reduce the incidence of the arrhythmogenic effects of antiarrhythmic drugs and a plea is made that the physician should be always on the alert for this complication.

Anti-Arrhythmia Agents↗
PubMed1991

Applicability of the stimulus-T interval for antitachycardia pacing.

UNLABELLED: At the onset of tachycardia, the refractory period (RP) changes together with the tachycardia termination window. We evaluated dogs with total atrioventricular (AV) block to determine if stimulus-T interval (STI) can be used to adjust the coupling interval(s) of an antitachycardia pacemaker in relation to changes in RP. Endocardial STI was recorded continuously together with six surface ECG leads. Steady-state (greater than 2 min) RP was determined for drive cycle lengths (DCL) 400 msec and 900 msec. The test pulse (TP) coupling interval, with DCL 900 msec, was chosen to be equal to the RP of DCL 400 msec. DCL was then changed to 400 msec until TP captured. STI of DCL of beat before capture was gained was measured. DCL was then changed back to 900 msec and the interval determined when capture was lost. TP was then lengthened by 5 msec and the procedure repeated until TP captured immediately upon changing to DCL 400 msec. RESULTS: The difference between RP at onset of pacing at DCL of 400 msec and RP when capture was achieved with the shortest coupling interval was 35-50 (mean 40) msec. This required 35-90 (mean 62) seconds. The correlation coefficient RP to STI was greater than 0.95. CONCLUSIONS: (1) RP changed by as much as 35-50 msec at the onset of an abrupt increase in rate in a 35-90-second period; and (2) STI enables estimation of RP on a beat-to-beat basis. Capture can therefore be predicted from the previous beat and the coupling interval adjusted accordingly in an antitachycardia pacing mode.

Animals↗
PubMed1991

Bovine inhibin immediately inhibits the electrophysiological response to chorionic gonadotrophin in ovarian follicles of Xenopus laevis.

Inhibin was originally isolated from ovarian tissue using, as a bioassay, its ability to diminish synthesis and secretion of gonadotrophins in pituitary cells after several days. Inhibin is known also to modify responses to gonadotrophins in the ovary after stimulation times of hours or days. Here we show that action for less than 4 min of purified bovine inhibin on ovarian follicles from Xenopus laevis causes a specific, dose-responsive (greater than 10 U/ml) inhibition of the membrane hyperpolarization produced by stimulation with chorionic gonadotrophin. The CG-induced change in follicle membrane potential has previously been shown to be caused by potassium efflux produced by rises in intracellular cAMP. Inhibin did not affect similar hyperpolarization stimulated by 10 microM adenosine. The apparent Ca(2+)-dependent Cl- currents which are often associated with CG action, were not inhibited by inhibin. At concentrations up to 2000 U/ml, inhibin did not significantly alter the timing of CG-induced germinal vesicle breakdown in the oocytes, which may suggest functional action on other developmental processes.

Animals↗