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M Dolder

Publications and source records attributed to M Dolder.

10 recordsLinked to original sources
PubMed1990

3-(Trifluoromethyl)-3-(m-isothiocyanophenyl)diazirine: synthesis and chemical characterization of a heterobifunctional carbene-generating crosslinking reagent.

A new hydrophobic heterobifunctional photocrosslinking reagent 3-(trifluoromethyl)-3-(m-isothiocyanophenyl)diazirine (TRIMID), a carbene precursor, and its radioiodinated analogue [125I]TRIMID, have been synthesized and chemically characterized. The reagents were applied for membrane protein modification in human erythrocyte membranes and purple membranes from Halobacterium halobium. Covalent labeling of the anion transport protein (band 3) via the isothiocyanate function was confirmed. Radiolabeled TRIMID was detected in at least two thermolysin-generated transmembrane fragments of the anion transport protein, and half-maximal inhibition of the erythrocyte anion transport activity was attained with 2.2 mM reagent. In bacteriorhodopsin (BR), a common binding site for the monofunctional phenylisothiocyanate and the bifunctional crosslinking reagent was identified: preincubation of purple membranes with TRIMID suppressed phenylisothio-[14C]-cyanate binding to BR. [125I]TRIMID was recovered in V-1, the N-terminal segment of BR, which includes the phenylisothiocyanate binding site Lys-41. Light-induced intramolecular crosslinking of band 3-derived thermolytic fragments was not observed, although the carbene was generated in situ and photocrosslinking of the protease V8 fragments of BR was not detected. Chemical and physicochemical characteristics of the new reagent are discussed with regard to limitations imposed for photoinduced site-directed crosslink formation.

Anion Exchange Protein 1, Erythrocyte↗
PubMed1979

[Echocardiography].

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Echocardiography↗
PubMed1978

[Experimental coronary ligation in swine: reduction of myocardial infarct and hemodynamic and metabolic changes by means of the calcium antagonist RO 11-1781].

In a comparative study the effect of the new calcium antagonist Ro 11-1781 on experimental infarct size and left ventricular function in the pig has been investigated. The calcium antagonist was administered 30 min prior to ligation of the left anterior descending coronary artery and twice daily on the following 4 days. For morphometric assessment of infarct size the ventricular myocardium was cut into slices and stained with nitro-benztoluene. There was a significant reduction in infarct size of about 25% in the calcium antagonist-treated group in comparison with the control group. After coronary occlusion left ventricular function is equally depressed in both groups, as is myocardial lactate extraction, which becomes negative.

Animals↗
PubMed1978

[Ventricular arrhythmias in the acute stage of experimental swine myocardial infarct; effect of the beta blocker pindolol and the calcium antagonist Ro 11-1781].

A study was designed to examine ventricular arrhythmias in the acute phase of experimental myocardial infarction in the pig and to evaluate possible antiarrhythmogenic influence of the beta-adrenergic blocking drug pindolol (Visken) and the calcium antagonist Ro 11-1781. Ventricular fibrillation (VF) occurred in 17 of 18 animals, in 4 almost immediately after coronary occlusion and in 12 with a delay of about 17 min. VF was almost always induced by episodes of ventricular tachycardia (VT) which were started by single ventricular premature beats (VPBs). VPBs occurred in 3 phases, whereas VT and VF coincided only with phase 1 and phase 3. The prematurity index QR/QT of single VPBs decreased significantly with time after coronary occlusion. The beta-adrenergic blocking drug pindolol and the calcium antagonist Ro 11-1781 did not prevent VT or VF.

Acute Disease↗
PubMed1977

[Effect of pindolol (Visken) on the size and hemodynamics of the exerimental myocardial infarct in the pig].

In a comparative study the effect of pindolol (Visken, Sandoz) on experimental infarct size and left ventricular function in the pig has been investigated. Pindolol was given 30 min prior to the ligation of the left anterior descending coronary artery and on the following 5 days twice daily in a dosage of 0.05 mg/kg body weight. For morphometric assessment of infarct size the ventricular myocardium was cut into slices and stained with nitro-benztoluene. There is a significant reduction of infarct size (by one third) in the pindolol-treated group as compared to the controls. In addition, deterioration of left ventricular function is less marked in the pindolol-treated group.

Animals↗
PubMed1976

[Frequency and prevention of ventricular arrhythmias after acute myocardial infarct].

In a controlled study using mexiletine and placebo, the incidence of ventricular arrhythmias after acute myocardial infarction (AMI) has been compared. The study covered 40 male patients who had sustained AMI and who in the first 48 h after onset of infarction had exhibited ventricular tachycardia, R on T-, multiform or close-coupled ventricular ectopic beats. Half of the patients were given either mexiletine (250 mg 8-hourly) or placebo. On the 4th and 10th day after onset of infarction a continuous 24-hour ECG was performed. 76% of the patients receiving placebo showed serious ventricular arrhythmias compared with 32% receiving mexiletine (p less than 0.05). These results demonstrate (1) the frequency of ventricular arrhythmias in a group of patients already at risk, and (2) the efficacy of an oral antiarrhythmic agent like mexiletine in the management of these rhythm disorders.

Arrhythmias, Cardiac↗
PubMed1976

[Sinus node syndrome].

The sick sinus syndrome is caused by dysfunction of the sinus node and includes various forms of arrhythmia. In its chronic form the underlying disease may affect not only the sinus node but also the atrial, junctional and intraventricular conduction tissue. The most important clinical symptoms are, in decreasing order, dizziness, syncope, palpitations, cardiac failure, systemic embolism, and cerebrovascular insult. The main diseases causing dysfunction of the sinus node are coronary heart disease, myocarditis, and rheumatic fever. The diagnosis is based on history, clinical findings, ECG, specific provocative tests and, if necessary, long-term ECG monitoring. The sick sinus syndrome is most frequently seen in patients aged over 50 years. Treatment with drugs alone, such as atropin, catecholamines, digitalis or antiarrhythmic drugs is often difficult becuase of the frequent changes between bradycardic and tachycardic arrhythmia. In chronic and progressive cases, the best treatment is implantation of a cardiac pacemaker.

Arrhythmia, Sinus↗