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Biomedical subjects

H Refsum

Publications and source records attributed to H Refsum.

At least 91 records · Page 5Linked to original sources
PubMed1977

A comparison of the effects of ouabain, noradrenaline and nifedipine on the contractile force of the isolated rat atrium at different calcium levels.

The effects of ouabain 5 x 10-5 M, noradrenaline 10-7 M and nifedipine 100 mug/1 on the contractile force of the isolated rat left atrium were tested and compared at varying concentrations of calcium in the Ringer solution. The effect of ouabain was small, developed slowly and almost independently of the calcium concentration. Noradrenaline, which increases Ca++ influx during excitation, caused an increase in the contractile force which was complete within 2 min. The percentage as well as the absolute increase in contractile force was pronounced at lower, but small at higher calcium concentrations. Nifedipine, which reduces Ca++ influx during excitation, caused a decrease in contractile force which was complete within 2-4 min. The nifedipine-induced depression in contractile force decreased with a rise in the calcium concentration. It is assumed that the ouabain-induced increase in contractile force in the rat, is not mediated by an increase in the magnitude of the inward calcium current, and other modes of action for the inotropic effect of glycosides are discussed.

Animals↗
PubMed1977

The effect of calcium and beat interval on the contractile force and refractoriness of the isolated rat atrium in the absence and presence of nifedipine: a possible mechanism for the negative staircase phenomenon.

An increase in the calcium concentration of the Ringer solution increased the contractile force and reduced the effective refractory period of the isolated rat left atrium paced at a frequency of 60 per min. An increase in the frequency of stimulation decreased the contractile force (negative staircase) and reduced the effective refractory period; these effects being most pronounced at the highest calcium levels. A calcium-antagonistic drug, nifedipine, decreased the contractile force and the effective refractory period. The effect of an increased frequency of stimulation on the contractile force at different calcium levels in the absence and presence of nifedipine paralleled its effect on the effective refractory period. This observation suggests that both these phenomena are caused by a decreased quantity of inflowing calcium ions during the period of exciation, and thus might explain the absence of positive staircase in the rat myocardium.

Action Potentials↗
PubMed1976

Effects of levomepromazine, chlorpromazine and their sulfoxides on isolated rat atria.

The effects of levomepromazine, chlorpromazine and their sulfoxides were studied on spontaneously beating and on electrically driven rat atria in vitro. Levomepromazine, chlorpromazine and levomepromazine sulfoxide produced a dose-dependent decrease in the work index of spontaneously beating atria and in the contractile force of electrically driven atria, while chlorpromazine sulfoxide was relatively inactive in these respects. At higher concentrations, levomepromazine sulfoxide caused a pronounced increase in the threshold for electrical stimulation and the effective refractory period. Compared to chlorpromazine, levomepromazine looses less of its cardio-depressive effect through sulfoxidation.

Animals↗
PubMed1976

Anticholinergic and cardiodepressive effects of levomepromazine and two of its metabolites on isolated rat atria.

The effects of monodesmethyl levomepromazine on effective refractory period (ERP) threshold for electrical stimulation and contractile force on isolated rat atria were compared to the effects of levomepromazine and levomepromazine sulfoxide. All agents caused an apparently dose-dependent increase in ERP, and antagonized acetylcholine-induced reductions in ERP. Levomepromazine and monodesmethyl levomepromazine decreased excitability and contractile force to a similar extent.

Acetylcholine↗
PubMed1975

Effects of N-acetylprocainamide as compared with procainamide in isolated rat atria.

The actions of procainamide and its major metabolite N-acetylprocainamide were tested and compared on isolated rat atria. While procainamide exerted a negative chronotropic and iontropic effect, N-acetylprocainamide had the opposite effect. It is suggested that a N-acetylprocainamide-induced increase in myocardial work can counteract the negative inotropic action of procainamide and thus to some extent explain the variable results with the latter compound on myocardial performance reported from in vivo experiments. Procainamide increased the refractory period and reduced the excitability of isolated rat atria. N-acetylprocainamide, on the other hand, caused negligible effects on these parameters.

Animals↗