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Biomedical subjects

H Refsum

Publications and source records attributed to H Refsum.

At least 235 records · Page 13Linked to original sources
PubMed1981

Ventricular diastolic pressure-volume relations and the pericardium. Effects of changes in blood volume and pericardial effusion in dogs.

We investigated the role of the pericardium in the mechanism of shifts in the left ventricular (LV) diastolic pressure-volume relation produced by changes in circulating blood volume and by pericardial effusion. Twelve closed-chest anesthetized dogs were instrumented with pericardial and pleural balloons and intracardiac catheters for pressure measurements. We measured the volumes of the pericardium and the left and right ventricles by computed tomography (CT), integrating the area of CT cross-sections measured at 1-cm intervals from the cardiac apex to the aortic arch. The volumes of the pericardium and the cardiac chambers were changed by infusing 40 and 80 ml of dilute contrast medium into the pericardial space, by bleeding, and by rapidly infusing saline intravenously. Pericardial effusions of 80 ml reduced mean right ventricular volumes to 59% of control, whereas LV volumes were less severely compromised (81% of control). Total pericardial volume and pressure increased. Intravenous saline infusions, which raised right atrial pressure 10-15 mm Hg, produced increases of this magnitude in pericardial pressure. This was also the magnitude of the upward displacement in the LV diastolic pressure-volume relation after infusion. However, LV diastolic transmural pressure-volume coordinates fell along a single curve. Similar behavior was observed for the right ventricular diastolic pressure-volume relation. Pericardial transmural pressure-volume curves were described. When cardiac volume was altered by volume load and pericardial effusion, acute shifts in the LV diastolic pressure-volume relation were caused by changes in pericardial pressure, which, in turn, corresponded to changes in pericardial volume.

Animals↗
PubMed1980

Electrophysiological and mechanical effects of contrast media on isolated rat atria.

Cardiac complications caused by contrast media may occur during angiocardiography. The present study on spontaneously beating and electrically stimulated isolated rat atrial preparations investigated the direct effects on the myocardium of four different contrast media. A low-osmolar non-ionic compound, metrizamide, was compared with three ionic contrast media having different cation compositions: meglumine-Na-Ca metrizoate, meglumine-Na diatrizoate and meglumine iothalamate. The ionic contrast media at an organ bath concentration of 30 mg I.cm-3 produced a striking shortening of the effective refractory period. In addition, they reduced the spontaneous rate of contractions, prolonged sinus node recovery time and decreased excitability. Meglumine-Na diatrizoate and meglumine iothalamate induced great reductions in contractile force and "force-rate" product. Metrizamide influenced both the electrical and mechanical activities of the isolated rat atrial preparations to a smaller extent than the three ionic contrast media. The present study demonstrated direct arrhythmogenic and cardiodepressive effects of commonly used ionic contrast media. The low-osmolar non-ionic medium, metrizamide, appears to have lower cardiotoxicity than the ionic contrast media.

Animals↗
PubMed1979

Calcium, nifedipine and arrhythmias in isolated rat atria.

Arrhythmias were induced in isolated rat atrial muscle preparations by increasing the calcium concentration of the Ringer solution, while the potassium concentration was kept low. A rise in the resting tension occurred simultaneously. The release of aspartate aminotransferase (ASAT) from the fibrillating atria was not higher than the release from non-fibrillating atria pretreated with a calcium-antagonistic drug, nifedipine 100 microgram/l. It is suggested that calcium-induced rat atrial arrhythmias in the present experiments are caused by a direct effect on calcium influx through the excitable membrane and not as a result of myocardial lesion caused by calcium overload.

Animals↗
PubMed1979

The effect of nifedipine on the monophasic action potential and refractoriness of the right ventricle of the dog heart in situ after beta-adrenergic receptor blockade.

The effect of nifedipine, a calcium-antagonistic drug, was studied on the electrophysiology of the right ventricle in the dog heart in situ. Monophasic action potential recordings were obtained by the suction electrode technique and refractoriness was measured by means of programmed electrical stimulation. Pentobarbital anaesthesia was used. As the basic cardiac effects of nifedipine can be altered by the release of catecholamines from sympathetic nerves of the heart and vessels, the dogs were pretreated with the beta-adrenergic receptor blocking agent acebutolol which increased the action potential duration and the refractoriness. Intravenous injection of nifedipine 30 microgram/kg body weight decreased the times for 50 and 90 per cent repolarization of the monophasic action potential and to a smaller extent the effective and functional refractory period. It is suggested that nifedipine decreases the action potential duration and the refractoriness of the right ventricle of the dog heart in situ due to a direct effect of the drug on the myocardium.

Acebutolol↗
PubMed1978

Comparison of the electrophysiological effects of two neuroleptics, melperone and thioridazine, on isolated rat atria.

The effects of the two neuroleptics, melperone (a butyrophenone) and thioridazine (a phenothiazine), were compared on the electrical and mechanical activity of isolated rat atria. Both electrically stimulated and spontaneously beating atria were used. Melperone was found to prolong the effective refractory period while the threshold for electrical stimulation i.e. the excitability, was almost unaffected. Thioridazine caused a similar prolongation of the effective refractory period, but also decreased the excitability significantly. In contrast to melperone, thioridazine had a negative inotropic effect. The spontaneous pacemaker activity was depressed and the sinus node recovery time increased to a greater extent after melperone than after thioridazine. The results taken together with other recent data support the hypothesis that melperone may be a type III anti-arrhythmic according to the classification of Vaughan Williams, in contrast to thioridazine which has a quinidine-like action (type I). The results also indicate that melperone in addition to prolonging the effective refractory period, may act as an anti-arrhythmic agent by depressing automaticity.

Animals↗
PubMed1978

Acebutolol-induced changes in refractoriness and monophastic action potential of the right ventricle of the dog heart in situ.

The effect of acebutolol, a beta-adrenergic receptor blocking agent, on the electrophysiology of the right ventricle was studied in the dog heart in situ. Pentobarbital anaesthesia which is known to increase the sympathetic tone was used. Monophasic action potential recordings were obtained by the suction electode technique and refractoriness was measured by means of programmed electrical stimulation. A stepwise increase in the frequency of stimulation from 170 to 200, 230, and 260 per min caused a progressive decrease in the refractoriness as well as the duration of the monophasic action potential. Intravenous injection of acebutolol 2.0 mg.kg-1 increased the times for 50 and 90% repolarisation of the monophasic action potential. This increase is probably due to beta-adrenergic receptor blockade in the presence of alpha-adrenergic receptor stimulation. The effective and functional refractory periods, however, were increased to an even greater extent than the monophasic action potential duration. It is suggested that this is the result of a blockade of a catecholamine-induced increase in the velocity of the depolarisation.

Acebutolol↗
PubMed1978

Qualitative differences between beta-adrenergic and alpha-adrenergic inotropic effects in rat heart muscle.

If beta- and alpha-adrenergic inotropic effects are cyclic AMP dependent and cyclic AMP independent, respectively, they may be qualitatively different. The inotropic effects of beta-receptor stimulation (isoprenaline) and alpha-receptor stimulation (phenylephrine combined with propranolol) were characterized in isolated perfused rat hearts, rat atria and rat papillary muscles. The beta-effect reached its maximum before the alpha-effect. The alpha-effect followed a three-phasic time-course indicating both stimulatory and inhibitory components. The aortic pressure wave (perfused heart) indicated a shorter contraction phase after beta-stimulation than after alpha-stimulation. The time to peak tension (atrium, papillary muscle) was relatively shorter after isoprenaline than after alpha-stimulation, which tended to prolong it. The contraction-relaxation cycles (atrium, papillary muscle) were examined by recording the isometric tension (T), its first (T') and second (T'') deri derivatives. alpha and beta-stimulation both increased Tmax, T'max (maximal rate of tension rise), T'min (maximal rate of tension decline) and T''min (maximal rate of transition from rise to decline of tension). Isoprenaline increased T'min (papillary muscle) and T''min (atrium, papillary muscle) relatively more than did alpha-stimulation, i.e. the relaxing processes were activated relatively more by beta-stimulation. The results indicate different mechanisms for the two adrenergic inotropic effects. The relatively larger activation of relaxation by beta-stimulation is assumed to be caused by clic AMP.

Adrenergic alpha-Agonists↗
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↗