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H Tritthart

Publications and source records attributed to H Tritthart.

At least 37 records · Page 2Linked to original sources
PubMed1975

Calcium movements controlling mammalian myocardial contractility: analog computation of contractile behavior assuming a multicompartmented model.

We present a model to be displayed on a medium scale analog computer, which describes excitation-contraction (E-C) coupling of the mammalian myocardium in terms of calcium movements occurring, on a sarcomere level, in a multicompartment system, Despite the fact that its mathematical formulations are oversimplifications of the mechanism involved, because the number of differential equations had to be limited, the model predicts with fair accuracy a large variety of inotropic phenomena thought to be the result of factors influencing cardiac E-C coupling in one way or another. Therefore, in its basic assumption, the overall concept might be correct, and if so, it should be possible to use the model in order to make predictions which can be tested experimentally and can help in understanding results which are otherwise difficult to interpret.

Action Potentials↗
PubMed1975

Inhibition of calcium-dependent action potentials in mammalian myocardium by specific inhibitors of the transmembrane calcium conductivity (verapamil, D 600).

Cat papillary muscles were depolarized from about -80 mV to -50 mV by addition of KCl to Tyrode's solution. This causes an inactivation of the Na-carrying system so that the remaining transmembrane inward current is due, in practice, to Ca. Such action potentials show a reduced rate of rise, a greater overshoot, and a shorter duration. These parameters vary somewhat with the strength of stimulation and, particularly, with frequency. Excitability as well as contractility of the K-depolarized fibers are completely abolished by Ca withdrawal or by addition of verapamil or D 600, which block the transmembrane Ca inward current specifically. Conversely, extra Ca or epinephrine overcomes the verapamil and C 600 effects by increasing the transmembrane Ca influx. As soon as the papillary muscles are returned to Tyrode's solution with normal K0 the Na-carrying system is reactivated. Then Ca withdrawal or Ca-antagonistic compounds lose their inhibitory influence on excitation, whereas excitation-contraction uncoupling persists.

Action Potentials↗
PubMed1975

The role of myocardial membrane leakage channels in the production of fibrillation: studies with an analog computer model.

The conditions under which automatic activity and fibrillation can occur were studied through the use of an analog model. Parameters (transmembrane active and passive properties) were established from biological data of mammalian myocardial fibers. The definition of instability of membrane potential can be given by the following functions of inward and outward steady state current (I) to voltage relationships of the membrane. 1) With decreasing angle between the tangent of the slope of the Iout and (-1) Iin, instability increases at constant potential. 2) Instability is also a function of the membrane potential as related to peak inward current (nonsteady state) at a given angle. 3) Maximum peak inward current and minimum angle produced such instability as to cause fibrillation. The most likely explanation is that automaticity and/or fibrillation is induced by leakage currents which change the normal current/voltage relatiosnhip in the described manner. The membrane leakage currents could be specific to sodium or unspecific.

Biological Transport, Active↗
PubMed1972

Effects of pethidine and nalorphine on the mechanical and electrical activities of mammalian isolated ventricular muscle.

1. The strength of the isometric mechanical contraction of electricallydriven ventricular muscle has been recorded simultaneously with the resting and action potentials; the effects of pethidine and of nalorphine on these parameters have been studied.2. When lower concentrations of pethidine (0.22-6.5 mug/ml) were perfused, isometric peak tension was decreased in parallel with the maximum upstroke velocity of the action potential; these actions are considered to result from membrane stabilization. At higher concentrations (11.8-109 mug/ml) pethidine usually produced, in addition, a progressive decrease in the resting and action potentials associated with marked irregularities in, or even abolition of, the mechanical response. It is suggested that these effects of the higher doses might be due to a depression of ATPase activity in the myocardial membrane.3. Compared with pethidine, nalorphine had similar, but weaker, actions.

Action Potentials↗