Time Course Of Contracture Research Articles

Potassium contractures and mechanical activation in rat skeletal muscle: effects of multivalent cations, temperature and tetracaine.

The effects of cations, temperature and tetracaine on potassium-induced contractures of rat soleus and extensor digitorus longus (e.d.l.) muscles were investigated. In the soleus, the threshold for the potassium contracture was lower (10-20 vs 20-40 mM), the peak amplitude was up to fourteen times larger, and the time course was about one half that in the e.d.l. muscle. The extent of inactivation of a test potassium contracture was directly related to the concentration of potassium in the conditioning solution and the period of exposure. Removal of calcium reduced the amplitude and time course of potassium contractures in both preparations. Addition of cobalt (10 mM) reduced the amplitude but prolonged the time course of contractures. Exposure of muscles to tetracaine (10(-5)-10(-6) M for 30 min) increased, but higher concentrations reduced, the amplitude of potassium contractures. When present for one minute, tetracaine (1 mM) moved the potassium activation curve to higher, and the potassium inactivation curve to lower, potassium concentrations.

Effect of external calcium and of temperature on contraction in snake muscle fibers.

The effect of external calcium and of temperature on the contractile responses has been studied in voltage clamped snake twitch muscle fibers. Increasing [Ca(++)](o) from 0.2 to 7.0 mM raised contractile threshold by 15-20 mV, the latter coinciding with the appearance of delayed rectification. The duration of contracture, the rates of rise and decay of tension depended on the level of depolarization and [Ca(++)](o). The minimum duration of repolarization necessary to restore the contractile response was much shorter in high [Ca(++)](o). When the bathing solution was cooled to 10 from 20 degrees C the time-course of contracture was markedly prolonged and the outward current was reduced without significant change in maximum tension. The threshold for contraction tended to be somewhat lower at the lower temperature. The contractile repriming was much slower at low temperature. However, reduction in temperature slowed the rate of recovery much less at low [Ca(++)](o) than at normal [Ca(++)](o).

Differentiation of inotropic mechanisms by experiments on cardiac contracture

1. Contractures of guinea-pig papillary muscles, induced either by potassium withdrawal or by high potassium concentrations, were investigated under the influence of noradrenaline and dihydro-ouabain, respectively. 2. Noradrenaline in concentrations between 10−7 M and 10−5 M enhances contractures induced by high [K+]0. There is a parallel shift of the relation between contracture force and [K+]0 towards lower potassium concentrations. The effect of noradrenaline on the time course of contracture equals the effect of a rise in [Ca2+]0. The contracture-enhancing effect of noradrenaline is not accompanied by an influence on potassium-dependent depolarization. 3. Even at high concentrations (3.5×10−5 M), noradrenaline does not increase contractures induced by potassium withdrawal. 4. In concentrations which increase the force of contraction (10−5–4×10−5M) dihydro-ouabain, in contrast to noradrenaline, enhances potassium-withdrawal contractures. Dihydro-ouabain does not change the hyperpolarization of the cardiac cells elicited by potassium withdrawal. 5. There is no noteworthy contracture after potassium withdrawal and simultaneous reduction of [Na+]0 to 25 mM, if [Ca2+]0 is only 1.6 mM. However, contracture develops under these conditions after a brief transitory rise of [Na+]0 to 140 mM. This contracture is increased and prolonged by dihydro-ouabain. 6. Contractures induced by elevation of [K+]0 can be enhanced by high concentrations of dihydro-ouabain (6×10−5–2×10−4 M). The maximal effect of dihydroouabain on potassium contracture is greater than that on potassium-withdrawal contracture. 7. It is concluded that noradrenaline enhances contractures of papillary muscles by an influence on a steady Ca entry from the extracellular solution in dependence upon [K+]0 and membrane depolarization, respectively. On the other hand, dihydroouabain increases contracture force by the same mechanism as potassium with-drawal, i.e., by an inhibition of the sodium pump with consequent increase in exchange of intracellular sodium against extracellular calcium.