Contractures in a superfused frog's ventricle

Abstract

1. A new perfused preparation of frog's ventricle is described, whose main advantage is that there are short diffusion distances between the cells and the washing fluid. 2. This preparation responds within a few seconds to alterations in sodium, potassium or calcium concentration, or alteration in the osmotic pressure of the bathing fluid. The speed of these alterations is consistent with the diffusional distances involved measured histologically. 3. On depolarizing the preparation with Ringer + excess potassium, tension development starts at about ‐25 mV and is still increasing at ‐8 mV (the lowest voltage studied). As in earlier experimetns in frog ventricle (Niedergerke, 1956b) and in skeletal muscle (Hodgkin & Horowicz, 1960) the relation between potential and tension is very steep. 4. Sodium free contractures (Lüttgau & Niedergerke, 1958) are very rapid in onset with this preparation. To maintain the tension developed, a rapid rate of washing is necessary for 1–2 min. After this, slow washing is sufficient. It is proposed that this is due to the leaching out of cellular sodium. 5. In fresh preparations the twitch and maximum K contracture are of similar size when stimulated at 30/min in 1–2 m M‐Ca. With the onset of hypodynamia the twitch tension falls, but the K contracture remains unaltered. In hypodynamic ventricles the sensitivity of the twitch to the ratio [Ca]/[Na]2 declines, whereas that of the K contractures remains unaltered. Hypodynamia therefore does not affect the contractile elements themselves. 6. During the staircase phenomenon the K contracture and twitch size alter in a similar manner, as previously described by Niedergerke. The sodium free contracture, however, remains unaltered. This tends to favour the hypothesis that the staircase phenomenon is due to effects at the cell membrane rather than in the cell interior. 7. Maximum K contractures occur at a [Ca]/[Na]2 ratio of about 0·7 × 10−4 m M−1, a figure similar to that obtained in earlier experiments (Lüttgau & Niedergerke, 1958). 8. The length—tension curves of K contractures are similar to those previously described for heart muscle, using single twitches to generate tension. 9. Application of K free solutions produced no rapid contractures in this preparation.

The effect of adrenaline on the tension developed in contractures and twitches of the ventricle of the frog

“…This twitch prolongs the time to peak con-tracture tension by a variable but small amount. As the peak tension declines relatively slowly with a T, of 40-60 sec (Lamb & McGuigan, 1966) this should not greatly affect the tension developed, and comparison of equivalent points on contracture records before and after adrenaline confirmed that in fact this had less than a 5 % effect on peak twitch tension. It might be supposed however that the presence of this spike could be reducing the contracture tension in some other way, and experiments were carried out in situations where this initial twitch could be abolished.…”

“…Half ventricles were pinned out cutsideuppermost by two entomological pins and irrigated with a jet of Ringer solution (Lamb & McGuigan, 1966). The third 'corner' of the ventricle was connected by a short length of Arbrasilk 4/0 thread to a Grass FTO 3 transducer used on its most sensitive range.…”

The ionic dependence of the strength and spontaneous relaxation of the potassium contracture induced in the heart of the frog Rana pipiens

“…In the present work, using a variation of the [K]o to alter the membrane potential, no N-shaped tension-depolarization curves have been found. It is interesting to note that other reports using the potassium contracture method also provide simple sigmoidal curves (Lamb & McGuigan, 1966;Gibbons & Fozzard, 1971 (Fig. 5), tension increasing parabolically between 3 and 25 mM-K (-75 to -40 mV resting potential) followed by a more linear increase as the membrane potential is lowered from -40 to -15 mV (25-100 mM-K).…”

Calcium‐sodium antagonism on the frog's heart: a voltage‐clamp study.

“…Theoretically, the rate of Ca extrusion by the Ca-Na exchange mechanism will be unchanged if both [Ca] Contraction in a Na-free medium. After removal of external Na, development of reversible contractures without any marked depolarization has been observed in frog ventricular and atrial preparations (Luttgau & Niedergerke, 1958;Lamb & McGuigan, 1966;Vassort, 1973;Chapman, 1974), guinea-pig auricles and atrial trabeculae of calf hearts (Scholz, 1969a, b) and ventricular strips of the goldfish heart (Busselen & Carmeliet, 1973). The simplest interpretation of a Na-lack contracture is that transmembrane exchange of internal Ca for external Na is inhibited in a Na-free medium and the control of the internal Ca level is left to some other mechanism which, under normal conditions, is inferior to the pumping mechanism of the sarcolemma.…”

“…The system is thought to operate close to equilibrium at any potential, thereby determining the INTRODUCTION It has long been known that force development in cardiac muscle is promoted by Ca ions and depressed by Na ions in the bathing medium (Ringer, 1883;Clark, 1913;Daly & Clark, 1921). The antagonistic effects have been quantified by the observation that the contractile strength of the frog heart, both ventricle and auricle, depends largely on the ratio of [Ca]o/[Na]2 (Wilbrandt & Koller, 1948;Luttgau & Niedergerke, 1958;Lamb & McGuigan, 1966;Chapman & Tunstall, 197t). This relation holds for twitch tension initiated by an action potential as well as contractures induced by high-K solutions.…”