The rest- and excitation-dependent shifts of Ca and 45Ca in the isolated, perfused ventricles of guinea-pig hearts were investigated. As much as 50% of the total Ca content (2.2 mmol/kg ww) found in the ventricular muscle stimulated at a steady rate of 60/min, was released into perfusate during 4 min of rest. In the preparations perfused with 45Ca containing solution during the 4 min of rest or during the last 20 s of rest only, a single beat resulted in extra uptake of 0.359 and 0.287 mmol of labelled calcium (45Ca) per kg ww, respectively. Single post-rest excitation evoked in the ventricles which were previously perfused with radioactive solution for 64 min, resulted in increase in tissue 45Ca content by 0.229 mmol/kg ww. In these preparations, the gain in 45Ca is equivalent to the net Ca uptake. Continued post-rest stimulation at the rate of 60/min resulted in recovery of pre-rest content of 45Ca and of total Ca. Gain of 45Ca was paralleled by recovery of contractile force. Uptake of 45Ca in the preparations stimulated at the steady rate of 60/min was 0.137 mmol/kg ww and its value did not depend on the number of beats during exposure to the isotope. Thus 45Ca uptake over a number of steady-state beats may be regarded as equal to the uptake in a single beat. This uptake is by orders of magnitude larger than reported previously by other authors. It is proposed that contraction is triggered by Ca influx into the excited cells (Ca1), and that the response of contractile proteins to this trigger is controlled by a large intracellular Ca2 fraction whose volume is rate-dependent.
Ca shifts in the isolated, perfused ventricular muscle of guinea-pig hearts were investigated with the aid of 45Ca under the conditions of complete equilibration of preparations with the isotope-containing solution. In some series of experiments total Ca content was also measured by means of atomic absorption spectrophotometry. The content of 45Ca at the end of 70 min equilibration period during which the ventricles were stimulated at a rate of 60/min was 1.66 +/- 0.09 mmol/kg w.w. This content dropped to 0.42 +/- 0.09 mmol/kg w.w. within 4 min of rest. Contractile force also decreased to 21% of control. Both the content of 45Ca and contractile force returned to the pre-rest values within the 4 min of post-rest stimulation. The difference between the total Ca content in the rested and stimulated muscle was comparable to the respective difference in 45Ca contents. A significant linear correlation between this 45Ca fraction which was lost at rest and recovered during the post-rest stimulation, and contractile force was found under the following experimental conditions: I. post-rest recovery, II. decay during rest, III. post-rest stimulation at various rates. These results are consistent with the hypothesis proposing that this Ca fraction is involved in the frequency-dependent control of contractile force.
The purpose of this study was to investigate the effect of prolonged (14 days) intragastric administration of Mn2+ (0.25 mmol/kg daily) on Ca2+ exchange and contractility of rat ventricular myocardium. Left-ventricular pressure and its first derivative (dP/dt) were recorded by means of a balloon catheter inserted via the left atrium into the left ventricle of the rat heart perfused by Langendorff method. Ca2+ exchange in the stimulated and rested ventricular myocardium was investigated with the aid of 45Ca under the conditions of complete equilibration of preparations with a solution containing 45Ca2+. The "cellular" 45Ca2+ content was calculated by subtraction of 45Ca2+ dissolved in the free water of extracellular space from the total tissue 45Ca2+ content. The cellular 45Ca2+ content in the stimulated (60/min) ventricles of control rats (without Mn2+) was 0.83 +/- 0.09 mmol/kg wet weight (w.w.). Ten minutes of rest resulted in a gain of 0.06 mmol 45Ca/kg w.w. (not statistically significant). Fourteen days' exposure to Mn2+ resulted in an increase of the mean 45Ca content to 1.61 +/- 0.09 mmol/kg w.w. in the stimulated preparations and to 1.35 +/- 0.06 mmol/kg w.w. in the rested ones (p less than 0.001). Thus, the control rest preparations did not change their Ca2+ content, while in the rats treated with Mn2+ the rest resulted in an increase at exchangeable Ca by 52%. The maximal ventricular developed pressure (Pmax) after 14 days of Mn2+ administration was increased by 35% and dP/dtmax was 228% of the value in the control group.(ABSTRACT TRUNCATED AT 250 WORDS)
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