From the study of movements of Ca**++ in frog cardiac muscle, Niedergerke (1963)
postulated that Ca**++ necessary for the cardiac contraction is stored in a
Langer et al (1967) and DeCaro (1967) also found a close relationship between the
change of Ca**++ flux kinetics and the change of contractile force. According to
the studies of several investigators, Ca Ⅱ (Bailey and Dressel 1968) or phase Ⅰ
and Ⅱ (Langer 1965, Langer et al 1967, 1971) in the Ca**++ washout curve was
associated with cardiac contractility.
This investigation was aimed to elucidate the anatomical region of the
contractile active Ca**++ pool. At the same time, it was assumed in this study that
Ca**++ in the sarcoplasmic reticulum represent one of the major intracolluar Ca**++
pool and cardiac contractility was also dependent on the intracellular Ca**++
concentration. Consequently, this experiment was performed at different
temperatures to activate or inhibit the deactivating process of activated Ca**++ in
the intracellular space to see if changes in the contractility decay curve existed
at different temperatures.
The isolated hearts of rabbits and turtles (Amyda maackii) were attached to the
perfusion apparatus according to the method employed by bailey and Dressel (1968).
The isolated hearts were initially perfused with a full ringer solution
containing 2 mg/ml of inulin for 1hr, and then Ca**++ and inulin-free Ringer
solution was perfused while the isometric tension was recorded and a serial sample
of perfusion fluid dripping from the cardiac apex was collected for 10 sec.
throughout experimental period.
The above procedure was performed at 22℃, 30℃ and 38℃ on the rabbit heart and
10-15℃, 20℃, 30℃ and 35℃ on the turtle heart.
After determination of Ca**++ and inulin concentration of the samples, the
Ca**++, inulin washout curve and the contractile tension decay curve were analysed
according to the method of Riggs (1963).
The results were summarized as follows;
1. In the rabbit heart, there are 2 inulin compartments, 3 Ca**++ compartments
and single exponential decay of contractile tension. In the turtle heart, there are
1-2 inulin compartments, 1-2 Ca**++ compartments and 1-2 phases of contractile
tension decay. The fact that the inulin space was divided into 2 compartments in
the washout carve in these hearts indicates the presence of heterogeneity in
cardiac perfusion, i.e., over-perfused and under-perfused area.
2. Ca Ⅰ and CaⅡ in these hearts were found to have Ca**++ in the ECF
compartments because their half times in the washout curves were far smaller than
those of the inulin washout curves in the rabbit heart and similar to those of the
inulin washout curves in the turtle heart.
Ca Ⅱ in the rabbit heart may have originated from the intracellular Ca**++
store. But no Ca Ⅲ in the turtle heart was found. This may be due to the fact that
the intracellular Ca**++ pool in the turtle heart was too small to detect using
this experimental procedure since sarcoplasmic reticulumn in the turtle heart is
3. In the rabbit heart, there were no changes in the half time of Ca Ⅰ, Ca Ⅱ, ,
inulin Ⅰ and inulin Ⅱ at different temperatures, but the half time of Ca Ⅲ was
significantly prolongea at lower temperatures, and the half time of the contractile
tension decay tended to be prolonged at lower temperatures but this was not
significant. In the turtle heart, there were no changes in the half time of Ca Ⅰ,
Ca Ⅱ, inulin Ⅰ, inulin Ⅱ and phase Ⅰof the contractile tension decay at
different temperatures, but the half time of phase Ⅱ of the contractile tension
decay was significantly prolonged at lower temperatures. This finding indicates
that intracellular Ca**++ in these hearts was also responsible particulary for
meantaining the cardiac contractility at the lower temperatures.
4. The half times of contractile tension decay were shorter than those of Ca Ⅱ
in the Ca**++ washout curves in both animal hearts.
According to the above results it was shown that Ca**++ in ECF is primarily and
Ca**++ in the intracellualr space is partially associated with the cardiac