Objective: 

In the given investigation cytoplasmic contents of potassium and its physiological analog rubidium are determined in cardiomyocytes of rat under acute ischemia.

Methods: 

The experiments were carried out on male Wistar rats. An isolated heart was perfused by Langendorff`s procedure. Ischemic depletion was created by perfusion with Tirode´s solution deep deoxygenated and in the absence of glucose. An isolated cardiac papillary muscle was frozen in liquid propane and placed in a cryomicrotome chamber, where it was cut at –30°C into 10 mm thick cryosections. After low-temperature dehydration in vacuum the cryosections were mounted in the holder of a JSM-U3 microanalyzer microscope (JEOL, Japan). Applying Electron Probe Microanalysis cytoplasmic contents of elements were measured. The potassium or rubidium concentration in the cell was determined from the intensity of the Ka line in the characteristic spectrum of an element that was excited in a sample by accelerated electrons of the probe.

Results: 

It was found that after 60 minute of acute ischemia the potassium concentration in cardiac myocells decreased from the control level 1221 mM to 542 mM (these and all results below are presented as mean and standard deviation). The potassium deficiency approached 811 mM and rubidium was accumulated to 221 mM when perfusion with rubidium was applied.

Conclusions: 

The data obtained exhibit that for initial acute ischemia phase the active transport is involved in the uptake of rubidium which competes with potassium entry in cardiac myocell. Then deep deenergization leads to the intracellular potassium depletion and rubidium retention. This suggests that Rb⁺ is physiologically not complete analog for K⁺.