Prevention of cellular edema directly caused by hypothermic cardioplegia: studies in isolated human and rabbit atrial myocytes.

OBJECTIVES

This study tested the hypothesis that edema during hypothermic cardioplegia is caused by the hypotonicity of the perfusate at cold temperatures.

METHODS

The volume of isolated human and rabbit atrial myocytes was measured by video microscopy under nonischemic conditions. Each cell served as its own control.

RESULTS

After equilibration in 37 degrees C physiologic buffer (Tyrode's solution), exposure to 9 degrees C St. Thomas' Hospital solution for 20 minutes caused human atrial cells to swell by 20% and rabbit atrial cells to swell by 10%. Cell volume fully recovered on rewarming in 37 degrees C physiologic solution. Cell swelling was due to the composition of St. Thomas' Hospital solution rather than hypothermia alone. Exposure to 9 degrees C physiologic solution did not significantly affect cell volume. Swelling of myocytes was largely prevented by replacing most of the Cl- in St. Thomas' Hospital solution with an impermeant anion so that the product of the concentrations of K+ and Cl- were the same as in the physiologic solution.

CONCLUSIONS

This study suggests that cell swelling during hypothermic cardioplegia is caused in part by the composition of the cardioplegic solution. The volume of cardiac myocytes appears to follow a Donnan equilibrium in the cold, and the perfusate KCl product determines water movement. Thus, the tonicity of hyperkalemic cardioplegic solutions can be adjusted to a physiologic value by replacing most Cl- by an impermeant anion. Following this simple principle, a reformulation of cardioplegic solutions may be able to minimize iatrogenic myocardial edema.