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.

Pulmonary hydraulic impedance response to cromakalim (BRL 34915) in newborn pigs.

Cromakalim (BRL 34915), a novel vasodilator, is used clinically to manage systemic hypertension. Its effects on the intact newborn pulmonary circulation remain unclear. The purpose of this study was to determine the response of both the mean and pulsatile pulmonary hemodynamic parameters to intravenous infusion of BRL 34915 (0.1 mg/kg/min for 10 min) in 48-hr-old open-chest Yorkshire pigs. Animals were divided into two groups: Group I pigs had a high mean baseline pulmonary artery pressure (PAP) (> 17 mm Hg), while Group II pigs had a low to normal baseline mean PAP (< 17 mm Hg). Following instrumentation for high-fidelity recordings of PAP and flow, baseline data were acquired. Employing Fourier analysis, characteristic impedance (Zo), input mean impedance (Zm), impedance harmonic moduli (units in dyn sec cm-5), and phase angles (radians) were determined. Pulmonary vascular resistance (PVR) was calculated and aortic pressure (AP, mm Hg) was also measured. All values = mean +/- SEM. Group I animals ("high tone") underwent a decrease in PAP (17.9 +/- 1.6 mm Hg vs 13.6 +/- 1.9 mm Hg, P = 0.008) and PVR (4310 +/- 816 dyn sec cm-5 vs 3713 +/- 687 dyn sec cm-5, P = 0.04). Group II animals ("low tone") responded with an increase in PAP (11.5 +/- 0.4 mm Hg vs 16.6 +/- 1.8 mm Hg, P = 0.029). AP decreased in Group I (40 +/- 3.8 mm Hg vs 21.5 +/- 2.8 mm Hg, P = 0.008) and Group II (51.2 +/- 10.8 mm Hg vs 31.2 +/- 10.9 mm Hg, P = 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)