Aims: 

Excitability and contraction of cardiac muscle from brain dead heart donors critically influence the success of cardiac transplantation. We have examined membrane physiology, Ca²⁺ handling and contraction of cardiac muscle and properties of coronary arteries from the hearts of brain dead pigs.

Methods: 

A porcine model of 12–20 hrs of brain death was developed. Comparisons were made with non-treated pigs. Cardiomyocytes and trabecular preparations were examined using whole cell patch clamp and microelectrode techniques. Calcium handling and calcium sensitivity were determined using confocal imaging and permeabilized preparations. Coronary arteries were examined in a wire-myograph.

Results: 

Action potentials in isolated cardiomyocytes and trabecular muscle were significantly shorter in the brain dead group. No difference was found in the resting membrane potential. The alteration in the action potential was associated with impaired cellular shortening and attenuated Ca²⁺ transients. L-type Ca^2+, inward (IK1) and delayed K⁺ currents were detected (IKr and IKs), while the transient outward K⁺ current (Ito) was absent. No significant differences in the recorded currents were detected between groups. Coronary arteries exhibited increased sensitivity to the thromboxane analogue (U46619) and unaltered endothelium dependent relaxation.

Conclusion: 

Brain death was associated with moderate shortening of the action potential, leading to attenuated Ca²⁺ transients and cellular shortening which might lower the contractility after transplantation. Changes in K⁺ channels could not be detected. Increased reactivity of coronary arteries could be associated with an increased risk of vascular spasm, although endothelial relaxant function was well preserved.