Excitability and contraction of cardiac muscle from
brain-dead donors critically influence the success of
heart transplantation. Membrane physiology, Ca2+-handling, and force production of cardiac muscle and the contractile properties of coronary arteries were studied in hearts of
brain-dead pigs. Cardiac muscle and vascular function after 12 h
brain death (
decapitation between C2 and C3) were compared with properties of fresh tissue. In both isolated cardiomyocytes (whole-cell patch clamp) and trabecular muscle (conventional
microelectrodes), action potential duration was shorter in
brain dead, compared to controls. Cellular shortening and Ca2+ transients were attenuated in the
brain dead, and linked to lower
mRNA expression of
L-type calcium channels and a slightly lower ICa,L, current, as well as to a lower expression of
phospholamban. The current-voltage relationship and the current above the equilibrium potential of the inward K+ (IK1) channel were altered in the
brain-dead group, associated with lower
mRNA expression of the
Kir2.2 channel. Delayed K+ currents were detected (IKr, IKs) and were not different between groups. The transient outward K+ current (Ito) was not observed in the pig heart. Coronary arteries exhibited increased contractility and sensitivity to the
thromboxane analogue (
U46619), and unaltered endothelial relaxation. In conclusion,
brain death involves changes in cardiac cellular excitation which might lower contractility after
transplantation. Changes in the
inward rectifier K+ channel can be associated with an increased risk for
arrhythmia. Increased reactivity of coronary arteries may lead to increased risk of vascular
spasm, although endothelial relaxant function was well preserved.