Table 2.

Functional parameters of ex vivo heart preparations

Heart preparation	Oxygen consumption (whole heart)	Time to 66% maximal NADH during ischaemia (ventricles)	Coronary flow reserve	Percentage reduction in ventricular APD after 15 min ischaemia
Ejecting heart	9.2 ml (100 g)−1 min−1[1] (BiV ejecting)* 3.1 µmol g−1 min−1[2] (LV ejecting)	17 ± 10 s[4]	7 ml min−1 (LV ejecting)[2]	~53%[5,6,7]
Langendorff: contracting	3.8 ml (100 g)−1 min−1[1] (unloaded)* 2.5 µmol g−1 min−1[2]† 6.0 ml per beat g−1[3] (working) 2.7 ml per beat g−1[3] (unloaded)	44 ± 21 s[4]	29 ml min−1[2]	~53%[8,9,10]
Langendorff: non-contracting	1.74 ml (100 g)−1 min−1[1] (KCl arrest)* 0.7 µmol g−1 min−1[2] (KCl arrest) 1.4 ml per beat g−1[3] (BDM) 0.9 ml per beat g−1[3] (KCl arrest)	100 ± 64 s[4]	31 ml min−1 (KCl arrest)[2]	~22%[11]

Whole-heart oxygen consumption rates from three studies are listed for the three primary types of ex vivo heart preparations. Upon the initiation of ischaemia, the fastest accumulation of NADH occurs within preparations with the highest oxygen consumption rate. Ejecting heart preparations may have less coronary flow reserve than Langendorff preparations. Reductions in APD occur more slowly and to a lesser extent after 10 min of ischaemia in electromechanically uncoupled hearts. Dog: [1]; and rabbit: [2–10]. Studies are as follows:

^[1]Gibbs et al. (1980);

^[2]Heineman et al. (1992);

^[3]Yaku et al. (1993);

^[4]Wengrowski et al. (2014);

^[5]Wolk et al. (1998);

^[6]Wolk et al. (1999);

^[7]Wolk et al. (2000);

^[8]Botsford & Lukas (1998);

^[9]Saltman et al. (2000);

^[10]Horimoto et al. (2002); and

^[11]Smith et al. (2012).

^*Data from open-chest dog with 20% haematocrit.

^†Loading condition unclear. Abbreviations: APD, action potential duration; BDM, 2,3-butanedione monoxime; BiV, biventricular; and LV, left ventricle.