Table 3.

Pharmacological activation of prosurvival kinases in a model of donor heart preservation.

Agent (s)1	Storage time (h)	Poststorage CO recov2	Prosurvival kinase phosphorylation3			Other salient findings	Ref.
			Akt	ERK	STAT3
GTN (0.1 mg/mL)	6	2.5	0	+	nd4	↓ cleaved Casp 3	[61]
Carip (10 μM)	6	3.5	0	++	nd4	↓ cleaved Casp 3	[61]
INO 1153 (1 μM)	6	2.5	+++	+	nd4	Recovery of function abolished by Akt inhib	[62]
Zonip (1 μM)	6	14	0	+++	+++	Zonip abolished LDH release; ↓ cleaved Casp 3; Inhib of STAT3 phos abolished recovery of f'n.	[63]
Neureg (14 nM)	6	13	++	+++	+++	Recovery of function abolished by Akt inhib	[64]
EPO (5 units/mL)	6	16	0	0	+++	Inhib of STAT3 phos abolished recovery of f'n.	[65]
Neureg + GTN + Carip	10	13	++	0	+	Triple supplement ↓ contraction band necrosis	[64]

¹Agent(s) added to Celsior arresting and storage solution. Abbreviations/drug classes are as follows: GTN—glyceryl trinitrate (nitric oxide donor); Carip—cariporide, Zonip—zoniporide, (both sodium/hydrogen exchange inhibitors); INO 1153—poly(ADPribose) polymerase inhibitor; Neureg—recombinant human Neuregulin-1 peptide; EPO—erythropoietin. ²Recovery of cardiac output expressed as fold increase over Celsior-stored hearts (P ≤ 0.05); ³increase in survival kinase phosphorylation over Celsior-stored hearts; +++: intense; ++: moderate; +: weak; ⁴nd-not determined;