Table 5.

Ac-ANX-A1_2–26 fails to restore recovery of LV function following I–R injury in hearts isolated from both male and female ANX-A1^−/− mice ex vivo

LVDP (% baseline, min post reperfusion)
Experimental group	0	1	2	5	10	20	30	40	AUC × 103	n
Untreated wild-type I–R	45 ± 12	87 ± 17	58 ± 6	50 ± 7	48 ± 7	57 ± 7	63 ± 8	64 ± 8	2.31 ± 0.29	11
Ac-ANX-A12–26-treated wild-type I–R	25 ± 4	87 ± 11	67 ± 4	52 ± 8	53 ± 10	77 ± 8	81 ± 6	82 ± 6	2.89 ± 0.27	6
Untreated ANX-A1−/− I–R	23 ± 3	57 ± 6a	35 ± 5a	13 ± 3a	16 ± 3a	29 ± 4a	31 ± 4a	31 ± 4a	1.05 ± 0.14a	14
Ac-ANX-A12–26-treated ANX-A1−/− I–R	51 ± 32	59 ± 7	62 ± 16	20 ± 5	23 ± 5	35 ± 8b	36 ± 7b	37 ± 7b	1.36 ± 0.22b	8

Analysis of the time course of recovery of LVDP over 40 min of reperfusion on two-way anova indicates that: P_{(min post reperfusion)} < 0.001; P_{(experimental group)} < 0.001; P_{(interaction)} = NS. Analysis of AUC for LVDP on two-way anova indicates that P_(genotype) < 0.0001; P_{(experimental group)} = 0.08; P_{(interaction)} = NS.

^aP < 0.05 versus untreated wild-type.

^bP < 0.05 versus Ac-ANX-A1_2–26-treated wild-type mice.