Effects of the AMP-activated protein kinase inhibitor compound C on the postconditioned rat heart

Table 2 Effects of 10 μM compound C (CC) treatment of postconditioned ischemic-reperfused rat hearts on changes in absorbance at 540 nm up to 5 min in subsequently isolated mitochondria

	Ca²⁺ 100 µM	Ca²⁺ 150 µM	Ca²⁺ 200 µM	Ca²⁺ 300 µM	Ca²⁺ 400 µM	Ca²⁺ 500 µM
C	1.37 ± 0.2	1.75 ± 0.3	1.87 ± 0.1	2.56 ± 0.1^a	2.62 ± 0.2^a	2.68 ± 0.1^a
IPOC	2.00 ± 0.3	2.4 ± 0.5	2.70 ± 0.5	3.20 ± 0.3	4.3 ± 0.2^a,b	4.70 ± 0.2^a,b
C + CC	0.57 ± 0.10	0.65 ± 0.10	0.76 ± 0.12	1.76 ± 0.4^a	1.80 ± 0.3^a	1.96 ± 0.3^a
IPOC + CC	0.81 ± 0.3	1.12 ± 0.20	1.29 ± 0.3	2.60 ± 0.3^a	2.80 ± 0.2^a	2.83 ± 0.4^a

Ischemic postconditioning was induced by six cycles of 10-s reperfusion interspersed with 10-s no-flow ischemia immediately after sustained ischemia in absence or presence of CC added to the perfusion medium during the first 5 min of reperfusion. Mitochondria were prepared as described in the “Materials and methods”. MPTP opening was initiated by addition of CaCl₂ (100–500 μM) and was followed by monitoring of the classic decrease of absorbance at 540 nm at 25 °C as described in “Materials and methods”. Values are mean ± SEM (n = 8). Decrease of absorbance is expressed as a percentage of the respective initial value
^a p < 0.05 versus Ca²⁺ 100 µM, Ca²⁺ 150 µM, Ca²⁺ 200 µM
^b p < 0.05 versus Ca²⁺ 300 µM

ISSN: 1880-6562