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. 1999 Aug;80(4):189–196. doi: 10.1046/j.1365-2613.1999.00114.x

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© 1999 Blackwell Science Ltd

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Cardiac myocytes were exposed to simulated lethal hypoxic/ischaemic injury for 6 h. Immediately after this period, the stimulated ischaemic buffer was removed and replaced with normal growth medium supplemented with CT-1 (2 ng/ml) only () and in the presence of 50μm PD98059 (▪) or 10μm SB203580 (). IR NT, cardiac myocytes reoxygenated in the absence of CT-1 (□). The inhibitors were added to the cells 10 min before the addition of CT-1. The cells were incubated under normoxic, oxygenated conditions for 2 h. Subsequent to this period the cells were harvested and cell death following ischaemia/reoxygenation (IR) was assessed by trypan blue exclusion. *P < 0.05.

Inline graphic — Cardiac myocytes were exposed to simulated lethal hypoxic/ischaemic injury for 6 h. Immediately after this period, the stimulated ischaemic buffer was removed and replaced with normal growth medium supplemented with CT-1 (2 ng/ml) only () and in the presence of 50μm PD98059 (▪) or 10μm SB203580 (). IR NT, cardiac myocytes reoxygenated in the absence of CT-1 (□). The inhibitors were added to the cells 10 min before the addition of CT-1. The cells were incubated under normoxic, oxygenated conditions for 2 h. Subsequent to this period the cells were harvested and cell death following ischaemia/reoxygenation (IR) was assessed by trypan blue exclusion. *P < 0.05.