Fig. 3. (  A ) Representative Western blot of phospho–protein kinase C (PKC)-δ and phospho–PKC-ϵ from left ventricular samples acquired at 10 min after reperfusion (n = 4 for each group). Expression of phospho–PKC-δ was significantly increased in postconditioning (POST). Administration of aprotinin (APRO) upon reperfusion abolished increased expression of phospho–PKC-δ in POST + APRO. There was no significant difference in expression of phospho–PKC-ϵ among groups. (  B ) Densitometric evaluation of four experiments as the  x -fold increase in average light density (AVI)  versus control (CTL). The results are presented as the ratio of phospho–PKC-δ and phospho–PKC-ϵ to total PKC-δ and total PKC-ϵ, respectively. The average light intensity was multiplied by 10 to facilitate presentation of an  x -fold increase. Data are mean ± SD. *  P < 0.05: POST  versus CTL, CTL + APRO, and POST + APRO. 

Fig. 3. (  A ) Representative Western blot of phospho–protein kinase C (PKC)-δ and phospho–PKC-ϵ from left ventricular samples acquired at 10 min after reperfusion (n = 4 for each group). Expression of phospho–PKC-δ was significantly increased in postconditioning (POST). Administration of aprotinin (APRO) upon reperfusion abolished increased expression of phospho–PKC-δ in POST + APRO. There was no significant difference in expression of phospho–PKC-ϵ among groups. (  B ) Densitometric evaluation of four experiments as the  x -fold increase in average light density (AVI)  versus control (CTL). The results are presented as the ratio of phospho–PKC-δ and phospho–PKC-ϵ to total PKC-δ and total PKC-ϵ, respectively. The average light intensity was multiplied by 10 to facilitate presentation of an  x -fold increase. Data are mean ± SD. *  P < 0.05: POST  versus CTL, CTL + APRO, and POST + APRO. 

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