Failure to protect the myocardium against ischemia/reperfusion injury after chronic atorvastatin treatment is recaptured by acute atorvastatin treatment
A potential role for phosphatase and tensin homolog deleted on chromosome ten?
Kwabena Mensah, MBChB,
Mihaela M. Mocanu, PhD and
Derek M. Yellon, DSc, FACC*
Hatter Institute and Centre for Cardiology, University College London Hospital and Medical School, London, United Kingdom.
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Figure 1 Infarction developed in the risk zone in hearts treated for one or three days with atorvastatin or methylcellulose. *p < 0.05. I/R = ischemia/reperfusion.
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Figure 2 Infarction developed in the risk zone in hearts treated for one or two weeks with atorvastatin or methylcellulose. + = a supplementary dose of atorvastatin given a few hours before ischemia/reperfusion (I/R). *p < 0.05.
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Figure 3 Level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in hearts treated with methylcellulose or atorvastatin for one or three days. (A) Western blots; (B) relative densitometry.
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Figure 4 Level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in hearts treated with methylcellulose or atorvastatin for one week. (A) Representative blots; (B) relative densitometry. *p < 0.05.
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Figure 5 Level of phosphatase and tensin homolog deleted on chromosome ten (PTEN) in hearts treated with methylcellulose or atorvastatin for two weeks. (A) Representative blots; (B) relative densitometry. *p < 0.05.
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