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Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.

Turrell HE, Thaitirarot C, Crumbie H, Rodrigo G - Physiol Rep (2014)

Bottom Line: However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity.These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC.We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Sciences, University of Leicester, Glenfield General Hospital, Leicester, UK.

No MeSH data available.


Related in: MedlinePlus

The SBFI fluorescence measurement of intracellular sodium. Record of SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), during perfusion of a control myocyte with MI‐Tyrode.
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fig01: The SBFI fluorescence measurement of intracellular sodium. Record of SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), during perfusion of a control myocyte with MI‐Tyrode.

Mentions: It has been shown previously that the fluorescence signal of SBFI (F(340) and F(380)) is sensitive to changes in NADH during metabolic inhibition with cyanide (Donoso et al. 1992). This study also showed that the in vivo fluorescence response of SBFI was different to the in vitro characteristics, with the F(380) signal showing a decrease in intensity in response to an increase in [Na+]i and F(340)‐signal not responding to changes in [Na+]i. Figure 1 shows the SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), in which a rapid increase in the F(340) fluorescence is detected in MI‐Tyrode, as reported previously (Donoso et al. 1992). However, this rapid increase was absent in F(380) signal, which did show a gradual decrease as expected for an increase in [Na+]i. The ratio F(340/380), indicates two phases a rapid increase, which was due to the large increase in F(340) responding to the increase in [NADH], and the gradual increase reflecting an increase in [Na+]i which is in agreement with the previous report (Donoso et al. 1992).


Remote ischemic preconditioning of cardiomyocytes inhibits the mitochondrial permeability transition pore independently of reduced calcium-loading or sarcKATP channel activation.

Turrell HE, Thaitirarot C, Crumbie H, Rodrigo G - Physiol Rep (2014)

The SBFI fluorescence measurement of intracellular sodium. Record of SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), during perfusion of a control myocyte with MI‐Tyrode.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4255825&req=5

fig01: The SBFI fluorescence measurement of intracellular sodium. Record of SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), during perfusion of a control myocyte with MI‐Tyrode.
Mentions: It has been shown previously that the fluorescence signal of SBFI (F(340) and F(380)) is sensitive to changes in NADH during metabolic inhibition with cyanide (Donoso et al. 1992). This study also showed that the in vivo fluorescence response of SBFI was different to the in vitro characteristics, with the F(380) signal showing a decrease in intensity in response to an increase in [Na+]i and F(340)‐signal not responding to changes in [Na+]i. Figure 1 shows the SBFI‐fluorescence record at F(340) and F(380) and the ratio F(340/380), in which a rapid increase in the F(340) fluorescence is detected in MI‐Tyrode, as reported previously (Donoso et al. 1992). However, this rapid increase was absent in F(380) signal, which did show a gradual decrease as expected for an increase in [Na+]i. The ratio F(340/380), indicates two phases a rapid increase, which was due to the large increase in F(340) responding to the increase in [NADH], and the gradual increase reflecting an increase in [Na+]i which is in agreement with the previous report (Donoso et al. 1992).

Bottom Line: However, only conventional-IPC reduced the Ca(2+)-loading during metabolic inhibition and this was independent of any change in sarcKATP channel activity but was associated with a reduction in Na(+)-loading, reflecting a decrease in Na/H exchanger activity.These data show that remote-IPC inhibits MPT pore opening to a similar degree as conventional IPC, however, the contribution of MPT pore inhibition to protection against reperfusion injury is independent of Ca(2+)-loading in remote IPC.We suggest that inhibition of the MPT pore and not Ca(2+)-loading is the common link in cardioprotection between conventional and remote IPC.

View Article: PubMed Central - PubMed

Affiliation: Department of Cardiovascular Sciences, University of Leicester, Glenfield General Hospital, Leicester, UK.

No MeSH data available.


Related in: MedlinePlus