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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

Intracellular pH in conventional and remotely preconditioned myocytes in response to an NH4Cl acid‐pulse (A) (i) Record of intracellular pH from a control naïve‐myocyte (black trace), conventional IPC‐myocyte (dark gray trace), and remote IPC myocyte (light gray), in response to 20 mmol/L NH4Cl for 5 min. Mean data ± SEM of the rat of recovery of intracellular pH from the acid load induced by the NH4Cl pulse in control naïve myocytes (black), conventional IPC myocytes (dark gray), and remotely conditioned myocytes (light gray). ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control naïve myocytes = 3 hearts; 16 cells, conventional IPC myocytes = 3; 25, remote IPC = 3; 21. (B) (i). Representative record of Fura‐2 ratio from a single control myocytes during MI and reenergization, and (ii). In the presence of amiloride. This result was seen in seven cells from three different hearts.
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fig06: Intracellular pH in conventional and remotely preconditioned myocytes in response to an NH4Cl acid‐pulse (A) (i) Record of intracellular pH from a control naïve‐myocyte (black trace), conventional IPC‐myocyte (dark gray trace), and remote IPC myocyte (light gray), in response to 20 mmol/L NH4Cl for 5 min. Mean data ± SEM of the rat of recovery of intracellular pH from the acid load induced by the NH4Cl pulse in control naïve myocytes (black), conventional IPC myocytes (dark gray), and remotely conditioned myocytes (light gray). ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control naïve myocytes = 3 hearts; 16 cells, conventional IPC myocytes = 3; 25, remote IPC = 3; 21. (B) (i). Representative record of Fura‐2 ratio from a single control myocytes during MI and reenergization, and (ii). In the presence of amiloride. This result was seen in seven cells from three different hearts.

Mentions: The resting intracellular pH was not affected by IPC or rIPC with a pH of 7.22 ± 0.02 (n = 3; 16) in control myocytes; 7.17 ± 0.02 (n = 3; 25) in IPC‐myocytes, and 7.21 ± 0.05 (n = 3; 21) in rIPC‐myocytes. Addition of NH4Cl (20 mmol/L) to the superfusate caused in a rapid intracellular alkalinization, which on washout of NH4Cl resulted a rapid acidification and the peak acidification was similar in all three myocyte groups (Figure 6A). However, the rate of recovery from the acid load, as determined from the exponential time constant for the recovery, was significantly reduced to 80.1 ± 6.2 sec in IPC‐myocytes from 50.7 ± 2.5 sec in control myocytes (P < 0.001). The exponential time constant was not altered in rIPC‐myocytes at 54.4 ± 2.9 sec (NS).


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)

Intracellular pH in conventional and remotely preconditioned myocytes in response to an NH4Cl acid‐pulse (A) (i) Record of intracellular pH from a control naïve‐myocyte (black trace), conventional IPC‐myocyte (dark gray trace), and remote IPC myocyte (light gray), in response to 20 mmol/L NH4Cl for 5 min. Mean data ± SEM of the rat of recovery of intracellular pH from the acid load induced by the NH4Cl pulse in control naïve myocytes (black), conventional IPC myocytes (dark gray), and remotely conditioned myocytes (light gray). ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control naïve myocytes = 3 hearts; 16 cells, conventional IPC myocytes = 3; 25, remote IPC = 3; 21. (B) (i). Representative record of Fura‐2 ratio from a single control myocytes during MI and reenergization, and (ii). In the presence of amiloride. This result was seen in seven cells from three different hearts.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig06: Intracellular pH in conventional and remotely preconditioned myocytes in response to an NH4Cl acid‐pulse (A) (i) Record of intracellular pH from a control naïve‐myocyte (black trace), conventional IPC‐myocyte (dark gray trace), and remote IPC myocyte (light gray), in response to 20 mmol/L NH4Cl for 5 min. Mean data ± SEM of the rat of recovery of intracellular pH from the acid load induced by the NH4Cl pulse in control naïve myocytes (black), conventional IPC myocytes (dark gray), and remotely conditioned myocytes (light gray). ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control naïve myocytes = 3 hearts; 16 cells, conventional IPC myocytes = 3; 25, remote IPC = 3; 21. (B) (i). Representative record of Fura‐2 ratio from a single control myocytes during MI and reenergization, and (ii). In the presence of amiloride. This result was seen in seven cells from three different hearts.
Mentions: The resting intracellular pH was not affected by IPC or rIPC with a pH of 7.22 ± 0.02 (n = 3; 16) in control myocytes; 7.17 ± 0.02 (n = 3; 25) in IPC‐myocytes, and 7.21 ± 0.05 (n = 3; 21) in rIPC‐myocytes. Addition of NH4Cl (20 mmol/L) to the superfusate caused in a rapid intracellular alkalinization, which on washout of NH4Cl resulted a rapid acidification and the peak acidification was similar in all three myocyte groups (Figure 6A). However, the rate of recovery from the acid load, as determined from the exponential time constant for the recovery, was significantly reduced to 80.1 ± 6.2 sec in IPC‐myocytes from 50.7 ± 2.5 sec in control myocytes (P < 0.001). The exponential time constant was not altered in rIPC‐myocytes at 54.4 ± 2.9 sec (NS).

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