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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

Ca2+‐homeostasis in conventional and remotely preconditioned myocytes subject to MI and reenergization. (A) Simultaneous recordings of [Ca2+]i from (i) seven control myocytes; (ii) nine conventional IPC‐myocytes, and (iii) nine rIPC‐myocytes from a single field of view during metabolic inhibition (8 min) and reenergization (10 min). (B) The mean Fura 2 ratio at the end of 8 min MI and 10 min reenergization for control naïve myocytes (black), conventional IPC‐myocytes (dark gray), and remote IPC‐myocytes (light gray). (C) Percentage of myocytes with a diastolic Fura‐2 ratio <2.0 after 10 min of reenergization. (D) Percentage of myocytes contracting in response to field stimulation after 10 min of reenergization. Mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control myocytes = 6 hearts; 23 observations and 185 myocytes, conventional IPC = 6; 28, and 254, remote IPC = 6; 33, and 315.
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fig03: Ca2+‐homeostasis in conventional and remotely preconditioned myocytes subject to MI and reenergization. (A) Simultaneous recordings of [Ca2+]i from (i) seven control myocytes; (ii) nine conventional IPC‐myocytes, and (iii) nine rIPC‐myocytes from a single field of view during metabolic inhibition (8 min) and reenergization (10 min). (B) The mean Fura 2 ratio at the end of 8 min MI and 10 min reenergization for control naïve myocytes (black), conventional IPC‐myocytes (dark gray), and remote IPC‐myocytes (light gray). (C) Percentage of myocytes with a diastolic Fura‐2 ratio <2.0 after 10 min of reenergization. (D) Percentage of myocytes contracting in response to field stimulation after 10 min of reenergization. Mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control myocytes = 6 hearts; 23 observations and 185 myocytes, conventional IPC = 6; 28, and 254, remote IPC = 6; 33, and 315.

Mentions: Data are presented as mean of the experimental observations ± SEM, with the number of hearts and experimental observation indicated as (n = hearts; experiments). For calculations of percent necrotic cells (Fig. 2), the mean from four randomly selected fields‐of‐view containing >100 cells per experimental observation counted and the mean of this mean reported. For calculation of Fura‐2 ratio and percentage Fura‐2 ratio <2.0, the mean from a field‐of‐view containing 8–12 cells per experimental observation was calculated and for recovery of contractile function the mean from a field‐of‐view containing 15–20 cells calculated, and the mean of these mean reported (Fig. 3). Statistical significance was determined using a one‐way ANOVA with Tukey's post hoc test using GraphPad Prism5. P <0.05 were considered statistically significant.


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)

Ca2+‐homeostasis in conventional and remotely preconditioned myocytes subject to MI and reenergization. (A) Simultaneous recordings of [Ca2+]i from (i) seven control myocytes; (ii) nine conventional IPC‐myocytes, and (iii) nine rIPC‐myocytes from a single field of view during metabolic inhibition (8 min) and reenergization (10 min). (B) The mean Fura 2 ratio at the end of 8 min MI and 10 min reenergization for control naïve myocytes (black), conventional IPC‐myocytes (dark gray), and remote IPC‐myocytes (light gray). (C) Percentage of myocytes with a diastolic Fura‐2 ratio <2.0 after 10 min of reenergization. (D) Percentage of myocytes contracting in response to field stimulation after 10 min of reenergization. Mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control myocytes = 6 hearts; 23 observations and 185 myocytes, conventional IPC = 6; 28, and 254, remote IPC = 6; 33, and 315.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

fig03: Ca2+‐homeostasis in conventional and remotely preconditioned myocytes subject to MI and reenergization. (A) Simultaneous recordings of [Ca2+]i from (i) seven control myocytes; (ii) nine conventional IPC‐myocytes, and (iii) nine rIPC‐myocytes from a single field of view during metabolic inhibition (8 min) and reenergization (10 min). (B) The mean Fura 2 ratio at the end of 8 min MI and 10 min reenergization for control naïve myocytes (black), conventional IPC‐myocytes (dark gray), and remote IPC‐myocytes (light gray). (C) Percentage of myocytes with a diastolic Fura‐2 ratio <2.0 after 10 min of reenergization. (D) Percentage of myocytes contracting in response to field stimulation after 10 min of reenergization. Mean ± SEM; *P < 0.05, **P < 0.01, ***P < 0.001, one‐way ANOVA followed by Tukey's post hoc test for significance. Control myocytes = 6 hearts; 23 observations and 185 myocytes, conventional IPC = 6; 28, and 254, remote IPC = 6; 33, and 315.
Mentions: Data are presented as mean of the experimental observations ± SEM, with the number of hearts and experimental observation indicated as (n = hearts; experiments). For calculations of percent necrotic cells (Fig. 2), the mean from four randomly selected fields‐of‐view containing >100 cells per experimental observation counted and the mean of this mean reported. For calculation of Fura‐2 ratio and percentage Fura‐2 ratio <2.0, the mean from a field‐of‐view containing 8–12 cells per experimental observation was calculated and for recovery of contractile function the mean from a field‐of‐view containing 15–20 cells calculated, and the mean of these mean reported (Fig. 3). Statistical significance was determined using a one‐way ANOVA with Tukey's post hoc test using GraphPad Prism5. P <0.05 were considered statistically significant.

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