Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43
Abstract
:1. Introduction
2. Results
2.1. Electrophysiological Effects of IPoC in Isolated Rat Hearts Submitted to Regional Ischemia
2.2. Connexin 43 Is Not Essential for IPoC Effects in Isolated Mice Hearts Submitted to Global Myocardial Ischemia
2.3. Adenosine Receptors and PKC Activations, but Not KATP Channels, Are Needed for IPoC Antiarrhythmic Protection
2.4. Adenosine Intermitet (ADOi) Administration during Reperfusion Reproduced Some of the Electrophysiological Effects of IPoC
3. Discussion
4. Materials and Methods
4.1. Animal Models
4.2. Experimental Protocols
4.3. Electrophysiological Studies
4.3.1. Arrhythmias
4.3.2. Electrograms and Action Potentials
4.3.3. Impedance
4.4. Intercellular Chemical Communication
4.5. Statistical Analysis
5. Conclusions
Author Contributions
Funding
Acknowledgments
Conflicts of Interest
Abbreviations
APD | action potential duration |
IPoC | ischemic postconditioning |
PKC | protein kinase C |
KATP | ATP-dependent potassium channels |
Cx32 | connexin 32 |
Cx43 | connexin 43 |
CPT | adenosine A1 receptor antagonist, cyclopentyl theophylline |
SCH | adenosine A2A receptor antagonist, SCH 58261 |
MRS | adenosine A3 receptor antagonist, MRS-1523 |
GLI | non selective KATP blocker, glibenclamide |
LY | Licifer Yellow |
RD | Rhodamine |
References
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Experimental Groups | Ventricular Tachycardia | Ventricular Fibrillation |
---|---|---|
Control | 45.0 (10–142) | 476.0 (198–555) |
IPoC | 17.0 (3–146) | 5.0 (0–115) ** |
CPT | 11.0 (0–41) | 459.0 (228–555) |
IPoC + CPT | 68.0 (28–235) | 250.5 (121–291) |
DMSO | 45.0 (24–123) | 529.0 (205–582) |
IPoCd | 27.5 (3–146) | 10.5 (0–141) ** |
SCH | 50.5 (33–110) | 398.5 (124–460) |
IPoC + SCH | 64.0 (25–128) | 282.0 (112–505) |
MRS | 35.0 (8–99) | 520.0 (233–563) |
IPoC + MRS | 82.5 (20–186) | 263.0 (0–415) |
CHE | 41.0 (20–51) | 467.5 (295–545) |
IPoC + CHE | 71.5 (38–133) | 360.0 (224–460) |
GLI | 401.0 (260–542) ** | 61.5 (18–75) * |
IPoC + GLI | 33.5 (12–63) | 66.0 (12–90) * |
ADOi10 | 141.0 (60–242) | 91.5 (30–135) * |
ADOi100 | 120.5 (22–195) | 66.5 (0–106) * |
GIPoC | 39.5 (18–87) | 48.0 (0–78) ** |
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Diez, E.R.; Sánchez, J.A.; Prado, N.J.; Ponce Zumino, A.Z.; García-Dorado, D.; Miatello, R.M.; Rodríguez-Sinovas, A. Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43. Int. J. Mol. Sci. 2019, 20, 5927. https://doi.org/10.3390/ijms20235927
Diez ER, Sánchez JA, Prado NJ, Ponce Zumino AZ, García-Dorado D, Miatello RM, Rodríguez-Sinovas A. Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43. International Journal of Molecular Sciences. 2019; 20(23):5927. https://doi.org/10.3390/ijms20235927
Chicago/Turabian StyleDiez, Emiliano Raúl, Jose Antonio Sánchez, Natalia Jorgelina Prado, Amira Zulma Ponce Zumino, David García-Dorado, Roberto Miguel Miatello, and Antonio Rodríguez-Sinovas. 2019. "Ischemic Postconditioning Reduces Reperfusion Arrhythmias by Adenosine Receptors and Protein Kinase C Activation but Is Independent of KATP Channels or Connexin 43" International Journal of Molecular Sciences 20, no. 23: 5927. https://doi.org/10.3390/ijms20235927