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Showing 1 to 12 of 13 entries
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Ischemic injury of the developing heart.

Experimental and clinical cardiology

Ost'ádal B, Ost'ádalová I, Skárka L, Kolár F, Kopecký J.
PMID: 19649230
Exp Clin Cardiol. 2002;7(2):93-8.

CARDIAC TOLERANCE TO ISCHEMIA CHANGES SIGNIFICANTLY DURING ONTOGENETIC DEVELOPMENT: the immature heart appears to be more resistant to ischemic injury than the adult myocardium. The mechanisms of the higher tolerance of the developing heart have not yet been satisfactorily...

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Ost'ádal B, Ost'ádalová I, Skárka L, et al. Ischemic injury of the developing heart. Exp Clin Cardiol. 2002;7(2):93-8
Ost'ádal, B., Ost'ádalová, I., Skárka, L., Kolár, F., & Kopecký, J. (2002). Ischemic injury of the developing heart. Experimental and clinical cardiology, 7(2), 93-8.
Ost'ádal, Bohuslav, et al. "Ischemic injury of the developing heart." Experimental and clinical cardiology vol. 7,2 (2002): 93-8.
Ost'ádal B, Ost'ádalová I, Skárka L, Kolár F, Kopecký J. Ischemic injury of the developing heart. Exp Clin Cardiol. 2002;7(2):93-8. PMID: 19649230; PMCID: PMC2719176.
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Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial K(ATP) channels in mouse cardiomyocytes.

The Journal of clinical investigation

[No authors listed]
PMID: 23202740
J Clin Invest. 2012 Dec;122(12):4748. doi: 10.1172/JCI67553. Epub 2012 Dec 03.

No abstract available.

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Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial K(ATP) channels in mouse cardiomyocytes. J Clin Invest. 2012;122(12):4748doi: 10.1172/JCI67553.
(2012). Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial K(ATP) channels in mouse cardiomyocytes. The Journal of clinical investigation, 122(12), 4748. https://doi.org/10.1172/JCI67553
"Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial K(ATP) channels in mouse cardiomyocytes." The Journal of clinical investigation vol. 122,12 (2012): 4748. doi: https://doi.org/10.1172/JCI67553
Connexin 43 acts as a cytoprotective mediator of signal transduction by stimulating mitochondrial K(ATP) channels in mouse cardiomyocytes. J Clin Invest. 2012 Dec;122(12):4748. doi: 10.1172/JCI67553. Epub 2012 Dec 03. PMID: 23202740; PMCID: PMC3533571.
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Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury.

Experimental and clinical cardiology

Watanabe M, Wu J, Li S, Li C, Okada T.
PMID: 19641723
Exp Clin Cardiol. 2004;9(3):181-5.

During cardiac ischemia or hypoxia, increased levels of extracellular Mg show cardioprotective effects. The mechanisms of high level Mg-induced cardioprotection were examined in Langendorff perfused rat hearts. In the control group (1.2 mM Mg during hypoxia), the recovery of...

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Watanabe M, Wu J, Li S, et al. Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury. Exp Clin Cardiol. 2004;9(3):181-5
Watanabe, M., Wu, J., Li, S., Li, C., & Okada, T. (2004). Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury. Experimental and clinical cardiology, 9(3), 181-5.
Watanabe, Makino, et al. "Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury." Experimental and clinical cardiology vol. 9,3 (2004): 181-5.
Watanabe M, Wu J, Li S, Li C, Okada T. Mechanisms of cardioprotective effects of magnesium on hypoxia-reoxygenation-induced injury. Exp Clin Cardiol. 2004;9(3):181-5. PMID: 19641723; PMCID: PMC2716744.
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Pharmacological preconditioning with diazoxide slows energy metabolism during sustained ischemia.

Experimental and clinical cardiology

Schwartz LM, Reimer KA, Crago MS, Jennings RB.
PMID: 18650995
Exp Clin Cardiol. 2007;12(3):139-47.

Ischemic preconditioning (PC) is associated with slower destruction of the adenine nucleotide pool ( summation operatorAd) and slower rate of anaerobic glycolysis during ischemic stress. These changes are concordant with the preconditioned state, supporting an essential role of lowered...

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Schwartz LM, Reimer KA, Crago MS, et al. Pharmacological preconditioning with diazoxide slows energy metabolism during sustained ischemia. Exp Clin Cardiol. 2007;12(3):139-47
Schwartz, L. M., Reimer, K. A., Crago, M. S., & Jennings, R. B. (2007). Pharmacological preconditioning with diazoxide slows energy metabolism during sustained ischemia. Experimental and clinical cardiology, 12(3), 139-47.
Schwartz, Lisa M, et al. "Pharmacological preconditioning with diazoxide slows energy metabolism during sustained ischemia." Experimental and clinical cardiology vol. 12,3 (2007): 139-47.
Schwartz LM, Reimer KA, Crago MS, Jennings RB. Pharmacological preconditioning with diazoxide slows energy metabolism during sustained ischemia. Exp Clin Cardiol. 2007;12(3):139-47. PMID: 18650995; PMCID: PMC2323755.
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Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion.

Pathophysiology : the official journal of the International Society for Pathophysiology

Krenz M, Cohen MV, Downey JM.
PMID: 15006417
Pathophysiology. 2004 Apr;10(2):113-9. doi: 10.1016/j.pathophys.2003.10.006.

Epidemiological data suggest that a cardioprotective effect of acute alcohol exposure exists in humans. Recent studies in animal models indicate that transient alcohol exposure can indeed reduce myocardial infarct size and exert a preconditioning-like protective effect akin to ischemic...

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Krenz M, Cohen MV, Downey JM. Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion. Pathophysiology. 2004;10(2):113-9doi: 10.1016/j.pathophys.2003.10.006.
Krenz, M., Cohen, M. V., & Downey, J. M. (2004). Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion. Pathophysiology : the official journal of the International Society for Pathophysiology, 10(2), 113-9. https://doi.org/10.1016/j.pathophys.2003.10.006
Krenz, Maike, et al. "Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion." Pathophysiology : the official journal of the International Society for Pathophysiology vol. 10,2 (2004): 113-9. doi: https://doi.org/10.1016/j.pathophys.2003.10.006
Krenz M, Cohen MV, Downey JM. Protective and anti-protective effects of acute ethanol exposure in myocardial ischemia/reperfusion. Pathophysiology. 2004 Apr;10(2):113-9. doi: 10.1016/j.pathophys.2003.10.006. PMID: 15006417.
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The effect of mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat.

Korean journal of anesthesiology

Park YS, Bang JY, Hwang BY, Ryu HY, Jeong SM, Park PH.
PMID: 30625957
Korean J Anesthesiol. 2009 Dec;57(6):729-736. doi: 10.4097/kjae.2009.57.6.729.

BACKGROUND: A brief episode of cerebral ischemia confers transient ischemic tolerance to a subsequent ischemic challenge that is otherwise lethal to them. This study was purposed to evaluate the effect of mitochondrial adenosine triphosphate-sensitive potassium (KATP) channel blocker on...

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Park YS, Bang JY, Hwang BY, et al. The effect of mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat. Korean J Anesthesiol. 2009;57(6):729-736doi: 10.4097/kjae.2009.57.6.729.
Park, Y. S., Bang, J. Y., Hwang, B. Y., Ryu, H. Y., Jeong, S. M., & Park, P. H. (2009). The effect of mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat. Korean journal of anesthesiology, 57(6), 729-736. https://doi.org/10.4097/kjae.2009.57.6.729
Park, Young Soo, et al. "The effect of mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat." Korean journal of anesthesiology vol. 57,6 (2009): 729-736. doi: https://doi.org/10.4097/kjae.2009.57.6.729
Park YS, Bang JY, Hwang BY, Ryu HY, Jeong SM, Park PH. The effect of mitochondrial adenosine triphosphate-sensitive potassium (K(ATP)) channel blocker on ischemic preconditioning in hypoxic-ischemic brain injury model of neonatal rat. Korean J Anesthesiol. 2009 Dec;57(6):729-736. doi: 10.4097/kjae.2009.57.6.729. PMID: 30625957.
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The mitochondrial K-ATP channel opener diazoxide upregulates STIM1 and Orai1 via ROS and the MAPK pathway in adult rat cardiomyocytes.

Cell & bioscience

Gavali JT, Carrillo ED, García MC, Sánchez JA.
PMID: 32817784
Cell Biosci. 2020 Aug 13;10:96. doi: 10.1186/s13578-020-00460-w. eCollection 2020.

BACKGROUND: Openers of mitochondrial adenosine triphosphate-dependent potassium (mKATP) channels like diazoxide increase reactive oxygen species (ROS) production in cardiac cells and reduce CaRESULTS: Quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and western blot experiments showed that diazoxide increased expression...

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Gavali JT, Carrillo ED, García MC, et al. The mitochondrial K-ATP channel opener diazoxide upregulates STIM1 and Orai1 via ROS and the MAPK pathway in adult rat cardiomyocytes. Cell Biosci. 2020;10:96doi: 10.1186/s13578-020-00460-w.
Gavali, J. T., Carrillo, E. D., García, M. C., & Sánchez, J. A. (2020). The mitochondrial K-ATP channel opener diazoxide upregulates STIM1 and Orai1 via ROS and the MAPK pathway in adult rat cardiomyocytes. Cell & bioscience, 1096. https://doi.org/10.1186/s13578-020-00460-w
Gavali, Joice T, et al. "The mitochondrial K-ATP channel opener diazoxide upregulates STIM1 and Orai1 via ROS and the MAPK pathway in adult rat cardiomyocytes." Cell & bioscience vol. 10 (2020): 96. doi: https://doi.org/10.1186/s13578-020-00460-w
Gavali JT, Carrillo ED, García MC, Sánchez JA. The mitochondrial K-ATP channel opener diazoxide upregulates STIM1 and Orai1 via ROS and the MAPK pathway in adult rat cardiomyocytes. Cell Biosci. 2020 Aug 13;10:96. doi: 10.1186/s13578-020-00460-w. eCollection 2020. PMID: 32817784; PMCID: PMC7424994.
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Role of opioid delta1 receptors, mitochondrial K(ATP) channels, and protein kinase C during cardiocyte apoptosis.

Journal of molecular and cellular cardiology

Liu H, Zhang HY, McPherson BC, Baman T, Roth S, Shao Z, Zhu X, Yao Z.
PMID: 14703685
J Mol Cell Cardiol. 2003 Mar;35(3):337. doi: 10.1016/s0022-2828(02)00314-0.

No abstract available.

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Liu H, Zhang HY, McPherson BC, et al. Role of opioid delta1 receptors, mitochondrial K(ATP) channels, and protein kinase C during cardiocyte apoptosis. J Mol Cell Cardiol. 2003;35(3):337doi: 10.1016/s0022-2828(02)00314-0.
Liu, H., Zhang, H. Y., McPherson, B. C., Baman, T., Roth, S., Shao, Z., Zhu, X., & Yao, Z. (2003). Role of opioid delta1 receptors, mitochondrial K(ATP) channels, and protein kinase C during cardiocyte apoptosis. Journal of molecular and cellular cardiology, 35(3), 337. https://doi.org/10.1016/s0022-2828(02)00314-0
Liu, H, et al. "Role of opioid delta1 receptors, mitochondrial K(ATP) channels, and protein kinase C during cardiocyte apoptosis." Journal of molecular and cellular cardiology vol. 35,3 (2003): 337. doi: https://doi.org/10.1016/s0022-2828(02)00314-0
Liu H, Zhang HY, McPherson BC, Baman T, Roth S, Shao Z, Zhu X, Yao Z. Role of opioid delta1 receptors, mitochondrial K(ATP) channels, and protein kinase C during cardiocyte apoptosis. J Mol Cell Cardiol. 2003 Mar;35(3):337. doi: 10.1016/s0022-2828(02)00314-0. PMID: 14703685.
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Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats.

Experimental and therapeutic medicine

Liu ML, Wang ML, Lv JJ, Wei J, Wan J.
PMID: 29545864
Exp Ther Med. 2018 Apr;15(4):3425-3431. doi: 10.3892/etm.2018.5862. Epub 2018 Feb 13.

Adriamycin (ADR) is a chemotherapeutic drug used to treat tumors in a clinical setting. However, its use is limited by a side effect of cardiotoxicity. Glibenclamide (Gli), an inhibitor of mitochondrial ATP-dependent potassium (K-ATP) channels, blocks the cardioprotective effects...

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Liu ML, Wang ML, Lv JJ, et al. Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats. Exp Ther Med. 2018;15(4):3425-3431doi: 10.3892/etm.2018.5862.
Liu, M. L., Wang, M. L., Lv, J. J., Wei, J., & Wan, J. (2018). Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats. Experimental and therapeutic medicine, 15(4), 3425-3431. https://doi.org/10.3892/etm.2018.5862
Liu, Meng-Lin, et al. "Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats." Experimental and therapeutic medicine vol. 15,4 (2018): 3425-3431. doi: https://doi.org/10.3892/etm.2018.5862
Liu ML, Wang ML, Lv JJ, Wei J, Wan J. Glibenclamide exacerbates adriamycin-induced cardiotoxicity by activating oxidative stress-induced endoplasmic reticulum stress in rats. Exp Ther Med. 2018 Apr;15(4):3425-3431. doi: 10.3892/etm.2018.5862. Epub 2018 Feb 13. PMID: 29545864; PMCID: PMC5840948.
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Ex-vivo effect of roxithromycin on human and rat arterial vasoactivity.

Interactive cardiovascular and thoracic surgery

Berman M, Hasdai D, Raanani E, Georghiou GP, Kapustin L, Chepurko Y, Vidne BA, Hochhauser E.
PMID: 17670399
Interact Cardiovasc Thorac Surg. 2005 Jun;4(3):232-7. doi: 10.1510/icvts.2004.095505. Epub 2005 Mar 29.

BACKGROUND: Prior studies have suggested that inflammation and possibly bacterial infections play a role in atherogenesis and in the clinical pathogenesis of cardiovascular diseases. Treatment with the macrolide antibiotics has been associated with improved outcome from cardiovascular disease, although...

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Berman M, Hasdai D, Raanani E, et al. Ex-vivo effect of roxithromycin on human and rat arterial vasoactivity. Interact Cardiovasc Thorac Surg. 2005;4(3):232-7doi: 10.1510/icvts.2004.095505.
Berman, M., Hasdai, D., Raanani, E., Georghiou, G. P., Kapustin, L., Chepurko, Y., Vidne, B. A., & Hochhauser, E. (2005). Ex-vivo effect of roxithromycin on human and rat arterial vasoactivity. Interactive cardiovascular and thoracic surgery, 4(3), 232-7. https://doi.org/10.1510/icvts.2004.095505
Berman, Marius, et al. "Ex-vivo effect of roxithromycin on human and rat arterial vasoactivity." Interactive cardiovascular and thoracic surgery vol. 4,3 (2005): 232-7. doi: https://doi.org/10.1510/icvts.2004.095505
Berman M, Hasdai D, Raanani E, Georghiou GP, Kapustin L, Chepurko Y, Vidne BA, Hochhauser E. Ex-vivo effect of roxithromycin on human and rat arterial vasoactivity. Interact Cardiovasc Thorac Surg. 2005 Jun;4(3):232-7. doi: 10.1510/icvts.2004.095505. Epub 2005 Mar 29. PMID: 17670399.
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Clinical application of ischemic preconditioning in the elderly.

Dose-response : a publication of International Hormesis Society

Abete P, Cacciatore F, Testa G, Della-Morte D, Galizia G, Ferrara N, Rengo F.
PMID: 20221286
Dose Response. 2009 Oct 16;8(1):34-40. doi: 10.2203/dose-response.09-023.Abete.

A mild stress such as brief ischemic episodes may protect the heart from a successive and more prolonged myocardial ischemia (ischemic preconditioning). This phenomenon is considered a typical "hormetic mechanism" by which the heart is immunized from pathological insults...

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Abete P, Cacciatore F, Testa G, et al. Clinical application of ischemic preconditioning in the elderly. Dose Response. 2009;8(1):34-40doi: 10.2203/dose-response.09-023.Abete.
Abete, P., Cacciatore, F., Testa, G., Della-Morte, D., Galizia, G., Ferrara, N., & Rengo, F. (2009). Clinical application of ischemic preconditioning in the elderly. Dose-response : a publication of International Hormesis Society, 8(1), 34-40. https://doi.org/10.2203/dose-response.09-023.Abete
Abete, Pasquale, et al. "Clinical application of ischemic preconditioning in the elderly." Dose-response : a publication of International Hormesis Society vol. 8,1 (2009): 34-40. doi: https://doi.org/10.2203/dose-response.09-023.Abete
Abete P, Cacciatore F, Testa G, Della-Morte D, Galizia G, Ferrara N, Rengo F. Clinical application of ischemic preconditioning in the elderly. Dose Response. 2009 Oct 16;8(1):34-40. doi: 10.2203/dose-response.09-023.Abete. PMID: 20221286; PMCID: PMC2836158.
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Insights into the cardioprotective function of adenosine A(1) and A(3) receptors.

Experimental and clinical cardiology

Shneyvays V, Mamedova LK, Leshem D, Korkus A, Shainberg A.
PMID: 19649238
Exp Clin Cardiol. 2002;7(2):138-45.

OBJECTIVES: Cardioprotection (delaying of irreversible damage in hypoxia or prevention of doxorubicin [DOX] toxicity) is achieved by increasing the energy supply, or decreasing the energy demand in the cell and may be regulated through adenosine (ADO) receptor (AR) signalling....

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Shneyvays V, Mamedova LK, Leshem D, et al. Insights into the cardioprotective function of adenosine A(1) and A(3) receptors. Exp Clin Cardiol. 2002;7(2):138-45
Shneyvays, V., Mamedova, L. K., Leshem, D., Korkus, A., & Shainberg, A. (2002). Insights into the cardioprotective function of adenosine A(1) and A(3) receptors. Experimental and clinical cardiology, 7(2), 138-45.
Shneyvays, Vladimir, et al. "Insights into the cardioprotective function of adenosine A(1) and A(3) receptors." Experimental and clinical cardiology vol. 7,2 (2002): 138-45.
Shneyvays V, Mamedova LK, Leshem D, Korkus A, Shainberg A. Insights into the cardioprotective function of adenosine A(1) and A(3) receptors. Exp Clin Cardiol. 2002;7(2):138-45. PMID: 19649238; PMCID: PMC2719165.
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