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Nitrate tolerance aggravates postischemic myocardial apoptosis and impairs cardiac functional recovery after ischemia.
Apoptosis. 2005 Dec; 10(6):1235-42.A

Abstract

OBJECTIVES

This study examined the effects of nitrate tolerance (NT) on myocardial ischemia reperfusion (MI/R) injury and elucidated the potential mechanisms involved. Furthermore, the effects of GSH on postischemic myocardial apoptosis in NT rats were investigated.

METHODS AND RESULTS

Male Sprague-Dawley rats were randomized to receive nitroglycerin (60 microg/kg/h) or saline for 12 h followed by 40 min of MI and 4 h of reperfusion. Myocardial apoptosis, infarct size, nitrotyrosine formation, plasma CK and LDH activity, and cardiac function were determined. MI/R resulted in significant apoptotic cell death, which was further increased in animals with NT. In addition, NT further increased plasma CK and LDH activity, enlarged infarct size, and impaired cardiac functional recovery after ischemia. Myocardial nitrotyrosine, a footprint for cytotoxic reactive nitrogen species formation, was further enhanced in the NT heart after MI/R. Treatment of NT animals with exogenous GSH inhibited nitrotyrosine formation, reduced apoptosis, decreased infarct size, and improved cardiac functional recovery.

CONCLUSION

Our results demonstrate that nitrate tolerance markedly enhances MI/R injury and that increased peroxynitrite formation likely plays a role in this pathologic process. In addition, our results suggest that GSH could decrease peroxynitrite formation and reduce MI/R injury in nitrate tolerant hearts.

Authors+Show Affiliations

Department of Physiology, Fourth Military Medical University, Xi-An, PR China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16215686

Citation

Fan, Q, et al. "Nitrate Tolerance Aggravates Postischemic Myocardial Apoptosis and Impairs Cardiac Functional Recovery After Ischemia." Apoptosis : an International Journal On Programmed Cell Death, vol. 10, no. 6, 2005, pp. 1235-42.
Fan Q, Gao F, Zhang L, et al. Nitrate tolerance aggravates postischemic myocardial apoptosis and impairs cardiac functional recovery after ischemia. Apoptosis. 2005;10(6):1235-42.
Fan, Q., Gao, F., Zhang, L., Christopher, T. A., Lopez, B. L., & Ma, X. L. (2005). Nitrate tolerance aggravates postischemic myocardial apoptosis and impairs cardiac functional recovery after ischemia. Apoptosis : an International Journal On Programmed Cell Death, 10(6), 1235-42.
Fan Q, et al. Nitrate Tolerance Aggravates Postischemic Myocardial Apoptosis and Impairs Cardiac Functional Recovery After Ischemia. Apoptosis. 2005;10(6):1235-42. PubMed PMID: 16215686.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Nitrate tolerance aggravates postischemic myocardial apoptosis and impairs cardiac functional recovery after ischemia. AU - Fan,Q, AU - Gao,F, AU - Zhang,L, AU - Christopher,T A, AU - Lopez,B L, AU - Ma,X L, PY - 2005/10/11/pubmed PY - 2008/3/26/medline PY - 2005/10/11/entrez SP - 1235 EP - 42 JF - Apoptosis : an international journal on programmed cell death JO - Apoptosis VL - 10 IS - 6 N2 - OBJECTIVES: This study examined the effects of nitrate tolerance (NT) on myocardial ischemia reperfusion (MI/R) injury and elucidated the potential mechanisms involved. Furthermore, the effects of GSH on postischemic myocardial apoptosis in NT rats were investigated. METHODS AND RESULTS: Male Sprague-Dawley rats were randomized to receive nitroglycerin (60 microg/kg/h) or saline for 12 h followed by 40 min of MI and 4 h of reperfusion. Myocardial apoptosis, infarct size, nitrotyrosine formation, plasma CK and LDH activity, and cardiac function were determined. MI/R resulted in significant apoptotic cell death, which was further increased in animals with NT. In addition, NT further increased plasma CK and LDH activity, enlarged infarct size, and impaired cardiac functional recovery after ischemia. Myocardial nitrotyrosine, a footprint for cytotoxic reactive nitrogen species formation, was further enhanced in the NT heart after MI/R. Treatment of NT animals with exogenous GSH inhibited nitrotyrosine formation, reduced apoptosis, decreased infarct size, and improved cardiac functional recovery. CONCLUSION: Our results demonstrate that nitrate tolerance markedly enhances MI/R injury and that increased peroxynitrite formation likely plays a role in this pathologic process. In addition, our results suggest that GSH could decrease peroxynitrite formation and reduce MI/R injury in nitrate tolerant hearts. SN - 1360-8185 UR - https://www.unboundmedicine.com/medline/citation/16215686/Nitrate_tolerance_aggravates_postischemic_myocardial_apoptosis_and_impairs_cardiac_functional_recovery_after_ischemia_ L2 - https://doi.org/10.1007/s10495-005-1455-5 DB - PRIME DP - Unbound Medicine ER -