Meng, Xianzhong, Brian D. Shames, Edward J. Pulido, Daniel R. Meldrum, Lihua Ao, Kyung S. Joo, Alden H. Harken, and Anirban Banerjee. Adrenergic induction of bimodal myocardial protection: signal transduction and cardiac gene reprogramming. Am. J. Physiol. 276 (Regulatory Integrative Comp. Physiol. 45): R1525–R1533, 1999.—This study tested the hypothesis that in vivo norepinephrine (NE) treatme...

Background—Tumor necrosis factor (TNF)-a has been implicated in the pathogenesis of heart failure and ischemiareperfusion injury. Effects of TNF-a are initiated by membrane receptors coupled to sphingomyelinase signaling and include altered metabolism and calcium cycling, contractile dysfunction, and cell death. We postulate that pressureoverload hypertrophy results in increased myocardial TNF-...

Okubo, Shinji, Yujirou Tanabe, Kenji Takeda, Michihiko Kitayama, Seiyu Kanemitsu, Rakesh C. Kukreja, and Noboru Takekoshi. Ischemic preconditioning and morphine attenuate myocardial apoptosis and infarction after ischemia-reperfusion in rabbits: role of -opioid receptor. Am J Physiol Heart Circ Physiol 287: H1786–H1791, 2004; 10.1152/ajpheart.01143.2003.—We examined whether ischemic preconditio...

Kuzume, Koh, Kazuyo Kuzume, Zhiping Cao, Lijuan Liu, and Donna M. Van Winkle. Long-term infusion of Met-enkephalin fails to protect murine hearts against ischemia-reperfusion injury. Am J Physiol Heart Circ Physiol 288: H1717–H1723, 2005. First published November 18, 2004; doi:10.1152/ajpheart.00257.2004.—Recently, we reported that exogenous administration of Met-enkephalin (ME) for 24 h reduce...

Wang M, Zhang W, Crisostomo P, Markel T, Meldrum KK, Fu XY, Meldrum DR. Endothelial STAT3 plays a critical role in generalized myocardial proinflammatory and proapoptotic signaling. Am J Physiol Heart Circ Physiol 293: H2101–H2108, 2007. First published August 3, 2007; doi:10.1152/ajpheart.00125.2007.—Signal transducer and activator of transcription (STAT) 3 is involved in mediating a broad ran...

Sambandam, Nandakumar, Dominique Morabito, Cory Wagg, Brian N. Finck, Daniel P. Kelly, and Gary D. Lopaschuk. Chronic activation of PPAR is detrimental to cardiac recovery after ischemia. Am J Physiol Heart Circ Physiol 290: H87–H95, 2006. First published September 9, 2005; doi:10.1152/ajpheart.00285.2005.— High fatty acid oxidation (FAO) rates contribute to ischemia-reperfusion injury of the m...

Wang, Lianguo, Gennady Cherednichenko, Lisa Hernandez, Jessica Halow, S. Albert Camacho, Vincent Figueredo, and Saul Schaefer. Preconditioning limits mitochondrial Ca21 during ischemia in rat hearts: role of KATP channels. Am J Physiol Heart Circ Physiol 280: H2321–H2328, 2001.—Prolonged myocardial ischemia results in an increase in intracellular calcium concentration ([Ca]i), which is thought ...

Zou, Lei, Bashir Attuwaybi, and Bruce C. Kone. Effects of NKB inhibition on mesenteric ischemia-reperfusion injury. Am J Physiol Gastrointest Liver Physiol 284: G713–G721, 2003. First published December 4, 2002; 10.1152/ ajpgi.00431.2002.—Mesenteric ischemia-reperfusion injury is a serious complication of shock. Because activation of nuclear factorB (NFB) has been implicated in this process, we...

TO THE EDITOR: We read with great interest, in the American Journal of Physiology-Heart and Circulatory Physiology, the article by Ge and colleagues (3) regarding neutrophil extracellular trap (NET)-induced myocardial no-reflow in ischemiareperfusion (I/R) injury. The authors demonstrated that NET formation was detected in I/R-challenged myocardium of animal model, and the combination treatment...

Virtually all cells exhibit metabolic flexibility and are capable of shifting their reliance on glycolysis relative to mitochondrial respiration. Such shifts can occur at different timescales through a variety of mechanisms, allowing cells to cope with prevailing nutrient availability or energetic demands. There is mounting evidence of the therapeutic potential of targeting such shifts. For exa...