Gutman, I. and Wahlenfeld, A.W.L. (1963) L-(+)-lactate. determination with LDH and NAD. In: Bergmeyer, H.U., Ed., Methods of Enzymatic Analysis, Academic Press, New York, 1464-1467.

has been cited by the following article:

• TITLE: Nitric oxide synthase mediates the apelin-induced improvement of myocardial postischemic metabolic and functional recovery

  AUTHORS: Oleg I. Pisarenko, Yulia A. Pelogeykina, Valentin S. Shulzhenko, Irina M. Studneva

  KEYWORDS: Apelin; Heart; Ischemia/Reperfusion Injury; L-NAME; Energy Metabolism

  JOURNAL NAME: Open Journal of Molecular and Integrative Physiology, Vol.2 No.1, February 17, 2012

  ABSTRACT: The adipocytokine apelin is capable to reduce myocardial ischemia/reperfusion injury in rodents. Cardioprotective activity of apelin may be attributed to upregulation of endothelial nitric oxide synthase (eNOS). This study was designed to examine metabolic and functional effects of a synthesized 12 C-terminal residue of apelin (A-12) and NG-nitro-L-arginine methyl ester (L-NAME), a non-selective eNOS inhibitor, in isolated working rat hearts subjected to global ischemia. Preischemic infusion of A-12 increased recovery of cardiac function during reperfusion compared with control and resulted in enhanced restoration of myocardial ATP, adenine nucleotide pool, phosphocreatine and reduction of myocardial lactate and lactate/pyruvate ratio. Coadministration of A-12 and L-NAME aggravated recovery of coronary flow and cardiac function compared with these indices after A-12 treatment. Cardiac dysfunction was associated with increase in lactate dehydrogenase release in myocardial effluent, reduction of glucose oxidation and abolishment of augmented restoration of high energy phosphates. The results clearly demonstrate involvement of NOS-dependent mechanisms in cardioprotection afforded by apelin.