Literature DB >> 8324803

Adenosine slows ischaemic metabolism in canine myocardium in vitro: relationship to ischaemic preconditioning.

R S Vander Heide1, K A Reimer, R B Jennings.   

Abstract

OBJECTIVE: Studies in rabbits suggest that the cardioprotective effects of adenosine against lethal cell injury may be related to production of adenosine and subsequent activation of adenosine A1 receptors. However, it is not known whether intracoronary adenosine therapy can mimic the metabolic sparing effects of preconditioning in rabbits or dogs. The purpose of this study was to determine the effect of intracoronary adenosine on ischaemic metabolism in totally ischaemic canine myocardium.
METHODS: Dog hearts (n = 13) were excised and the coronary arteries were perfused with an oxygenated Krebs' buffer containing glucose. Adenosine was added to the buffer perfusing the circumflex (treated) region. Following perfusion, control and treated beds from each heart were subjected to 90 min total ischaemia at 37 degrees C. Tissue levels of ATP and glycolytic intermediates were determined at several time points during the ischaemic incubation.
RESULTS: Adenosine significantly slowed the rate of ATP depletion, glycogen utilisation, and lactate accumulation during the first 20 minutes of total ischaemia.
CONCLUSIONS: The results suggest that adenosine is capable of slowing ischaemic metabolism and they are consistent with the hypothesis that adenosine may mediate ischaemic preconditioning.

Entities:  

Mesh:

Substances:

Year:  1993        PMID: 8324803     DOI: 10.1093/cvr/27.4.669

Source DB:  PubMed          Journal:  Cardiovasc Res        ISSN: 0008-6363            Impact factor:   10.787


  7 in total

1.  Loss of glycogen during preconditioning is not a prerequisite for protection of the rabbit heart.

Authors:  C Weinbrenner; P Wang; J M Downey
Journal:  Basic Res Cardiol       Date:  1996 Sep-Oct       Impact factor: 17.165

2.  Differential cardioprotection with selective inhibitors of adenosine metabolism and transport: role of purine release in ischemic and reperfusion injury.

Authors:  A S Abd-Elfattah; M E Jessen; J Lekven; A S Wechsler
Journal:  Mol Cell Biochem       Date:  1998-03       Impact factor: 3.396

3.  Suppression of the degradation of adenine nucleotides during ischemia may not be a sufficient mechanism for infarct size limitation by preconditioning.

Authors:  T Miura; K Suzuki; K Shimamoto; O Iimura
Journal:  Basic Res Cardiol       Date:  1996 Nov-Dec       Impact factor: 17.165

Review 4.  Biochemical dysfunction in heart mitochondria exposed to ischaemia and reperfusion.

Authors:  Giancarlo Solaini; David A Harris
Journal:  Biochem J       Date:  2005-09-01       Impact factor: 3.857

5.  Involvement of ATP-sensitive potassium channels in preconditioning protection.

Authors:  S Rohmann; H Weygandt; P Schelling; L Kie Soei; P D Verdouw; I Lues
Journal:  Basic Res Cardiol       Date:  1994 Nov-Dec       Impact factor: 17.165

6.  Reductions in mitochondrial O(2) consumption and preservation of high-energy phosphate levels after simulated ischemia in chronic hibernating myocardium.

Authors:  Qingsong Hu; Gen Suzuki; Rebeccah F Young; Brian J Page; James A Fallavollita; John M Canty
Journal:  Am J Physiol Heart Circ Physiol       Date:  2009-04-24       Impact factor: 4.733

7.  Attenuation of the antiarrhythmic effects of ischaemic preconditioning by blockade of bradykinin B2 receptors.

Authors:  A Vegh; J G Papp; J Parratt
Journal:  Br J Pharmacol       Date:  1994-12       Impact factor: 8.739

  7 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.