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This Article Full Text Full Text (PDF) All Versions of this Article: 90/4/497    most recent expphysiol.2004.029421v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Lu, J. Articles by Jia, B. Search for Related Content PubMed PubMed Citation Articles by Lu, J. Articles by Jia, B. Related Collections Heart/Cardiac Muscle

¹ Department of Pharmacology² Key Laboratory of Environment and Genes Related to Diseases of Ministry of Education, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, China

Conventional ischaemia-mimetic solutions contain several key components for inducing hypoxia, glucose deficiency, acidosis, lactate accumulation and hyperosmosis. The effect of each component on myocyte contractility during cardiac ischaemia was investigated in this study. A video-based edge-detection system was used to monitor single ventricular myocytes isolated from the rat. The effect of each factor was compared by preparing the following ischaemia-mimetic solutions: solution A, containing all of the above-mentioned factors; and solutions B, C, D, E and F, each with one of the factors excluded. The solutions that contained lactate severely reduced the contractility of the cardiomyocytes, but cell contraction did not differ significantly between the cardiomyocytes in these solutions. The effect of the solution without the acidosis-inducing component was weaker than that of the conventional ischaemia-mimetic solution. The solution lacking lactate produced the least depression of cell contractility. Lactate impaired cardiomyocyte contractility in a concentration-dependent manner. Our observations suggest that lactate is the main contributor to cardiac ischaemic injury and that its effects are attributable to acidosis and are concentration dependent. Imposition of hypoxia, glucose deficiency and hyperosmosis had little impact on the cardiomyocytes.

(Received 26 October 2004; accepted after revision 11 February 2005; first published online 11 February 2005)
Corresponding author W.-J. Zang: Department of Pharmacology, School of Medicine, Xi'an Jiaotong University, Xi'an, 710061, People's Republic of China. Email: zwj{at}mail.xjtu.edu.cn