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Basic Res Cardiol. 2000 Jun;95(3):243-9.

Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP.

Author information

1
The Hatter Institute, Department of Academic and Clinical Cardiology, University College Hospitals and Medical School, London, UK.

Abstract

Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel.

RESULTS:

PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 +/- 1.1%, ADO: 11.9 +/- 2.0% vs control: 36.4 +/- 1.1%; %PI positive: PC: 14.6 +/- 1.4%, ADO: 17.9 +/- 2.0% vs control: 34.4 +/- 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 +/- 2.8%; %PI positive 34.7 +/- 2.2%) and ADO + SB (%LDH release 25.3 +/- 2.9%; %PI positive 33.7 +/- 7.3)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 +/- 4.8%; %PI positive 29.5 +/- 2.0%) and ADO + 5-HD (%LDH release 36.9 +/- 4.0%; %PI positive 34.8 +/- 2%)].

CONCLUSION:

In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel.

PMID:
10879626
DOI:
10.1007/s003950050187
[Indexed for MEDLINE]

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