Cardiovascular Research

Reperfusion injury induces apoptosis in rabbit cardiomyocytes.

Authors: R A Gottlieb|||K O Burleson|||R A Kloner|||B M Babior|||R L Engler

Affiliations: + Expand

Abstract

The most effective way to limit myocardial ischemic necrosis is reperfusion, but reperfusion itself may result in tissue injury, which has been difficult to separate from ischemic injury. This report identifies elements of apoptosis (programmed cell death) in myocytes as a response to reperfusion but not ischemia. The hallmark of apoptosis, nucleosomal ladders of DNA fragments (approximately 200 base pairs), was detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only rabbit hearts. Granulocytopenia did not prevent nucleosomal DNA cleavage. In situ nick end labeling demonstrated DNA fragmentation predominantly in myocytes. The pattern of nuclear chromatin condensation was distinctly different in reperfused than in persistently ischemic tissue by transmission electron microscopy. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leading to late cell death.

---

Chemical List

Nucleosomes|||DNA

---

Reference List

J Clin Invest. 1993 Sep;92(3):1504-16|||FASEB J. 1993 Mar;7(5):470-8|||Nature. 1980 Apr 10;284(5756):555-6|||Int Rev Cytol. 1980;68:251-306|||Am J Pathol. 1983 Apr;111(1):98-111|||Pathol Annu. 1982;17 Pt 2:229-59|||J Pathol. 1984 Jan;142(1):67-77|||Pathology. 1984 Oct;16(4):406-10|||J Clin Invest. 1985 Nov;76(5):1713-9|||Proc Natl Acad Sci U S A. 1987 Mar;84(5):1404-7|||Fed Proc. 1987 May 15;46(7):2402-6|||Circ Res. 1987 Nov;61(5):757-60|||J Mol Cell Cardiol. 1988 Mar;20 Suppl 2:41-54|||Am J Physiol. 1988 Nov;255(5 Pt 2):H1060-8|||J Clin Invest. 1989 Mar;83(3):865-75|||Circulation. 1989 May;79(5):1137-42|||Circulation. 1989 Nov;80(5):1115-27|||Circulation. 1989 Dec;80(6):1816-27|||J Mol Cell Cardiol. 1989 Nov;21(11):1187-93|||Nature. 1990 Jan 11;343(6254):170-3|||Jpn Heart J. 1989 Sep;30(5):695-708|||Anticancer Res. 1990 Sep-Oct;10(5A):1153-9|||Lab Invest. 1990 Dec;63(6):770-9|||Biochem Cell Biol. 1990 Sep;68(9):1071-4|||Cell Prolif. 1991 Mar;24(2):203-14|||Circulation. 1991 Jul;84(1):350-6|||FASEB J. 1991 Aug;5(11):2529-37|||Proc Natl Acad Sci U S A. 1991 Aug 15;88(16):6961-5|||J Biol Chem. 1991 Oct 5;266(28):18580-5|||J Clin Invest. 1991 Oct;88(4):1216-23|||J Immunol. 1991 Nov 15;147(10):3408-12|||Biochem Biophys Res Commun. 1991 Dec 16;181(2):915-20|||J Clin Invest. 1992 Feb;89(2):602-9|||Am J Pathol. 1992 Apr;140(4):831-8|||Int J Clin Lab Res. 1992;21(4):300-3|||Cancer Res. 1992 Jun 15;52(12):3384-90|||J Biol Chem. 1992 Jun 5;267(16):10939-41|||J Cell Biol. 1992 Nov;119(3):493-501|||Am J Pathol. 1992 Dec;141(6):1471-9|||J Clin Invest. 1992 Dec;90(6):2593-7|||J Histochem Cytochem. 1993 Jan;41(1):7-12|||J Am Coll Cardiol. 1993 Apr;21(5):1245-53|||Br J Cancer. 1972 Aug;26(4):239-57