Caspase inhibition attenuates contractile dysfunction following cardioplegic arrest and rewarming in the setting of left ventricular failure

Journal of Cardiovascular Pharmacology

Volumn 44, Issue 6, 2004, Pages 645-650

  Yarbrough, William M ^b   Mukherjee, Rupak ^b   Squires, Christina E ^b   Reese, Emily S ^b   Leiser, Jennifer S ^b   Stroud, Robert E ^b   Sample, Jeffrey A ^b   Hendrick, Jennifer W ^b   Mingoia, Joseph T ^b   McLean, Julie E ^b   Hardin, Amy E ^b   Dowdy, Kathryn B ^b   Spinale, Francis G ^a  

^a MEDICAL UNIVERSITY OF SOUTH CAROLINA   (United States)

^b NONE

Author keywords

Caspase; Contractility; LV failure; Myocyte

Indexed keywords

BENZYLOXYCARBONYLVALYLALANYLASPARTYL FLUOROMETHYL KETONE; CASPASE 3 INHIBITOR; CASPASE INHIBITOR; ISOPRENALINE; POTASSIUM ION;

ADRENERGIC SYSTEM; ANIMAL MODEL; ARTICLE; BETA ADRENERGIC STIMULATION; BODY TEMPERATURE; CELL CULTURE; CELL ISOLATION; CONTROLLED STUDY; ENZYME ACTIVITY; ENZYME INHIBITION; HEART ARREST; HEART DISEASE; HEART FUNCTION; HEART LEFT VENTRICLE; HEART LEFT VENTRICLE FAILURE; HEART MUSCLE CELL; HEART MUSCLE CONTRACTILITY; HYPERKALEMIA; HYPOTHERMIA; MUSCLE FIBER CONTRACTION; NONHUMAN; PRIORITY JOURNAL; SWINE;

ADRENERGIC BETA-AGONISTS; ANIMALS; CARDIOPLEGIC SOLUTIONS; CARDIOTONIC AGENTS; CASPASES; CELL SEPARATION; ENZYME INHIBITORS; HEART ARREST, INDUCED; HEART FAILURE, CONGESTIVE; HYPERKALEMIA; MYOCARDIAL CONTRACTION; MYOCYTES, CARDIAC; REWARMING; SWINE; VENTRICULAR DYSFUNCTION, LEFT;

EID: 9744244874     PISSN: 01602446     EISSN: None     Source Type: Journal    
DOI: 10.1097/00005344-200412000-00004     Document Type: Article

References (24)

1. Gay WA Jr. Crystalloid potassium cardioplegia: concepts and early studies. Ann Thorac Surg. 1994;58:1285-1286.
2. Spinale FG. Cellular and molecular therapeutic targets for treatment of contractile dysfunction after cardioplegic arrest. Ann Thorac Surg. 1999; 68:1934-1941.
3. Vinten-Johansen J, Nakanishi K. Postcardioplegia acute cardiac dysfunction and reperfusion injury. J Cardiothorac Vasc Anesth. 1993;7(4 Suppl 2):6-18.
4. Chambers DJ. Mechanisms and alternative methods of achieving cardiac arrest. Ann Thorac Surg. 2003;75:S661-S666.
5. Suleiman MS, Halestrap AP, Griffiths EJ. Mitochondria: a target for myocardial protection. Pharmacol Ther. 2001;89:29-46.
6. Thornberry NA, Lazebnik Y. Caspases: enemies within. Science. 1998; 281:1312-1316.
7. Communal C, Sumandea M, de Tombe P, et al. Functional consequences of caspase activation in cardiac myocytes. Proc Natl Acad Sci USA. 2002; 99:6252-6256.
8. Haunstetter A, Izumo S. Toward antiapoptosis as a new treatment modality. Circ Res. 2000;86:371-376.
9. Holly TA, Drincic A, Byun Y, et al. Caspase inhibition reduces myocyte cell death induced by myocardial ischemia and reperfusion in vivo. J Mol Cell Cardiol. 1999;31:1709-1715.
10. Moretti A, Weig HJ, Ott T, et al. Essential myosin light chain as a target for caspase-3 in failing myocardium. Proc Natl Acad Sci USA. 2002;99: 11860-11865.
11. Okamura T, Miura T, Takemura G, et al. Effect of caspase inhibitors on myocardial infarct size and myocyte DNA fragmentation in the ischemia-reperfused rat heart. Cardiovasc Res. 2000;45:642-650.
12. Zhao ZQ, Vinten-Johansen J. Myocardial apoptosis and ischemic preconditioning. Cardiovasc Res. 2002;55:438-455.
13. Dorman BH, Hebbar L, Clair MJ, et al. Potassium channel opener-augmented cardioplegia: protection of myocyte contractility with chronic left ventricular dysfunction. Circulation. 1997;96(9 Suppl):II-9.
14. New RB, Sampson AC, King MK, et al. Effects of combined angiotensin II and endothelin receptor blockade with developing heart failure: effects on left ventricular performance. Circulation. 2000;102:1447-1453.
15. Spinale FG, Fulbright BM, Mukherjee R, et al. Relation between ventricular and myocyte function with tachycardia-induced cardiomyopathy. Circ Res. 1992;71:174-187.
16. Spinale FG, Mukherjee R, Iannini JP, et al. Modulation of the renin-angiotensin pathway through enzyme inhibition and specific receptor blockade in pacing-induced heart failure: II. Effects on myocyte contractile processes. Circulation. 1997;96:2397-2406.
17. Green PS, Leeuwenburgh C. Mitochondrial dysfunction is an early indicator of doxorubicin-induced apoptosis. Biochim Biophys Acta. 2002;1588:94-101.
18. Iyer R, Holian A. Involvement of the ICE family of proteases in silica-induced apoptosis in human alveolar macrophages. Am J Physiol. 1997; 273:L760-L767.
19. Edwards FH, Grover FL, Shroyer AL, et al. The Society of Thoracic Surgeons National Cardiac Surgery Database: current risk assessment. Ann Thorac Surg. 1997;63:903-908.
20. Huang JQ, Radinovic S, Rezaiefar P, et al. In vivo myocardial infarct size reduction by a caspase inhibitor administered after the onset of ischemia. Eur J Pharmacol. 2000;402:139-142.
21. Kovacs P, Bak I, Szendrei L, et al. Non-specific caspase inhibition reduces infarct size and improves post-ischaemic recovery in isolated ischaemic/reperfused rat hearts. Naunyn Schmiedebergs Arch Pharmacol. 2001;364:501-507.
22. Yaoita H, Ogawa K, Maehara K, et al. Attenuation of ischemia/ reperfusion injury in rats by a caspase inhibitor. Circulation. 1998;97: 276-281.
23. Feng J, Bianchi C, Li J, et al. Improved profile of bad phosphorylation and caspase 3 activation after blood versus crystalloid cardioplegia. Ann Thorac Surg. 2004;77:1384-1389.
24. Handy JR, Spinale FG, Mukherjee R, et al. Hypothermic potassium cardioplegia impairs myocyte recovery of contractility and inotropy. J Thorac Cardiovasc Surg. 1994;107:1050-1058.