Abstract
Diabetic patients are more prone to develop congestive heart failure and/or ischemic heart disease. Myocardial dysfunction is often attributed to diabetic cardiomyopathy that has been described in various clinical and experimental settings1,2. Deteriorations of heart contractile function as well as rhythm disorders are caused by the alterations in the cell membranes ion transport systems responsible for the maintenance of the homeostasis of Na+, K+ and Ca2+ and abnormal Ca2+ -handling3,4,5,6
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Kannel WB, McGee DL. Diabetes and cardiovascular risk factors. The Framingham Study. Circulation 1979;59:8–13.
Fein FS, Kornstein LB, Strobeck LJ, Capasso JM, Sonnenblick EH. Altered myocardial mechanics in diabetic rats. Circ Res 1980;47:922–933.
Ganguly PK, Pierce GN, Dhalla KS, Dhalla NS. Defective sarcoplasmic reticular calcium transport in diabetic cardiomyopathy. Am J Physiol 1983;244:E528–E535.
Khandoudi A, Bernard M, Cozzone P, Feuvray D.Intracellular pH and role of Na’/H’ exchange during ischemia and reperfusion of normal and diabetic rat hearts. Cardiovasc Res 1990;24:873–878.
Pierce GN, Ramjiawan B, Dhalla NS, Ferrari R. Nad/H’ exchange in cardiac sarcolemmal vesicles isolated from diabetic rats. Am J Physiol 1990;258:H255–E261.
Dhalla NS, Pierce GN, Panagia V, Singal PK, Beamish RE. Calcium movements in relation to heart function. Basic Res Cardiol 1982;77:117–139.
Opie LH. Myocardial ischemia, reperfusion and cytoprotection. Rev Port Cardiol 1996;15(10):703708.
Paulson D. The diabetic heart is more sensitive to ischemic injury. Cardiovasc Res 1997;34:104–112.
Murry CE, Jennings RB, Reimer KA. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 1986;74:1124–1136.
Liu GS, Downey JM. Preconditioning against infarction in rat heart does not involve pertussis toxin sensitive G protein. Cardiovasc Res 1993;27:608–611.
Cave AC. Preconditioning induced protection against postischemic contractile dysfunction: characteristics and mechanisms. J Mol Cell Cardiol 1995;27:969–979.
Vegh A, Komori S, Szekeres L, Parratt JR. Antiarrhythmic effects of preconditioning in anaesthetised dogs and rats. Cardiovasc Res 1992;26:487–495.
Tosaki A, Engelman DT, Engelman RM, Das DK. The evolution of diabetic response to ischemia/reperfusion and preconditioning in isolated working rat hearts. Cardiovasc Res 1996;31:526–536.
Bouchard JF, Lamontagne D. Protection afforded by preconditioning in the diabetic heart against ischemic injury. Cardiovasc Res 1998;37:82–90.
Walker MJA, Curtis MJ, Hearse DJ, Campbell RWF, Janse MJ, Yellon DM, Cobbe SM, Coker SJ, Harness JB, Harron DWG, Higgins AJ, Julian DJ, Lab MJ, Manning AS, Northover BJ, Parratt JR, Riemersma RA, Riva E, Russel DC, Sheridan DJ, Winslow E, Woodward B. The Lambeth conventions: guidelines for the study of arrhythmias in ischemia, infarction, and reperfusion. Cardiovasc Res 1988;22:447–455.
Ravingerova T, Tribulova N, Slezak J, Curtis MJ. Brief, intermediate and prolonged ischemia in the crystalloid perfused rat heart: Relationship between susceptibility to arrhythmias and degree of ultrastructural injury. J Mol Cell Cardiol 1995;27:1937–1951.
Curtis MJ. Characterisation, utilisation and clinical relevance of isolated perfused heart models of ischemia-induced ventricular fibrillation. Cardiovasc Res 1998;39:194–215.
Tani M, Neely JR. Hearts from diabetic rats are more resistant to in vitro ischemia: possible role of altered Cat` metabolism. Circ Res 1988;62: 931–940.
Feuvray D, Lopaschuk GD. Controversies on the sensitivity of the diabetic heart to ischemic injury: the sensitivity of the diabetic heart to ischemic injury is decreased. Cardiovasc Res 1997;34:113–120.
Malhotra A, Reich D, Reich D, Nakouzi A, Sanghi V, Geenen DL, Buttrick PM. Experimental diabetes is associated with functional activation of protein kinase C and phosphorylation of troponin I in the heart, which are prevented by angiotensin II receptor blockade. Circ Res 1997;81:1027–1033.
Rodrigues B, Cam MC, McNeill JH. Myocardial substrate metabolism: implications for diabetic cardiomyopathy. J Mol Cell Cardiol 1995;27;169–179.
Curtis MJ, Hearse DJ. Ischemia-induced and reperfusion-induced arrhythmias differ in their sensitivity to potassium: Implications for the mechanisms of initiation and maintenance of ventricular fibrillation. J Mol Cell Cardiol 1989;21:21–40.
Gamble J, Lopaschuk GD. Glycolysis and glucose oxidation during reperfusion of ischemic hearts from diabetic rats. Biochim Biophys Acta Mol Basis Dis 1994;1225:191–199.
Mitchell MB, Meng X, Ao L, Brown JM, Harken AH, Banerjee A. Preconditioning of isolated rat heart is mediated by protein kinase C. Circ Res 1995;76:73–81.
Gross GJ, Auchampach JA. Blockade of ATP-sensitive potassium channel prevents myocardial preconditioning in dogs. Circ Res 1992;70:223–233.
Hearse DJ. Myocardial protection in ischemia and reperfusion. Medicographia 1996;18:22–29.
Wolfe CL, Sievers RE, Visseren FLJ, Donnelly TJ. Loss of myocardial protection after preconditioning correlates with the time course of glycogen recovery within the preconditioned segment. Circulation 1993;87:881–892.
Tatsumi T, Matoba S, Kobara M, Keira N, Kawahara A, Tsuruyama K, Tanaka T, Katamura M, Nakagawa C, Ohta B, Yamahara Y, Asayama J, Nakagawa M. Energy metabolisms after ischemic preconditioning in streptozotocin-induced diabetic rat hearts. J Am Coll Cardiol 1998;31: 707–715.
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2001 Springer Science+Business Media New York
About this chapter
Cite this chapter
Ravingerova, T. et al. (2001). Response to Ischemia and Endogenous Myocardial Protection in the Diabetic Heart. In: Angel, A., Dhalla, N., Pierce, G., Singal, P. (eds) Diabetes and Cardiovascular Disease. Advances in Experimental Medicine and Biology, vol 498. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1321-6_36
Download citation
DOI: https://doi.org/10.1007/978-1-4615-1321-6_36
Publisher Name: Springer, Boston, MA
Print ISBN: 978-1-4613-5496-3
Online ISBN: 978-1-4615-1321-6
eBook Packages: Springer Book Archive