Abstract
Paradoxical and even beneficial effects of diabetes mellitus on the circulation system have been noted by several authors [1–3]. We found that diabetic hearts are more tolerant to high-frequency pacing [4] and that isolated, perfused diabetic rat hearts are less susceptible to ischemia—reperfusion injury in the substrate-free condition [5].
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Refereces
Tani M, Neely JR. 1988. Hearts from diabetic rats are more resistant to in vivo ischemia: possible role of altered Ca2+ metabolism. Circ Res 62:931–940.
Kusama Y, Hearse DJ, Avkiran M. 1992. Diabetes and susceptibility to reperfusion-induced ventricular arrhythmias. J Mol Cell Cardiol 24:411–421.
Khandoudi N, Bernard M, Cozzone P, Feuvrey D. 1990. Intracellular pH and role of Na+/H+ exchange during ischemia and reperfusion of normal and diabetic rat hearts. Cardiovasc Res 24:873–878.
Mochizuki S, Ozeki T, Tanaka F, Nagano M. 1991. Regulation of substrate utilization and ventricular function in diabetic hearts. In Nagano M, Dhalla NS (eds.), The Diabetic Heart. Raven Press: New York, pp. 351–364.
Mochizuki S, Tanaka F. Ejima M, Onodera T, Taniguchi M, Nagano M. 1994. Attenuation of susceptibility to ischemia/reperfusion in isolated, substrate free perfused hearts from diabetic rats. In Nagano M, Takeda N, Dhalla NS (eds.), The Adapted Heart. Raven Press: New York, pp. 423–429.
Neely JR, Liebermeister H, Battersby EJ, Morgan HE. 1967. Effect of pressure development of oxygen consumption by isolated rat heart. Am J Physiol 212:804–814.
Neely JR, Rovetto MJ, Whitmer JT, Morgan HE. 1973. Effect of ischemia on function and metabolism of isolated working rat heart. Am J Physiol 225:651–658.
Harris AS, Bisteni A, Russell RA, Brigham JC, Firestone JE. 1954. Excitatory factors in ventricular tachycardia resulting from myocardial ischemia. Potassium a major excitant. Science 119:200–203.
Hill JL, Gettes LS. 1980. Effect of acute coronary occlusion on local myocardial extracellular K+ activity in swine. Circulation 61:768–778.
Pierce GN, Dhalla NS. 1983. Sarcolemmal Na+/K+-ATPase activity in diabetic rat heart. Am J Physiol 245:C241–C247.
Heyliger CE, Prakash A, McNeil JH. 1987. Alterations in cardiac sarcolemmal Ca2+ pump activity during diabetes mellitus. Am J Physiol 252:H540–H544.
Case RB. 1971/72. Ion alterations during myocardial ischemia. Cardiology 56:245–262.
Weiss JN, Shieh R. 1994. Potassium loss during myocardial ischaemia and hypoxia: does lactate efflux play a role? Cardiovasc Res 28:1125–1132.
Kantor PF, Coetzee WA, Carmeliet EE, Dennis SC, Opie LH. 1990. Reduction of ischemic K+ loss and arrhythmias in rat hearrts. Effect of glibenclamide, a sulfonylurea. Circ Res 66:478–485.
Noma A. 1983. ATP-regulated K+ channels in cardiac muscle. Nature 305:147–148.
Grover GJ. 1994. Protective effects of ATP sensitive potassium channel openers in models of myocardial ischemia. Cardiovasc Res 28:778–782.
Gross GJ, Auchampach JA. 1992. Role of ATP-dependent potassium channels in myocardial ischaemia. Cardiovasc Res 26:1011–1016.
Antzelevitch C, DiDiego JM. 1992. Role of K+ channel activators in cardiac electrophy-siology and arrhythmias. Circulation 85:1627–1629.
Cole WC, McPherson CD, Sontag D. 1991. ATP-regulated K+ channels protect the myocardium against ischemia/reperfusion damage. Circ Res 69:571–581.
Sargent CA, Smith MA, Dzwonczyk S, Sleph PG, Grover GJ. 1991. Effect of potassium channel blockade on the anti-ischemic actions of mechanistically diverse agents. J Pharmacol Exp Ther 259:97–103.
Fosset M, De Weille JR, Green RD, Schmid-Antomarchi H, Lazdunski M. 1988. Antidiabetic sulfonylureas control action potential properties in heart cells via high affinity receptors that are linked to ATP-dependent K+ channels. J Biol Chem 263:7933–7936.
Bekheit SS, Restive M, Boutjdir M, Henkin R, Gooyanden K, Assadi M, Khatib S, Gough WB, El-Sherif N. 1990. Effects of glyburide on ischemia-induced changes in extracellular potassium and local myocardial activation: a potential new approach to the management of ischemia-induced malignant ventricular arrhythmias. Am Heart J 119:1025–1033.
Wollenben CD, Sanguinetti MC, Siegl PKS. 1989. Influence of ATP-sensitive potassium channel modulators in ischemia-induced fibrillation in isolated rat hearts. J Mol Cell Cardiol 21:783–788.
Cacciapouti F, Speizia R, Bianchi U, Lama D, D’Avino M, Varricchio M. 1991. Effectiveness of glibenclamide on myocardial ischemic ventricular arrhythmias in non-insulin-dependent diabetes mellitus. Am J Cardiol 67:843–847.
Davies NW, Standem NB, Stanfield PR. 1992. The effect of intracellular pH on ATP-dependent potassium channels of frog skeletal muscle. J Physiol 445:549–568.
Davies NW. 1990. Modulation of ATP-sensitive K+ channels in skeletal muscle by intracellular protons. Nature 343:375–377.
Cuevas J, Bassett AL, Cameron JS, Furukawa T, Myerburg RT, Kimura S. 1991. Effect of H+ on ATP-regulated K+ channel in feline ventricular myocytes. Am J Physiol 261:H755-H761.
Fan Z, Makielski JC. 1993. Intracellular H+ and Ca2+ modulation of tripsin-modified ATP-sensitive K+ channels in rabbit.ventricular myocytes. Circ Res 72:715–722.
Lederer WJ, Nichols CG. 1989. Nucleotide modulation of the activity of rat heart ATP-sensitive K+ channels in isolated membrane patches. J Physiol 419:193–211.
Anderson SE, Murphy E, Steenbergen C, London RE, Cala PM. 1990. Na-H exchange in myocardium: effects of hypoxia and acidification on Na and Ca. Am J Physiol 259:C940–C948.
Murphy E, Perlman M, London RE, Steenbergen C. 1991. Amiloride delays the ischemia-induced rise in cytoslic free calcium. Circ Res 68:1250–1258.
Mochizuki S, Seki S, Ejima M, Onodera T, Taniguchi M, Ishikawa S. 1993. Na+/H+ exchanger and reperfusion-induced ventricular arrhythmias in isolated perfused heart: possible role of amiloride. Mol Cell Biochem 119:151–157.
Pierce GN, Philipson KD. 1985. Na+-H+ exchange in cardiac sarcolemmal vesicles. Biochim Biophys Acta 818:109–116.
Luzdunski M, Freiin C, Vigne P. 1985. The sodium/hydrogen exchange in cardiac cells: its biochemical and pharmacological properties and its role in regulating internal concentrations of sodium and internal pH. J Mol Cell Cardiol 17:1029–1042.
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Mochizuki, S. et al. (1996). Diabetic State Reduces Ischemic K+ Loss and H+ Efflux in Isolated Rat Hearts. In: Dhalla, N.S., Singal, P.K., Takeda, N., Beamish, R.E. (eds) Pathophysiology of Heart Failure. Developments in Cardiovascular Medicine, vol 168. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-1235-2_29
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DOI: https://doi.org/10.1007/978-1-4613-1235-2_29
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