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Effects of Na+-H+ exchange blocker amiloride on left ventricular remodeling after anterior myocardial infarction in rats

Summary

We investigated the effects of amiloride, a Na+-H+ exchange blocker, on ventricular remodeling in an infarcted rat model. In the amiloride group, the left descending coronary artery was ligated and rats were given amiloride (1 mg/kg/day, n=11) in their drinking water for 4 weeks. In the control group, rats were given water for 4 weeks (n=8) after myocardial infarction. The rats were killed on day 28. Both the ratio of heart weight to body weight and that of left ventricular weight to body weight were significantly less in the amiloride group (p<0.05). The diameter of a myocardial fiber in the region adjacent to the operated area was significantly reduced in the amiloride group compared with the control group (p<0.05). Left ventricular cavity dimension was significantly smaller in the amiloride group than that in control group (p<0.05). Our findings suggest that amiloride prevents ventricular remodeling after myocardial infarction.

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References

  1. 1.

    Anversa P, Loud AV, Levicky V, Guideri G. Left ventricular failure induced by myocardial infarction: I. Myocyte hypertrophy.Am J Physiol 1985;248:H876-H882.

  2. 2.

    Anversa P, Loud AV, Levicky V, Guideri G. Left ventricular failure induced by myocardial infarction: II. Tissue morphometry.Am J Physiol 1985;248:H883-H889.

  3. 3.

    Olivettie G, Joseph MC, Leonard GM et al. Cellar basis of chronic ventricular remodeling after myocardial infarction in rats.Circ Res 1991;68:856–869.

  4. 4.

    Fletcher PJ, Pfeffer JM, Pfeffer MA, Braunwald E. Left ventricular diastolic pressure-volume relation in rats with healed myocardial infarction.Circ Res 1981;49:618–626.

  5. 5.

    Pfeffer MA, Pfeffer JM, Fishbein MC, et al. Myocardial infarction size and ventricular function in rats.Circ Res 1979;44:503–512.

  6. 6.

    Pfeffer MA, Pfeffer JM, Braunwald E. Influence of chronic captopril therapy on the infarcted left ventricule of the rat.Circ Res 1985;57:84–95.

  7. 7.

    Pfeffer MA, Pfeffer JM, Steinberg C, Finn P. Survival after an experimental myocardial: Beneficial effects of long-term therapy with captopril.Circulation 1985;72:406–412.

  8. 8.

    Pfeffer MA, Lamas GA, Vaughan DE, Paris AF, Braunwald E. Effect of captopril on progressive ventricular dilatation after anterior myocardial infarction.N Engl J Med 1988;319:80–86.

  9. 9.

    Tani M, Neely JR. Role of intracellular Na+ in Ca++ overload and depressed recovery of ventricular function of reperfused ischemic rat hearts: Possible involvement of H+-Na+ and Na+-Ca++ exchange. Circ Res 1989;65:1045–1056.

  10. 10.

    Harrison SM, Frampton JE, McCall E, Boyett MR, Orchard CH. Contraction and intracellular Ca++, Na+, and H+ during acidosis in rat ventricular myocytes.Am J Physiol 1992;262:C348–357.

  11. 11.

    Kennedy RH, Berlin JR, Ng Y-G, Akera T, Brody TM. Amiloride: Effects on myocardial force of contraction, sodium pump and Na+/Ca++ exchange.J Mol Cell Cardiol 1986;18:177–188.

  12. 12.

    Kim D, Cragoe JW, Smith TW. Relations among sodium pump inhibition, Na+-Ca++ exchange activities and Ca++-H+ interaction in cultured chick heart cells.Circ Res 1987;60:185–193.

  13. 13.

    Weiss RG, Lakatta EG, Gerstenblith G. Effects of amiloride on metabolism and contractility during reoxygenation in perfused rat heart.Circ Res 1990;66:1012–1022.

  14. 14.

    Duan J, Karmazyn M. Protective effects of amiloride on the ischemic reperfused rat heart. Relation to mitochondrial function.Eur J Pharmacol 1992;210:149–157.

  15. 15.

    Olivetti G, Ricci R, Beghi C, et al. Response of the border zone to myocardial infarction in rats.Am J Pathol 1986;125:476–483.

  16. 16.

    Morgan HE, Baker KM. Cardiac hypertrophy.Circulation 1991;83:13–25.

  17. 17.

    Hotokebuchi N, Yano T, Takeshita T, Nishi K. Acceleration of H extrusion via Na+-H+ exchange in guinea pig ventricular papillary muscle under intracellular acidic condition.Jpn J Physiol 1991;41:369–384.

  18. 18.

    Bogen DK, Rabinowitz SA, Needlemann A, McMahon TA, Abelmann WH. An analysis of the mechanical disadvantage of myocardial infarction in the canine left ventricule.Circ Res 1980;47:728–741.

  19. 19.

    Kojima K, Shiojima I, Yamazaki T, et al. Angiotensin II receptor antagonist TCV-116 induces regression of hypertensive left ventricular hypertrophy in vivo and inhibits the intracellular signaling pathway of stretch-mediated cardiomyocyte hypertrophy in vitro.Circulation 1994;89:2204–2211.

  20. 20.

    Kent RL, Hoober JK, Cooper G. Load responsiveness of protein synthesis in adult mammalian myocardium: Role of cardiac deformation linked to sodium influx.Circ Res 1989;64:74–85.

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Correspondence to Shuuichi Hasegawa MD.

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Hasegawa, S., Nakano, M., Taniguchi, Y. et al. Effects of Na+-H+ exchange blocker amiloride on left ventricular remodeling after anterior myocardial infarction in rats. Cardiovasc Drug Ther 9, 823–826 (1995). https://doi.org/10.1007/BF00879877

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Key Words

  • myocardial infarction
  • remodeling
  • amiloride
  • Na+-H+ exchange blocker
  • myocyte hypertrophy