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Reduction of myocardial damage and polymorphonuclear leukocyte accumulation following coronary artery occlusion and reperfusion by the thromboxane receptor antagonist BM 13.505.
J Cardiovasc Pharmacol. 1989 May; 13(5):715-22.JC

Abstract

This study was designed to assess the effect of the thromboxane receptor antagonist, BM 13.505, in limiting myocardial damage and polymorphonuclear leukocyte accumulation in rats subjected to coronary artery occlusion for 30 min with reperfusion for 24 h (MI/R). Myocardial injury and polymorphonuclear leukocyte infiltration were determined by measuring creatine phosphokinase (CPK) specific activity and myeloperoxidase (MPO) activity, respectively, in the left ventricular free wall (LVFW). Myocardial CPK levels were 8.24 +/- 0.33 U/mg protein in sham MI/R-vehicle-treated animals (n = 18), and were significantly decreased to 6.51 +/- 0.44 U/mg protein in MI/R-vehicle animals (n = 22). Myocardial MPO values were 2.4 +/- 0.5 U/g LVFW in sham MI/R animals, and significantly increased to 10.9 +/- 1.3 U/g LVFW in MI/R-vehicle animals. Administration of BM 13.505 (30 mg/kg, i.p.) 1 min prior to coronary occlusion resulted in CPK values of 7.83 +/- 0.45 U/mg protein and MPO levels of 6.1 +/- 0.9 U/g LVFW (p less than 0.05, compared to the MI/R-vehicle group). The survival rate in the MI/R-BM 13.505 group was 74 and 65% at 2 and 24 h, respectively, and was not different from the MI/R-vehicle group. There were no significant differences in mean arterial blood pressure or heart rate between the MI/R-vehicle and MI/R-BM 13.505 groups, indicating that changes in myocardial oxygen demand do not explain the protective effects. A lower dose did not reduce myocardial injury, indicating that the effects of BM 13.505 were dose dependent.(

ABSTRACT

TRUNCATED AT 250 WORDS)

Authors+Show Affiliations

Department of Pharmacology, Smith Kline and French Laboratories, King of Prussia, Pennsylvania 19406.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

2472519

Citation

Smith, E F., et al. "Reduction of Myocardial Damage and Polymorphonuclear Leukocyte Accumulation Following Coronary Artery Occlusion and Reperfusion By the Thromboxane Receptor Antagonist BM 13.505." Journal of Cardiovascular Pharmacology, vol. 13, no. 5, 1989, pp. 715-22.
Smith EF, Griswold DE, Egan JW, et al. Reduction of myocardial damage and polymorphonuclear leukocyte accumulation following coronary artery occlusion and reperfusion by the thromboxane receptor antagonist BM 13.505. J Cardiovasc Pharmacol. 1989;13(5):715-22.
Smith, E. F., Griswold, D. E., Egan, J. W., Hillegass, L. M., & DiMartino, M. J. (1989). Reduction of myocardial damage and polymorphonuclear leukocyte accumulation following coronary artery occlusion and reperfusion by the thromboxane receptor antagonist BM 13.505. Journal of Cardiovascular Pharmacology, 13(5), 715-22.
Smith EF, et al. Reduction of Myocardial Damage and Polymorphonuclear Leukocyte Accumulation Following Coronary Artery Occlusion and Reperfusion By the Thromboxane Receptor Antagonist BM 13.505. J Cardiovasc Pharmacol. 1989;13(5):715-22. PubMed PMID: 2472519.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reduction of myocardial damage and polymorphonuclear leukocyte accumulation following coronary artery occlusion and reperfusion by the thromboxane receptor antagonist BM 13.505. AU - Smith,E F,3rd AU - Griswold,D E, AU - Egan,J W, AU - Hillegass,L M, AU - DiMartino,M J, PY - 1989/5/1/pubmed PY - 1989/5/1/medline PY - 1989/5/1/entrez SP - 715 EP - 22 JF - Journal of cardiovascular pharmacology JO - J Cardiovasc Pharmacol VL - 13 IS - 5 N2 - This study was designed to assess the effect of the thromboxane receptor antagonist, BM 13.505, in limiting myocardial damage and polymorphonuclear leukocyte accumulation in rats subjected to coronary artery occlusion for 30 min with reperfusion for 24 h (MI/R). Myocardial injury and polymorphonuclear leukocyte infiltration were determined by measuring creatine phosphokinase (CPK) specific activity and myeloperoxidase (MPO) activity, respectively, in the left ventricular free wall (LVFW). Myocardial CPK levels were 8.24 +/- 0.33 U/mg protein in sham MI/R-vehicle-treated animals (n = 18), and were significantly decreased to 6.51 +/- 0.44 U/mg protein in MI/R-vehicle animals (n = 22). Myocardial MPO values were 2.4 +/- 0.5 U/g LVFW in sham MI/R animals, and significantly increased to 10.9 +/- 1.3 U/g LVFW in MI/R-vehicle animals. Administration of BM 13.505 (30 mg/kg, i.p.) 1 min prior to coronary occlusion resulted in CPK values of 7.83 +/- 0.45 U/mg protein and MPO levels of 6.1 +/- 0.9 U/g LVFW (p less than 0.05, compared to the MI/R-vehicle group). The survival rate in the MI/R-BM 13.505 group was 74 and 65% at 2 and 24 h, respectively, and was not different from the MI/R-vehicle group. There were no significant differences in mean arterial blood pressure or heart rate between the MI/R-vehicle and MI/R-BM 13.505 groups, indicating that changes in myocardial oxygen demand do not explain the protective effects. A lower dose did not reduce myocardial injury, indicating that the effects of BM 13.505 were dose dependent.(ABSTRACT TRUNCATED AT 250 WORDS) SN - 0160-2446 UR - https://www.unboundmedicine.com/medline/citation/2472519/Reduction_of_myocardial_damage_and_polymorphonuclear_leukocyte_accumulation_following_coronary_artery_occlusion_and_reperfusion_by_the_thromboxane_receptor_antagonist_BM_13_505_ L2 - http://ovidsp.ovid.com/ovidweb.cgi?T=JS&PAGE=linkout&SEARCH=2472519.ui DB - PRIME DP - Unbound Medicine ER -