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Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730).
Eur J Pharmacol. 1993 Jun 04; 236(3):477-81.EJ

Abstract

This study was designed to evaluate the cardioprotective effects of a solubilized human complement receptor, sCR1, in the rat subjected to myocardial infarction. Following coronary artery occlusion for 0.5 h and reperfusion for 24 h (MI/R group), myocardial infarct size (determined by planimetric analysis) was 18.3 +/- 2.1% of the left ventricle (n = 16), while myeloperoxidase activity (a biochemical marker of neutrophil activation) was increased from 0.94 +/- 0.09 U/g tissue in the sham occluded + vehicle group to 2.96 +/- 0.17 U/g tissue in the MI/R + vehicle treated group (P < 0.01). Injection of sCR1 (5 mg/kg i.v., 5 min prior to coronary artery occlusion) produced plasma concentrations of 154 +/- 4 microgram/ml 1 min prior to coronary artery occlusion, and concentrations of 86 +/- 2 and 58 +/- 3 micrograms/ml at 40 min and 125 min after dosing (n = 6). sCR1 reduced myocardial infarct size to 11.3 +/- 2.2% of the left ventricle, and attenuated the increase in myeloperoxidase activity to 2.11 +/- 0.20 U/g tissue (n = 18; P < 0.01, compared to the MI/R + vehicle group). Administration of sCR1 5 min prior to reperfusion afforded a 25.3% non-significant reduction in myocardial injury. These results suggest a beneficial effect of sCR1 in myocardial ischemia/reperfusion injury by reducing the infiltration of neutrophils and attenuating the extent of myocardial injury.

Authors+Show Affiliations

Department of Pharmacology, SmithKline Beecham Pharmaceuticals, King of Prussia, PA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

8395386

Citation

Smith, E F., et al. "Reduction of Myocardial Reperfusion Injury With Human Soluble Complement Receptor Type 1 (BRL 55730)." European Journal of Pharmacology, vol. 236, no. 3, 1993, pp. 477-81.
Smith EF, Griswold DE, Egan JW, et al. Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730). Eur J Pharmacol. 1993;236(3):477-81.
Smith, E. F., Griswold, D. E., Egan, J. W., Hillegass, L. M., Smith, R. A., Hibbs, M. J., & Gagnon, R. C. (1993). Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730). European Journal of Pharmacology, 236(3), 477-81.
Smith EF, et al. Reduction of Myocardial Reperfusion Injury With Human Soluble Complement Receptor Type 1 (BRL 55730). Eur J Pharmacol. 1993 Jun 4;236(3):477-81. PubMed PMID: 8395386.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reduction of myocardial reperfusion injury with human soluble complement receptor type 1 (BRL 55730). AU - Smith,E F,3rd AU - Griswold,D E, AU - Egan,J W, AU - Hillegass,L M, AU - Smith,R A, AU - Hibbs,M J, AU - Gagnon,R C, PY - 1993/6/4/pubmed PY - 1993/6/4/medline PY - 1993/6/4/entrez SP - 477 EP - 81 JF - European journal of pharmacology JO - Eur J Pharmacol VL - 236 IS - 3 N2 - This study was designed to evaluate the cardioprotective effects of a solubilized human complement receptor, sCR1, in the rat subjected to myocardial infarction. Following coronary artery occlusion for 0.5 h and reperfusion for 24 h (MI/R group), myocardial infarct size (determined by planimetric analysis) was 18.3 +/- 2.1% of the left ventricle (n = 16), while myeloperoxidase activity (a biochemical marker of neutrophil activation) was increased from 0.94 +/- 0.09 U/g tissue in the sham occluded + vehicle group to 2.96 +/- 0.17 U/g tissue in the MI/R + vehicle treated group (P < 0.01). Injection of sCR1 (5 mg/kg i.v., 5 min prior to coronary artery occlusion) produced plasma concentrations of 154 +/- 4 microgram/ml 1 min prior to coronary artery occlusion, and concentrations of 86 +/- 2 and 58 +/- 3 micrograms/ml at 40 min and 125 min after dosing (n = 6). sCR1 reduced myocardial infarct size to 11.3 +/- 2.2% of the left ventricle, and attenuated the increase in myeloperoxidase activity to 2.11 +/- 0.20 U/g tissue (n = 18; P < 0.01, compared to the MI/R + vehicle group). Administration of sCR1 5 min prior to reperfusion afforded a 25.3% non-significant reduction in myocardial injury. These results suggest a beneficial effect of sCR1 in myocardial ischemia/reperfusion injury by reducing the infiltration of neutrophils and attenuating the extent of myocardial injury. SN - 0014-2999 UR - https://www.unboundmedicine.com/medline/citation/8395386/Reduction_of_myocardial_reperfusion_injury_with_human_soluble_complement_receptor_type_1__BRL_55730__ L2 - https://linkinghub.elsevier.com/retrieve/pii/0014-2999(93)90487-3 DB - PRIME DP - Unbound Medicine ER -