Beneficial effects of a new prostacyclin analogue, KP-10614, on acute myocardial infarction in rats
| Autor: | Toshiji Kanayama, Susumu Mizogami, Yuko Kimura, Yoshikuni Tamao |
|---|---|
| Rok vydání: | 1992 |
| Předmět: |
Blood Platelets
Male medicine.medical_specialty Platelet Aggregation Myocardial Infarction Myocardial Ischemia Prostacyclin Rats Sprague-Dawley Leukocyte Count Left coronary artery Fibrinolytic Agents medicine.artery Internal medicine Heart rate Medicine Animals Platelet Myocardial infarction Iloprost Pharmacology Molecular Structure business.industry Hemodynamics medicine.disease Epoprostenol Rats medicine.anatomical_structure Blood pressure Ventricle Cardiology Cardiology and Cardiovascular Medicine business Ex vivo medicine.drug |
| Zdroj: | Journal of cardiovascular pharmacology. 20(4) |
| ISSN: | 0160-2446 |
| Popis: | The potential therapeutic value of a new prostacyclin analogue, (4z, 16s)-4,5,18,18,19,19-hexadehydro-16,20-dimethyl-delta 6(9a)- 9-(O)-methano-PGI1 (KP-10614), was studied in acute myocardial infarction in rats. Myocardial infarction was induced by ligation of the left coronary artery and ischemic injury was followed up to 4 h. The infarct size, evaluated by the area unstained by 2,3,5-triphenyltetrazolium chloride, reached 41.1 +/- 1.4% of the left ventricle at 4 h. KP-10614 (3 ng/kg/min x 4 h) reduced the infarct size at 4 h significantly (26.5 +/- 2.9%). At the same dose, KP-10614 inhibited ADP-induced ex vivo platelet aggregation significantly (21.5 +/- 4.0% of the control aggregation), but did not alter the arterial blood pressure or heart rate. To assess the role of platelets in myocardial infarction, circulating platelets were reduced by about 95% with rabbit antiserum to rat platelets. In platelet-depleted rats, the infarct size decreased significantly to 24.1 +/- 4.6% of the left ventricle at 4 h. These results suggest that platelets play an important role in expression of myocardial ischemic injury resulting from coronary artery occlusion in rats, and the ability of KP-10614 to decrease the infarct size appeared to be attributable, at least in part, to the inhibition of platelet aggregation or cellular metabolic effects produced by platelets at the site of tissue injury. |
| Databáze: | OpenAIRE |
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