6533b839fe1ef96bd12a6710

RESEARCH PRODUCT

Intravenous BQ-123 and phosphoramidon reduce ventricular ectopic beats and myocardial infarct size in dogs submitted to coronary occlusion and reperfusion

Amparo Ayuso MoyaAntonio M Alberola AguilarFrancisco Revert-rosJuan Chiva BeltránLuis SuchSusana SanchoJosé Luis GarcíaEduardo San Martı́n

subject

Endothelin Receptor Antagonistsmedicine.medical_specialtyMyocardial InfarctionIschemiaBlood PressureCoronary DiseaseMyocardial ReperfusionPeptides Cyclicchemistry.chemical_compoundDogsInternal medicineHeart rateAnimalsMedicinecardiovascular diseasesMyocardial infarctionAntihypertensive AgentsPharmacologyBQ-123Endothelin-1Receptors Endothelinbusiness.industryPhosphoramidonGlycopeptidesReceptor Endothelin Amedicine.diseaseVentricular Premature ComplexesBlood pressurechemistryCoronary occlusionAnesthesiaInjections IntravenousVentricular Fibrillationcardiovascular systemCardiologyDrug Therapy CombinationbusinessEndothelin receptor

description

Abstract The aim of this work was to investigate the influence of endothelin on myocardial ischemia and reperfusion in anaesthetized dogs. Animals were submitted to left thoracotomy and 120 min of left anterior descending coronary occlusion, followed by 180 min of reperfusion. Arterial blood pressure and electrocardiogram (ECG) were recorded in order to analyze heart rate (HR)–pressure product and production of ectopic beats. Infarcted areas were identified by a macroscopic staining method and infarct size was expressed as percentage of risk zone. To inhibit the effects of endothelin in a group of animals, we administered intravenously an endothelin synthesis inhibitor (phosphoramidon) and in another group, an endothelin-1 A receptor blocker (BQ-123). Phosphoramidon decreased the HR–pressure product during reperfusion period, and both, phosphoramidon and BQ-123 decreased infarct size by 40% and the number of ventricular ectopic beats by 88% and 68%, respectively, as compared to the saline treated dogs. In conclusion, endothelin seems to play a deleterious role on the myocardium submitted to ischemia and reperfusion.

https://doi.org/10.1016/s0306-3623(01)00101-x