Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat

• Published in: Regulatory peptides Vol. 115; no. 3; pp. 211 - 218
• Main Authors: Kumari, Rashmi, Maulik, Mohua, Manchanda, Subhash Chandra, Maulik, Subir Kumar
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier B.V 15.10.2003; Amsterdam Elsevier
• Subjects: Adenosine Triphosphate - metabolism; Animals; Biological and medical sciences; Bradykinin - analogs & derivatives; Bradykinin - pharmacology; Bradykinin antagonist; Bradykinin Receptor Antagonists; Cat; Cats; Fundamental and applied biological sciences. Psychology; Ischemic-reperfusion injury; Myocardial Ischemia - metabolism; Myocardial Reperfusion Injury - drug therapy; Myocardial Reperfusion Injury - metabolism; Myocardial Reperfusion Injury - mortality; Myocardium - enzymology; Myocardium - metabolism; Oxidative Stress - drug effects; Protective Agents - pharmacology; Thiobarbituric Acid Reactive Substances - metabolism; Time Factors; Vertebrates: endocrinology; Ischemic-reperfusion injury; Bradykinin antagonist; Cat; Fissipedia; Carnivora; Peptide hormone; Neuropeptide; Felis catus; In vivo; Vertebrata; Mammalia; Reperfusion; Bradykinin; Antagonist
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/S0167-0115(03)00169-1

The effect of icatibant (Hoe-140), a selective bradykinin receptor (B 2) antagonist on myocardial ischemic-reperfusion injury was studied in open chest barbiturate anaesthetized cats. The left anterior descending coronary artery was occluded for 15 min, followed by 60 min of reperfusion. Saline or icatibant (200 μg/kg) was administered intravenously slowly over 2 min, 5 min before reperfusion. In the saline-treated group, myocardial ischemic-reperfusion injury was evidenced by depressed MAP, depressed peak positive and negative d P/d t and elevated left ventricular end-diastolic pressure and enhanced oxidative stress [elevated plasma thiobarbituric acid reactive substances (TBARS; a marker for lipid peroxidation), depressed myocardial GSH (reduced glutathione), superoxide dismutase (SOD), catalase] and depletion of adenosine triphosphate (ATP) along with rise in plasma creatine phosphokinase (CPK). Administration of icatibant resulted in complete hemodynamic recovery together with repletion of ATP and reduction in plasma TBARS without any significant change in myocardial SOD, catalase and GSH. The results of the present study suggest a protective role of icatibant in myocardial ischemic-reperfusion injury.