Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat
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 i...
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| Published in | Regulatory peptides Vol. 115; no. 3; pp. 211 - 218 |
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| Main Authors | , , , |
| Format | Journal Article |
| Language | English |
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Shannon
Elsevier B.V
15.10.2003
Amsterdam Elsevier |
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| Abstract | 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. |
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| AbstractList | 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 microg/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 dP/dt 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.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 microg/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 dP/dt 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. 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 microg/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 dP/dt 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. 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. |
| Author | Manchanda, Subhash Chandra Kumari, Rashmi Maulik, Mohua Maulik, Subir Kumar |
| Author_xml | – sequence: 1 givenname: Rashmi surname: Kumari fullname: Kumari, Rashmi email: rashmikumari_s@hotmail.com organization: Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 2 givenname: Mohua surname: Maulik fullname: Maulik, Mohua organization: Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 3 givenname: Subhash Chandra surname: Manchanda fullname: Manchanda, Subhash Chandra organization: Department of Cardiology, All India Institute of Medical Sciences, New Delhi 110029, India – sequence: 4 givenname: Subir Kumar surname: Maulik fullname: Maulik, Subir Kumar organization: Department of Pharmacology, All India Institute of Medical Sciences, New Delhi 110029, India |
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| Cites_doi | 10.1291/hypres.24.179 10.1161/01.CIR.93.3.544 10.1111/j.1476-5381.1995.tb16357.x 10.1016/S0003-4975(99)01025-5 10.1023/A:1006808507605 10.1038/sj.bjp.0702089 10.1016/0003-2697(79)90738-3 10.1161/01.CIR.66.6.1146 10.1016/S0735-1097(98)00441-0 10.1016/S0167-0115(00)00094-X 10.1016/S0196-9781(01)00401-6 10.1006/phrs.1997.0182 10.1016/S0002-9149(97)00466-9 10.1016/S0003-4975(99)01073-5 10.1097/00005344-199200209-00014 10.1067/mhj.2000.103920 10.1038/320454a0 10.1172/JCI108178 10.1006/jmcc.2000.1130 10.1093/cvr/28.2.166 10.1161/01.STR.14.2.157 10.1161/01.CIR.96.7.2317 10.1161/01.HYP.35.4.942 10.1006/phrs.1997.0181 10.1161/01.CIR.0000046268.59922.A4 10.1016/S0002-9149(98)00531-1 10.2337/diab.45.1.S51 10.1016/S0002-8703(99)70323-6 10.1016/S0033-0620(98)80001-7 10.1172/JCI119360 10.1016/0003-9861(59)90090-6 10.1016/S0022-2828(87)80568-0 |
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| Keywords | Ischemic-reperfusion injury Bradykinin antagonist Cat Fissipedia Carnivora Peptide hormone Neuropeptide Felis catus In vivo Vertebrata Mammalia Reperfusion Bradykinin Antagonist |
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| Snippet | The effect of icatibant (Hoe-140), a selective bradykinin receptor (B
2) antagonist on myocardial ischemic-reperfusion injury was studied in open chest... The effect of icatibant (Hoe-140), a selective bradykinin receptor (B(2)) antagonist on myocardial ischemic-reperfusion injury was studied in open chest... |
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| SubjectTerms | 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 |
| Title | Protective effect of bradykinin antagonist Hoe-140 during in vivo myocardial ischemic-reperfusion injury in the cat |
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