Protective effect of ACE inhibitors on ischemia-reperfusion-induced arrhythmias in rats: Is this effect related to the free radical scavenging action of these drugs?


BIRINCIOGLU M., AKSOY T., OLMEZ E., Acet A.

FREE RADICAL RESEARCH, cilt.27, sa.4, ss.389-396, 1997 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 27 Sayı: 4
  • Basım Tarihi: 1997
  • Doi Numarası: 10.3109/10715769709065778
  • Dergi Adı: FREE RADICAL RESEARCH
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.389-396
  • İnönü Üniversitesi Adresli: Evet

Özet

The antiarrhythmic effects of captopril, a sulphydryl-containing angiotensin converting enzyme (ACE) inhibitor, were compared with those of the non-sulphydryl-containing ACE inhibitor Lisinopril and the sulphydryl-containing agent glutathione in an in vivo rat model of coronary artery ligation. To produce arrhythmia, the left main coronary artery was occluded for 7 min, followed by 7 min of reperfusion. Captopril (3 mg kg(-1)) and lisinopril (0.1, 0.3 or 1 mg kg(-1)) caused marked decreases in mean arterial blood pressure (BP) and heart rate, whereas glutathione (5 mg kg(-1)) had no effect on them. The incidence of ventricular tachycardia (VT) on ischemia and reperfusion was significantly reduced by captopril and lisinopril. Captopril and 1 mg kg(-1) lisinopril also significantly decreased the number of VEB during occlusion and the duration of VT on reperfusion, respectively. These drugs also attenuated the incidence of reversible ventricular fibrillation (VF) and the number of ventricular ectopic beats (VEB) during reperfusion. However, glutathione only reduced the incidence of VT on reperfusion, significantly. These results suggest that, in this experimental model, ACE inhibitors limit the arrhythmias following ischemia-reperfusion and free radical scavenging action of these drugs does not have a major contributory role in their protective effect.