Parikh V, Singh M
Department of Pharmaceutical Sciences and Drug Research, Punjabi University, Patiala, India.
J Cardiovasc Pharmacol. 1997 Aug;30(2):149-56. doi: 10.1097/00005344-199708000-00001.
Our study was designed to investigate the role of resident cardiac mast cells in the cardioprotective effect of ischemic preconditioning. Ischemic/compound 48/80 preconditioning and treatment with compound 48/80, a mast cell degranulator (1 microg/ml), produced cardioprotective and antiarrhythmic effects in isolated perfused rat heart subjected to 30-min global ischemia followed by 30-min reperfusion. Four episodes of ischemic/compound 48/80 preconditioning and compound 48/80 treatment markedly reduced the release of lactate dehydrogenase (LDH) and creatine kinase (CK) in coronary perfusate and the incidence of ventricular premature beats (VPBs) and ventricular tachycardia or fibrillation (VT/VF) during the reperfusion phase. The release of mast cell peroxidase (MPO), a marker of mast cell degranulation in coronary perfusate, increased immediately after ischemic and compound 48/80 preconditioning. The cardioprotective and antiarrhythmic effect of ischemic/compound 48/80 preconditioning was lost within 60 min. It is proposed that the cardioprotective effect of ischemic preconditioning, which lasts for 60 min in isolated rat heart, may be ascribed to degranulation of resident cardiac mast cells.
我们的研究旨在探讨驻留心脏肥大细胞在缺血预处理的心脏保护作用中的作用。缺血/化合物48/80预处理以及用肥大细胞脱颗粒剂化合物48/80(1微克/毫升)进行处理,在经历30分钟全心缺血随后30分钟再灌注的离体灌注大鼠心脏中产生了心脏保护和抗心律失常作用。四次缺血/化合物48/80预处理和化合物48/80处理明显减少了冠状动脉灌注液中乳酸脱氢酶(LDH)和肌酸激酶(CK)的释放,以及再灌注期室性早搏(VPB)和室性心动过速或颤动(VT/VF)的发生率。肥大细胞过氧化物酶(MPO)是冠状动脉灌注液中肥大细胞脱颗粒的标志物,在缺血和化合物48/80预处理后立即增加。缺血/化合物48/80预处理的心脏保护和抗心律失常作用在60分钟内消失。有人提出,在离体大鼠心脏中持续60分钟的缺血预处理的心脏保护作用可能归因于驻留心脏肥大细胞的脱颗粒。