Protective effects of hyperpolarizing cardioplegia with pinacidil on myocardium in rats.
- Author:
Zhiwei HU
1
;
Kailun ZHANG
;
Wendong WANG
Author Information
1. Department of Cardiovascular Surgery, Xiehe Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430022.
- Publication Type:Journal Article
- MeSH:
Animals;
Cardioplegic Solutions;
pharmacology;
Cyclic Nucleotide-Gated Cation Channels;
Heart Arrest, Induced;
Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels;
In Vitro Techniques;
Ion Channels;
metabolism;
Male;
Myocardial Reperfusion Injury;
physiopathology;
prevention & control;
Myocardium;
metabolism;
Pinacidil;
pharmacology;
Potassium Channels;
Random Allocation;
Rats;
Rats, Wistar
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2002;22(1):31-33
- CountryChina
- Language:English
-
Abstract:
Whether the ATP-sensitive potassium channel opener pinacidil can provide myocardial protective effects in prolonged isolated global ischemic rat heart was investigated. On modified isolated rat working heart model, 40 hearts were divided into four groups randomly: Hyperpolarized arrest H-K solution containing pinacidil (50 mumol/L) (P1 and P2) and depolarized arrest St. Thomas' solution (S1 and S2) subjected to 15 degrees C hypothermia, 60 min (P1 and S1) or 120 min (P1 and S2) of ischemia and 30 min reperfusion. The experimental indices included cardioplegic efficiency, cardiac function, coronary blood flow, myocardial enzyme release, myocardial water and ATP content. Hyperpolarized arrest provided significantly better recovery of cardiac function than depolarized arrest. Postischemic coronary flow and myocardial ATP content were higher. The arrest time of electro-mechanical activities were longer than depolarized arrest. There were no differences among the groups in myocardial water contents. The hyperpolarized arrest solution containing pinacidil can provide a marked myocardial protective effect during prolonged hypothermic myocardial ischemia.