PMID- 16268504
OWN - NLM
STAT- MEDLINE
DCOM- 20070320
LR  - 20141120
IS  - 0513-4870 (Print)
IS  - 0513-4870 (Linking)
VI  - 40
IP  - 8
DP  - 2005 Aug
TI  - [Protection of oxyphenamone against cardiac arrest-reperfusion injury of isolated 
      rat hearts].
PG  - 705-10
AB  - AIM: To ascertain the protective effect of oxyphenamone, a novel inodilator, 
      against myocardial ischemia-reperfusion injury. METHODS: A model of global 
      myocardial ischemia-reperfusion injury (I-R) was established by arresting the 
      infusion to heart 40 min followed by reperfusion 30 min in the preparations of 
      rat Langendorff' s hearts. The protective effects of oxyphenamone were evaluated 
      by the cardiac function, the activity of creatine phosphokinase (CPK) in coronary 
      efflux, the myocardial energy metabolism and antioxidation, the membrane 
      fluidity, the activity of ATPase, the calcium content and ultrastructure of 
      mitochondria. RESULTS: Administration of oxyphenamone to the infused heart before 
      cardiac arrest and during reperfusion ameliorated the decreases of myocardial 
      contractile force and coronary flow and the increase of the activity of CPK in 
      coronary efflux induced by cardiac arrest-reperfusion (A-R). At the concentration 
      of 1-10 micromol x L(-1) oxyphenamone dose-dependently antagonized the decrease 
      of myocardial adenosine triphosphate (ATP) and creatine phosphate (PCr) induced 
      by A-R, increased the activities of myocardial superoxide dismutase (SOD) and 
      glutathione peroxidase (GSH-px), decreased mitochondrial malondialdehyde (MDA) 
      content and increased membrane fluidity, glutathione (GSH) content and the 
      activities of GSH-px and ATPase of mitochondria. The parameters mentioned above 
      even maintained at normal level when high concentration of oxyphenamone (10 
      micromol x L(-1)) was applied. Oxyphenamone also antagonized the mitochondrial 
      calcium overload and the ultrastructure damage of mitochondria induced by A-R 
      obviously. Addition of oxyphenamone (1-100 micromol x L(-1)) to the system of 
      Fe2+-cysteine or Fe2+-H2O2, which could produce oxygen free radicals, decreased 
      MDA content and increased GSH and membrane fluidity of mitochondria 
      significantly. CONCLUSION: With the results of examinations of the cardiac 
      physiological function, myocardial energy metabolism and antioxidation and the 
      calcium content and ultrastructure of mitochondria, it is indicated that 
      oxyphenamone could protect the isolated rat heart against cardiac 
      arrest-reperfusion injury markedly and the mechanism of its action may be related 
      to the antioxidative effect of this agent.
FAU - Fan, Li-li
AU  - Fan LL
AD  - Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union 
      Medical College, Beijing 100050, China. fanlili@public3.bta.net.cn
FAU - Li, Hua
AU  - Li H
FAU - Fan, Ming-jie
AU  - Fan MJ
FAU - Zhang, Run-dong
AU  - Zhang RD
LA  - chi
PT  - English Abstract
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - China
TA  - Yao Xue Xue Bao
JT  - Yao xue xue bao = Acta pharmaceutica Sinica
JID - 21710340R
RN  - 0 (Organic Chemicals)
RN  - 0 (Protective Agents)
RN  - 0 (oxyphenamone)
RN  - SY7Q814VUP (Calcium)
SB  - IM
MH  - Animals
MH  - Calcium/metabolism
MH  - Coronary Circulation/drug effects
MH  - Female
MH  - In Vitro Techniques
MH  - Male
MH  - Membrane Fluidity/drug effects
MH  - *Mitochondria, Heart/metabolism/physiology/ultrastructure
MH  - Myocardial Contraction/*drug effects
MH  - *Myocardial Reperfusion Injury/metabolism/physiopathology
MH  - Myocardium/*metabolism
MH  - Organic Chemicals/pharmacology
MH  - Protective Agents/pharmacology
MH  - Random Allocation
MH  - Rats
MH  - Rats, Wistar
EDAT- 2005/11/05 09:00
MHDA- 2007/03/21 09:00
CRDT- 2005/11/05 09:00
PHST- 2005/11/05 09:00 [pubmed]
PHST- 2007/03/21 09:00 [medline]
PHST- 2005/11/05 09:00 [entrez]
PST - ppublish
SO  - Yao Xue Xue Bao. 2005 Aug;40(8):705-10.