[Protective effect on ischemic depletion of nucleotide phosphates in heart, brain, and kidney by cyclophosphamide].
The levels of ATP, ADP, and AMP in heart, brain, and kidney suffering from 10-min ischemia after decapitation in rats were determined by a modified reverse-phase HPLC set with uv detection. The ischemic depletion of ATP was alleviated and the total amount of high energy phosphates was markedly reduced by the treatment of po cyclophosphamide 20 and 100 mg.kg-1 x 3 d. The protective effect on depleting the total amount of high energy phosphates which was better preserved than ATP in ischemic organs by cyclophosphamide was evidenced in a dose-related manner. Cyclophosphamide induced leukopenia in circulating blood. Two reasons for the anti-arrhythmic effect of cyclophosphamide are suggested: 1) the depletion of leukocyte reduced the plugging effect of neutrophil in myocardial capillaries; 2) blocking the KATP channel by elevating ATP level in myocardium.
Zhu
Y
Y
Research Division of Pharmacology, China Pharmaceutical University, Nanjing.
Fan
Y Z
YZ
Dai
D Z
DZ
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000378:metabolism*; D002545:Brain Ischemia / Q000378:metabolism; D002851:Chromatography, High Pressure Liquid / Q000379:methods; D003520:Cyclophosphamide / Q000494:pharmacology*; D005260:Female; D007511:Ischemia / Q000378:metabolism; D007668:Kidney / Q000098:blood supply / Q000378:metabolism*; D007958:Leukocyte Count / Q000187:drug effects; D008297:Male; D017202:Myocardial Ischemia / Q000378:metabolism; D009206:Myocardium / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley
D000255:Adenosine Triphosphate; D003520:Cyclophosphamide