摘要
用离体大鼠心脏灌流模型观察了卡托普利(captopril,CAP)对阿霉素(adriamycin,ADM)急性心肌毒性作用的影响。结果表明,ADM(6mg/L)灌注能造成心肌收缩力的严重损害,冠脉灌注压的明显升高和心肌丙二醛含量的增加;治疗剂量的CAP(40mg/L)并不能保护心肌,反而加重了ADM对心脏的毒性作用。作者认为,在防治ADM所致的心功能不全时应慎用CAP。
he acute effects of adriamycin (ADM)on force of
contraction,coronary perfusion andcardiac malondialdehyde(MDA)content were measured in
isolated rat hearts Derfused atconstant flow, Experimental hearts were perfused for 60min
with Kreb- Hesenleit solutioncontaining 6mg/L ADM. treatmental hearts were perfused with
6mg/L of ADM and 40 mg/Lof captopil. In the experimental group,contractile force steadily
decreased to 2.5%±1.8(P<0. 01) of inital levels while coronary perfusion pressure steadily
increased to 230±48%(P<0. 01).The cardiac MDA content increased
significantly(P<0.01).These results suggest-ed that the cardiotoxicity of adriamcin might be
related to lipid peroxidation,However,capto-pril,an angiotensin converting enzyme inhibitor
possessing anti-free radical effect,did notprotect against the effects of adriamycin, but
deteriorated the cardiac function of hearts per-fused with adriamycin,The mechanism retnains
to be investigated.
出处
《湖南医科大学学报》
CSCD
1994年第2期105-107,共3页
Bulletin of Hunan Medical University
关键词
阿霉素
卡托普利
心肌
adriamycin
captdpril
adverse
effects
myocardium
toxicity
malondialdehyde
disease models,animal:rats