摘要
用6-羟多巴胺(6-OHDA)抑制交感神经释放神经肽Y(NPY)的作用,观察内毒素血症时NPY对大白鼠心率(HR)、平均动脉压(MAP)、心输出量(CO)、中心静脉压(CVP)和总末梢血管阻力(TPR)变化的影响。结果表明:抑制NPY释放后再给予内毒素时,血浆中NPY含量上升24A%,同时动物的MAP和TPR与内毒素血症对照组相比,分别降低约9.5%和13.7%(P均<0.05)。注射外源性NPY后,MAP、CO和CVP与内毒素血症对照组相比,则分别升高34.6%、15.6%和156.5%(p均<0.01),而TPR则比单纯抑制NPY组升高32.5%(P<0.;01)。另外给予致死剂量内毒素后,动物的存活时间为50.70±9.17min;同时给予6-OHDA时,动物的存活时间则延长至176.60±48.30min(P<0.01)。提示内毒素血症早期,血浆中NPY含量的升高参与了血流动力学的调节。
We studied changes of plasma neuropeptide Y(NPY) and the relationship
between plasma NpYand changes of mean arterial pressure (MAP),heartrate(HR) ,cardiac
output(CO) ,central venous pres-sure(CVP)and total peripheral resistance (TPR) inrats with
endotoxemia.It was found that released volume of NPY by endotoxin was only increased
by24.4%when NPY was inhibited previously by6-hydroxydopamine(6-OHDA),and
meanwhile,MAP and TPR decreased Significantly by about9.5% and13.7%,respectively(p<0.05)
in compari-son with the control endotoxemia group-As soon asexogenous NPY was given,the
level of MAP, CO,CVP increased significantly(about 34.6%,15.6%,156.5%,respectively as
compared with the controlendotoxemia group),however,TPR was increased byabout
32.5%(p<0.01)compared with the NPY inhi-bition group,In addition,the mean survival time forrats
given a lethal dose of endotoxin was50.7±9.2minutes,but was increased to 176.6±48.3
minuteswhile 6-OHDA was simultaneously administered(p<0.01).It is considered that the
increased plasmaNPY,as an important compensatory mechanism,is involved in the regulation
of hemodynamics duringthe early stage of endotoxemia。
出处
《中国危重病急救医学》
CAS
CSCD
1994年第2期72-74,共3页
Chinese Critical Care Medicine
基金
八五军队医药卫生科研基金