脑卒中患者血浆神经降压素水平及其动态变化

Level of plasma neurotensin in patients with stroke and its dynamic changes

目的:观察脑出血、脑梗死、蛛网膜下腔出血患者血浆神经降压素(neurotensin,NT)水平改变及其动态变化,探讨NT参与各型脑卒中及其伴发病中的病理生理机制及对功能预后评估的意义。方法:2002-03/2003-09,实验在济南长城医院神经内科、山东大学附属第二医院神经内科、山东省立医院、山东大学齐鲁医院神经内科与泰山医学院微循环研究所完成。选择脑卒中138例,其中脑出血组46例,脑梗死组62例,蛛网膜下腔出血组30例。病例依病情轻重、病灶大小、病程、伴发病积分、有无高血压史等分组,选择28例健康查体者作为对照组。用放免法检测血浆NT浓度。结果:脑梗死组NT水平(467.31±363.42)ng/L显著高于对照组(76.54±59.53)ng/L(t=4.638,P<0.0001),于发病后24h内显著升高(228.10±123.13)ng/L,4～7d达高峰(648.01±337.38)ng/L,8～15d开始下降(525.67±264.11)ng/L,15d后仍在较高水平(392.57±262.35)ng/L;重型(762.91±446.0)ng/L与大灶组(404.39±206.49)ng/L显著高于轻型(153.86±130.47)ng/L与小灶组(200.27±137.64)ng/L(P<0.01),伴发病积分≥6分组NT水平(623.11±377.97)ng/L显著高于<6分组(236.74±132.22)ng/L(t=3.506,P<0.001),高血糖组NT水平(673.26±331.00)ng/L显著高于正常血糖组(328.16±216.69)

AIM:To observe the change of plasma neurotensin(NT) in patients with cerebral hemorrhage,cerebral infarction and subarachnoid hemorrhage,and investigate the clinical significance of NT in pathogenetic and physiological mechanisms of cerebral hemorrhage,cerebral infarction and subarachnoid hemorrhage and the prognosis. METHODS:The experiment was finished in the Department of Neurology,Jinan Changcheng Hospital;Department of Neurology,Second Affiliated Hospital of Shandong University;Shandong Provincial Hospital;Department of Neurology,Qilu Hospital of Shandong University and Institute of Microcirculation,Taishan Medical College from March 2002 to September 2003.The levels of neurotensin in plasma were measured by radioimmunoassay in 138 cases with cerebrovascular disease and 28 healthy control subjects. 138 patients were divided into cerebral hemorrhage group(46 cases),cerebral infarction group(62 cases) and subarachnoid hemorrhage group(30 cases).The groups were divided by severe condition,volume of cerebral infarction and cerebral hemorrhage,course of disease,syndromic integra,history of high blood pressure,etc. RESULTS:The level of neurotensin in plasma in the cerebral infarction group [(467.31±363.42) ng/L] was significantly higher than that in control group [(76.54±59.53 ) ng/L](t= 4.638,P< 0.000 1). It started to increase significantly during the first day[(228.10±123.13) ng/L] and reached peak from 4 to 7 days[(648.01±337.38) ng/L],it began to decrease from the eighth to fifteen days[(525.67±264.11) ng/L], and it was higher than that in control group after 15 days[(392.57±262.35) ng/L].It was higher in the groups of severe condition[(762.91±446.0) ng/L] and large volume[(404.39 ±206.49) ng/L] of cerebral infarction than that in the groups of mild condition[(153.86±130.47) ng/L](P< 0.01) and small volume of cerebral infarction[(200.27±137.64) ng/L](P< 0.01).It was higher in the groups of ≥6 scores of some complicated diseases[(623.11±377.97) ng/L],high blood sugar[(673.26±331.00) ng/L] and atrial fibrillation[(800.36 ±308.86) ng/L] than that in the groups of < 6 scores of some complicated diseases[(236.74 ±132.22) ng/L],normal blood sugar[(328.16 ±216.69) ng/L] and non atrial fibrillation[(395.48±224.92) ng/L](P< 0.01).The levels of neurotensin in plasma in the cerebral hemorrhage group[(347.13±200.11) ng/L] was increased than that in control group [(76.54±59.53) ng/L](t=4.176,P< 0.000 1). It started to increase significantly during the first day[(151.61±101.57) ng/L] and reached peak from 1 to 3 days[(495.83±224.23) ng/L], it began to decrease from the eighth day[(181.85±102.56) ng/L],and it was higher than that in control group after 15 days[(156.62±29.46) ng/L].It was higher in the groups of severe condition[(450.90±242.82) ng/L] and large volume[(431.07 ±237.82) ng/L] of cerebral hemorrhage than that in the groups of mild condition[(135.03±77.26) ng/L] and small volume of cerebral hemorrhage[(216.56±165.79) ng/L](P< 0.01).It was higher in the groups of ≥6 scores of some complicated diseases[(425.18±234.75) ng/L],high blood sugar[(519.21±280.62) ng/L],high blood pressure[(408.91 ±217.00) ng/L] and alimentary canal bleeding(449.00±238.58) ng/L than that in the groups of < 6 scores of some complicated diseases[(200.80 ±136.10) ng/L], normal blood sugar[(273.86±189.62) ng/L],normal blood pressure [(150.57±88.14) ng/L] and non alimentary canal bleeding[(188.68±112.55) ng/L](P< 0.01).The levels of neurotensin in plasma in the subarachnoid hemorrhage group[(500.40±345.21) ng/L] was increased than that in control group[(76.54±59.53) ng/L](t=4.921,P< 0.000 1). It started to increase during the first day[(411.17±165.72) ng/L] and reached peak on day 1 to 3[(583.86±311.61) ng/L],it began to decrease from the eighth day[(297.48±106.94) ng/L[,and it was higher than that in control group after 15 days[(153.74±126.21) ng/L].It was higher in the group of delayed ischemic deficits of subarachnoid hemorrhage[(598.08 ±395.77) ng/L] than that in the group of non delayed ischemic defi