中华急诊医学杂志
中華急診醫學雜誌
중화급진의학잡지
CHINESE JOURNAL OF EMERGENCY MEDICINE
2010年
12期
1249-1252
,共4页
秦文玲%曹红%谷玲%王琪%朱鸿
秦文玲%曹紅%穀玲%王琪%硃鴻
진문령%조홍%곡령%왕기%주홍
急性脑梗死%神经肽Y%结构型一氧化氮合酶%诱导型一氧化氮合酶%梗死体积%NIHSS评分
急性腦梗死%神經肽Y%結構型一氧化氮閤酶%誘導型一氧化氮閤酶%梗死體積%NIHSS評分
급성뇌경사%신경태Y%결구형일양화담합매%유도형일양화담합매%경사체적%NIHSS평분
Acute cerebral infarction%Neuropeptide Y%Structural nitric oxide synthase%Inducible nitric oxide synthase%Size of cerebral infarction%NIHSS score
目的 观察急性脑梗死(ACI)患者血浆神经肽Y(NPY)、血清一氧化氮合酶(NOS)水平的动态变化,探讨二者的关系及其临床意义.方法 采用前瞻性对照研究的方法.脑梗死(CI)组为大连医科大学附属一院神经科2008年5月至2009年3月的住院患者,共30例(男21例,女9例),年龄(58.07±12.15)岁.首次发病,病程48 h以内,符合中华神经科学会及中华神经外科学会1996年制定的脑梗死诊断标准.排除半年内患急性心肌梗死、周围血管病、感染、肿瘤、严重脏器功能障碍等疾病.对照组均为同期健康体检者,共27例(男15例,女12例),年龄(55.00±11.03)岁.两组具有可比性.采集对照组及CI组(发病48 h内和病后10 d)空腹肘静脉血,用放免法检测NPY水平,化学比色法检测NOS水平.计算责任梗死灶体积,应用美国国立卫生研究院卒中量表(NIHSS)进行神经功能缺失程度评定.样本间的构成比采用x2检验,组间差别的分析采用t检验,双变量间单因素相关分析采用直线相关分析.结果 ①NPY水平两组差异无统计学意义(P＜0.05).②结构型NOS(cNOS)水平发病48 h内比对照组显著降低,与梗死体积、同期NIHSS评分呈显著负相关(P＜0.05),与NIHSS评分的差值呈显著正相关(P＜0.05).病后10 d比发病48 h内显著升高.③诱导型NOS(iNOS)水平发病48 h内比对照组显著升高(P＜0.05),与梗死体积、同期NIHSS评分呈显著正相关(P＜0.05),与NIHSS评分的差值呈显著负相关(P＜0.05).病后10 d比发病48 h内显著降低(P＜0.05).④CI组NPY水平与cNOS,iNOS水平没有显著相关(P＜0.05).NPY水平的差值与cNOS水平的差值呈显著负相关(P＜0.05).结论 ACI患者血浆NPY水平变化不显著,与病情无明显相关.发病48 h内血清cNOS水平与病情呈显著负相关,iNOS水平与病情呈显著正相关,其水平可以反应CI的严重程度.发病48 h内和病后10 d血浆NPY水平的变化与血清cNOS水平的变化呈显著负相关.
目的 觀察急性腦梗死(ACI)患者血漿神經肽Y(NPY)、血清一氧化氮閤酶(NOS)水平的動態變化,探討二者的關繫及其臨床意義.方法 採用前瞻性對照研究的方法.腦梗死(CI)組為大連醫科大學附屬一院神經科2008年5月至2009年3月的住院患者,共30例(男21例,女9例),年齡(58.07±12.15)歲.首次髮病,病程48 h以內,符閤中華神經科學會及中華神經外科學會1996年製定的腦梗死診斷標準.排除半年內患急性心肌梗死、週圍血管病、感染、腫瘤、嚴重髒器功能障礙等疾病.對照組均為同期健康體檢者,共27例(男15例,女12例),年齡(55.00±11.03)歲.兩組具有可比性.採集對照組及CI組(髮病48 h內和病後10 d)空腹肘靜脈血,用放免法檢測NPY水平,化學比色法檢測NOS水平.計算責任梗死竈體積,應用美國國立衛生研究院卒中量錶(NIHSS)進行神經功能缺失程度評定.樣本間的構成比採用x2檢驗,組間差彆的分析採用t檢驗,雙變量間單因素相關分析採用直線相關分析.結果 ①NPY水平兩組差異無統計學意義(P＜0.05).②結構型NOS(cNOS)水平髮病48 h內比對照組顯著降低,與梗死體積、同期NIHSS評分呈顯著負相關(P＜0.05),與NIHSS評分的差值呈顯著正相關(P＜0.05).病後10 d比髮病48 h內顯著升高.③誘導型NOS(iNOS)水平髮病48 h內比對照組顯著升高(P＜0.05),與梗死體積、同期NIHSS評分呈顯著正相關(P＜0.05),與NIHSS評分的差值呈顯著負相關(P＜0.05).病後10 d比髮病48 h內顯著降低(P＜0.05).④CI組NPY水平與cNOS,iNOS水平沒有顯著相關(P＜0.05).NPY水平的差值與cNOS水平的差值呈顯著負相關(P＜0.05).結論 ACI患者血漿NPY水平變化不顯著,與病情無明顯相關.髮病48 h內血清cNOS水平與病情呈顯著負相關,iNOS水平與病情呈顯著正相關,其水平可以反應CI的嚴重程度.髮病48 h內和病後10 d血漿NPY水平的變化與血清cNOS水平的變化呈顯著負相關.
목적 관찰급성뇌경사(ACI)환자혈장신경태Y(NPY)、혈청일양화담합매(NOS)수평적동태변화,탐토이자적관계급기림상의의.방법 채용전첨성대조연구적방법.뇌경사(CI)조위대련의과대학부속일원신경과2008년5월지2009년3월적주원환자,공30례(남21례,녀9례),년령(58.07±12.15)세.수차발병,병정48 h이내,부합중화신경과학회급중화신경외과학회1996년제정적뇌경사진단표준.배제반년내환급성심기경사、주위혈관병、감염、종류、엄중장기공능장애등질병.대조조균위동기건강체검자,공27례(남15례,녀12례),년령(55.00±11.03)세.량조구유가비성.채집대조조급CI조(발병48 h내화병후10 d)공복주정맥혈,용방면법검측NPY수평,화학비색법검측NOS수평.계산책임경사조체적,응용미국국립위생연구원졸중량표(NIHSS)진행신경공능결실정도평정.양본간적구성비채용x2검험,조간차별적분석채용t검험,쌍변량간단인소상관분석채용직선상관분석.결과 ①NPY수평량조차이무통계학의의(P＜0.05).②결구형NOS(cNOS)수평발병48 h내비대조조현저강저,여경사체적、동기NIHSS평분정현저부상관(P＜0.05),여NIHSS평분적차치정현저정상관(P＜0.05).병후10 d비발병48 h내현저승고.③유도형NOS(iNOS)수평발병48 h내비대조조현저승고(P＜0.05),여경사체적、동기NIHSS평분정현저정상관(P＜0.05),여NIHSS평분적차치정현저부상관(P＜0.05).병후10 d비발병48 h내현저강저(P＜0.05).④CI조NPY수평여cNOS,iNOS수평몰유현저상관(P＜0.05).NPY수평적차치여cNOS수평적차치정현저부상관(P＜0.05).결론 ACI환자혈장NPY수평변화불현저,여병정무명현상관.발병48 h내혈청cNOS수평여병정정현저부상관,iNOS수평여병정정현저정상관,기수평가이반응CI적엄중정도.발병48 h내화병후10 d혈장NPY수평적변화여혈청cNOS수평적변화정현저부상관.
Objective To observe the dynamic changes in plasma levels of neuropeptide Y (NPY) in patients with acute cerebral infarction (ACI) and the serum nitric oxide synthase (NOS) in order to find out the relationship between each other as well as their clinical significance. Method A prospective and control study was done in 30 patients with ACI including 21 male and 9 female with average age of (58.07 ± 12. 1S) years admitted from May 2008 to March 2009. These patients hit the diagnostic criteria for cerebral infarction (CI) set by the Chinese Society for Neruoscience and the Chinese Association of Neurosurgery in 1996 for their first attack of CI was treated within 48 hours. Patients with acute myocardial infarction, peripheral vascular disease, infection, tumor,or severe organic functional impairment, etc within six months were excluded. Another 27 healthy subjects asking for routine physical examination including 15 male and 12 female with average age of (55.00± 11.03) years were included as control group at the same period. The two groups were comparable. The blood samples of fasted subjects of control group and CI patients 48 hours after and within 10 days after attack were taken to examine the level of NPY by using radioimmunoassay and the level of serum NOS by using chemical colorimetry. The size of responsible focus of CI was calculated, and the degree of neurological deficits were estimated with Stroke Scales set by the American National Institutes Of Health (NIHSS). The chi-square test was used for constituent ratios within samples, while t -test was applied to analysis of differences between two groups, and linear was used for bivariate simple correlation analysis. Results (1) There was no significant difference in NPY between two groups. (2) The level of constructional NOS (cNOS) within 48 hours after attack in CI group was significantly lower than that in control group, and it was significantly and negatively correlated with the size of infarction and the NIHSS scores at the same period, whereas it significantly and positively correlated with difference in NIHSS scores, while it increased more significantly 10 days after attack than it did within 48 hours after attack. (3) The level of inducible NOS (iNOS) within 48 hours after attack in CI group was significantly higher than that in control group, and it was significantly and positively correlated with the size of infarctionand NIHSS scores at the same period, and it significantly and negatively crrelated with the difference in NIHSS scores, while it decreased more significantly 10 days after attack than it did within 48 hours after attack. (4) The level of NPY was not correlated with both cNOS and iNOS in CI group. The difference in levels of NPY was negatively and significantly correlated with the difference in levels of cNOS. Conclusions There was no significant change in plasma NPY level in ACI patients, and it was not correlated significantly with the disease itself. The serum cNOS was negatively correlated with the disease itself significantly within 48 hours after attack. The iNOS level was positively correlated with the disease itself significantly, and it reflected the severity of CI within 48 hours after attack. The changes of NPY level in plasma were significantly and negatively correlated with the changes of cNOS level in serum within 48 hours and 10 days after attack.
