山东医药
山東醫藥
산동의약
SHANDONG MEDICAL JOURNAL
2003年
7期
4-6
,共3页
阻塞性睡眠呼吸暂停低通气综合征%经鼻持续气道正压通气%血管内皮细胞%纤溶系统
阻塞性睡眠呼吸暫停低通氣綜閤徵%經鼻持續氣道正壓通氣%血管內皮細胞%纖溶繫統
조새성수면호흡잠정저통기종합정%경비지속기도정압통기%혈관내피세포%섬용계통
为探讨经鼻持续气道正压通气(nCPAP)治疗前后阻塞性睡眠呼吸暂停低通气综合征(OSAHS)患者血管内皮细胞及纤溶系统的变化及临床意义,选择年龄、性别、体重指数(BMI)无明显差异的OSAHS患者38例和健康者对照组32例,用多导睡眠呼吸监测仪进行监测,以凝固法测定纤维蛋白原(Fg),发色底物法测组织纤溶酶原激活物活性(tPA:A)、纤溶酶原激活物抑制物-1活性(PAI-1:A),酶联免疫法测vonWillebrand因子(vWF)、组织纤溶酶原激活物抗原(tPA:Ag)、纤溶酶原含量(PLg:Ag)和纤溶酶原激活物抑制物-1含量(PAI-1:Ag).结果OSAHS组与对照组比较,vWF、Fg、PAI-1:Ag、PAI-1:A明显升高(P分别＜0.01,0.001,0.001,0.01),PLg:Ag、tPA:A、tPA:Ag、最低血氧饱和度(SaO2low)明显降低(P分别＜0.01,0.001,0.001,0.01).nCPAP治疗后与治疗前比较,vWF、Fg、PAI-1:Ag、PAI-1:A明显降低(P分别＜0.05,0.01,0.01,0.01),PLg:Ag、tPA:A、tPA:Ag、最低SaO2明显升高(P分别＜0.05,0.001,0.001,0.01).提示OSAHS患者血管内皮细胞损伤,凝血功能增强,纤溶系统功能减弱;nCPAP治疗能部分纠正各指标的异常.
為探討經鼻持續氣道正壓通氣(nCPAP)治療前後阻塞性睡眠呼吸暫停低通氣綜閤徵(OSAHS)患者血管內皮細胞及纖溶繫統的變化及臨床意義,選擇年齡、性彆、體重指數(BMI)無明顯差異的OSAHS患者38例和健康者對照組32例,用多導睡眠呼吸鑑測儀進行鑑測,以凝固法測定纖維蛋白原(Fg),髮色底物法測組織纖溶酶原激活物活性(tPA:A)、纖溶酶原激活物抑製物-1活性(PAI-1:A),酶聯免疫法測vonWillebrand因子(vWF)、組織纖溶酶原激活物抗原(tPA:Ag)、纖溶酶原含量(PLg:Ag)和纖溶酶原激活物抑製物-1含量(PAI-1:Ag).結果OSAHS組與對照組比較,vWF、Fg、PAI-1:Ag、PAI-1:A明顯升高(P分彆＜0.01,0.001,0.001,0.01),PLg:Ag、tPA:A、tPA:Ag、最低血氧飽和度(SaO2low)明顯降低(P分彆＜0.01,0.001,0.001,0.01).nCPAP治療後與治療前比較,vWF、Fg、PAI-1:Ag、PAI-1:A明顯降低(P分彆＜0.05,0.01,0.01,0.01),PLg:Ag、tPA:A、tPA:Ag、最低SaO2明顯升高(P分彆＜0.05,0.001,0.001,0.01).提示OSAHS患者血管內皮細胞損傷,凝血功能增彊,纖溶繫統功能減弱;nCPAP治療能部分糾正各指標的異常.
위탐토경비지속기도정압통기(nCPAP)치료전후조새성수면호흡잠정저통기종합정(OSAHS)환자혈관내피세포급섬용계통적변화급림상의의,선택년령、성별、체중지수(BMI)무명현차이적OSAHS환자38례화건강자대조조32례,용다도수면호흡감측의진행감측,이응고법측정섬유단백원(Fg),발색저물법측조직섬용매원격활물활성(tPA:A)、섬용매원격활물억제물-1활성(PAI-1:A),매련면역법측vonWillebrand인자(vWF)、조직섬용매원격활물항원(tPA:Ag)、섬용매원함량(PLg:Ag)화섬용매원격활물억제물-1함량(PAI-1:Ag).결과OSAHS조여대조조비교,vWF、Fg、PAI-1:Ag、PAI-1:A명현승고(P분별＜0.01,0.001,0.001,0.01),PLg:Ag、tPA:A、tPA:Ag、최저혈양포화도(SaO2low)명현강저(P분별＜0.01,0.001,0.001,0.01).nCPAP치료후여치료전비교,vWF、Fg、PAI-1:Ag、PAI-1:A명현강저(P분별＜0.05,0.01,0.01,0.01),PLg:Ag、tPA:A、tPA:Ag、최저SaO2명현승고(P분별＜0.05,0.001,0.001,0.01).제시OSAHS환자혈관내피세포손상,응혈공능증강,섬용계통공능감약;nCPAP치료능부분규정각지표적이상.
