中华医学杂志
中華醫學雜誌
중화의학잡지
National Medical Journal of China
2013年
35期
2782-2785
,共4页
李素玮%刘大为%王小亭%张斌%陈秀凯%柴文昭%张宏民%杨全会%何怀武
李素瑋%劉大為%王小亭%張斌%陳秀凱%柴文昭%張宏民%楊全會%何懷武
리소위%류대위%왕소정%장빈%진수개%시문소%장굉민%양전회%하부무
休克,脓毒性%休克%感染%左心室-动脉偶联
休剋,膿毒性%休剋%感染%左心室-動脈偶聯
휴극,농독성%휴극%감염%좌심실-동맥우련
Shock,septic%Shock%Infection%Ventricular-arterial coupling
目的 探讨感染性休克左心室-动脉偶联关系的变化及机制.方法 通过静脉注射内毒素建立感染性休克兔模型,随机分为2组,假手术组(S组,n=6),内毒素组(E组,n=6)；分别在0h点(手术完成后30 min),2h点(注射内毒素或生理盐水后1h)和4h点(注射内毒素或生理盐水后3h),行超声检查及血流动力学监测,记录各血流动力学指标.结果 E组2h点左心室收缩末弹性(Ees)低于0h点,(75.7±5.2) mm Hg/ml比(90.8±7.2) mm Hg/ml；4 h点Ees低于2h点,(58.5±3.6)mm Hg/ml比(75.7±5.2)mm Hg/ml;差异均有统计学意义(均P＜0.05).E组2h点和4h点左心室舒张末容积(LVDV)均小于0h点,(3.3±0.2)ml比(3.6±0.3)ml和(3.3±0.2) ml比(3.6±0.3)ml；4 h点左心室顺应性(Ced)低于0h和2h点,(0.6±0.1)ml/mm Hg比(0.7±0.1)mL/mm Hg和(0.6±0.1)ml/mm Hg比(0.8±0.1)ml/mm Hg,差异均有统计学意义(均P＜0.05).E组2h和4h点有效动脉弹性(Ea)均低于0h点,(41.4±2.9) mm Hg/ml比(50.5±3.2) mm Hg/ml和(40.1 ±2.7)比(50.5±3.2) mm Hg/ml,差异均有统计学意义(均P＜0.05).E组4h点Ea/Ees高于0h和2h点,(0.7±0.1)比(0.6±0.1)和(0.7±0.1)比(0.6±0.1),差异均有统计学意义(均P ＜0.05)；Ea/Ees2 h点与0h点差异无统计学意义,(0.6±0.1)比(0.6±0.1),P＞0.05.结论 感染性休克代偿期左心室-动脉偶联关系无显著变化,感染休克失代偿期偶联不匹配,主要与心肌收缩功能相对心室后负荷降低更显著有关,可能与心脏舒张功能障碍有关.
目的 探討感染性休剋左心室-動脈偶聯關繫的變化及機製.方法 通過靜脈註射內毒素建立感染性休剋兔模型,隨機分為2組,假手術組(S組,n=6),內毒素組(E組,n=6)；分彆在0h點(手術完成後30 min),2h點(註射內毒素或生理鹽水後1h)和4h點(註射內毒素或生理鹽水後3h),行超聲檢查及血流動力學鑑測,記錄各血流動力學指標.結果 E組2h點左心室收縮末彈性(Ees)低于0h點,(75.7±5.2) mm Hg/ml比(90.8±7.2) mm Hg/ml；4 h點Ees低于2h點,(58.5±3.6)mm Hg/ml比(75.7±5.2)mm Hg/ml;差異均有統計學意義(均P＜0.05).E組2h點和4h點左心室舒張末容積(LVDV)均小于0h點,(3.3±0.2)ml比(3.6±0.3)ml和(3.3±0.2) ml比(3.6±0.3)ml；4 h點左心室順應性(Ced)低于0h和2h點,(0.6±0.1)ml/mm Hg比(0.7±0.1)mL/mm Hg和(0.6±0.1)ml/mm Hg比(0.8±0.1)ml/mm Hg,差異均有統計學意義(均P＜0.05).E組2h和4h點有效動脈彈性(Ea)均低于0h點,(41.4±2.9) mm Hg/ml比(50.5±3.2) mm Hg/ml和(40.1 ±2.7)比(50.5±3.2) mm Hg/ml,差異均有統計學意義(均P＜0.05).E組4h點Ea/Ees高于0h和2h點,(0.7±0.1)比(0.6±0.1)和(0.7±0.1)比(0.6±0.1),差異均有統計學意義(均P ＜0.05)；Ea/Ees2 h點與0h點差異無統計學意義,(0.6±0.1)比(0.6±0.1),P＞0.05.結論 感染性休剋代償期左心室-動脈偶聯關繫無顯著變化,感染休剋失代償期偶聯不匹配,主要與心肌收縮功能相對心室後負荷降低更顯著有關,可能與心髒舒張功能障礙有關.
목적 탐토감염성휴극좌심실-동맥우련관계적변화급궤제.방법 통과정맥주사내독소건립감염성휴극토모형,수궤분위2조,가수술조(S조,n=6),내독소조(E조,n=6)；분별재0h점(수술완성후30 min),2h점(주사내독소혹생리염수후1h)화4h점(주사내독소혹생리염수후3h),행초성검사급혈류동역학감측,기록각혈류동역학지표.결과 E조2h점좌심실수축말탄성(Ees)저우0h점,(75.7±5.2) mm Hg/ml비(90.8±7.2) mm Hg/ml；4 h점Ees저우2h점,(58.5±3.6)mm Hg/ml비(75.7±5.2)mm Hg/ml;차이균유통계학의의(균P＜0.05).E조2h점화4h점좌심실서장말용적(LVDV)균소우0h점,(3.3±0.2)ml비(3.6±0.3)ml화(3.3±0.2) ml비(3.6±0.3)ml；4 h점좌심실순응성(Ced)저우0h화2h점,(0.6±0.1)ml/mm Hg비(0.7±0.1)mL/mm Hg화(0.6±0.1)ml/mm Hg비(0.8±0.1)ml/mm Hg,차이균유통계학의의(균P＜0.05).E조2h화4h점유효동맥탄성(Ea)균저우0h점,(41.4±2.9) mm Hg/ml비(50.5±3.2) mm Hg/ml화(40.1 ±2.7)비(50.5±3.2) mm Hg/ml,차이균유통계학의의(균P＜0.05).E조4h점Ea/Ees고우0h화2h점,(0.7±0.1)비(0.6±0.1)화(0.7±0.1)비(0.6±0.1),차이균유통계학의의(균P ＜0.05)；Ea/Ees2 h점여0h점차이무통계학의의,(0.6±0.1)비(0.6±0.1),P＞0.05.결론 감염성휴극대상기좌심실-동맥우련관계무현저변화,감염휴극실대상기우련불필배,주요여심기수축공능상대심실후부하강저경현저유관,가능여심장서장공능장애유관.
Objective To explore the variations of left ventricular-arterial coupling and elucidate its mechanisms in septic shock.Methods Septic shock rabbits were established by an intravenous injection of endotoxin.A total of 12 rabbits were divided randomly into sham operation group (S,n =6) and endotoxin injection group (E,n =6).Ultrasonic echocardiography and hemodynamic monitoring were conducted at 0 h (30-min post-operation),2 h (1-hour after endotoxin or saline injection) and 4 h (3-hour after endotoxin or saline injection) and the relative hemodynamic indices were recorded.Results (1) In E group,endsystolic elastance (Ees) at 2 h was lower than that at 0 h(75.72 ±5.16 vs 90.77 ±7.17 mm Hg/ml) and Ees at 4 h was lower than that at 2 h (58.45 ± 3.63 vs 75.72 ± 5.16 mm Hg/ml,P ＜0.05).(2) In E group,left ventricular diastolic volume (LVDV) at 2 h and 4 h were both lower than that at 0 h (3.26 ± 0.21 vs 3.58 ±0.25 ml,3.27 ±0.19 vs 3.58 ±0.25 ml).And left ventricular end diastolic compliance (Ced) at 4 h were lower than that at 0 h and 2 h (0.61 ±0.05 vs 0.74 ±0.07 ml/mm Hg,0.61 ±0.05 vs 0.75±0.08 ml/mmHg,P＜0.05).(3) In E group,Ea at 2 h and 4 h was lower than that at 0 h (41.35 ±2.87 vs 50.46 ±3.22 mm Hg/ml,40.13 ±2.68 vs 50.46 ±3.22 mm Hg/ml,P ＜0.05).(4)In E group,Ea/Ees at 4 h was higher than that at 0 h and 4 h (0.70 ± 0.07 vs 0.57 ± 0.06,0.70 ± 0.07 vs 0.56 ± 0.05,P ＜ 0.05).And Ea/Ees at 2 h had no significant difference with that at 0 h (0.56 ± 0.05 vs 0.57 ± 0.06,P ＜ 0.05).Conclusion During compensatory stage of septic shock,left ventricular-arterial coupling shows no significant variation.However,during decompensatory stage of septic shock,there is significant left ventricular-arterial decoupling.The main reason for decoupling lies in that the decrease of left myocardial contractility is more significant than that of left ventricular afterload.And ventricular diastolic dysfunction may also participate.
