中华围产医学杂志
中華圍產醫學雜誌
중화위산의학잡지
CHINESE JOURNAL OF PERINATAL MEDICINE
2014年
6期
388-395
,共8页
胡雪峰%黄丽萍%贲晓明%张宝贤%刘江勤
鬍雪峰%黃麗萍%賁曉明%張寶賢%劉江勤
호설봉%황려평%분효명%장보현%류강근
窒息,新生儿%氧吸入疗法%复苏术%每搏输出量%超氧化物歧化酶
窒息,新生兒%氧吸入療法%複囌術%每搏輸齣量%超氧化物歧化酶
질식,신생인%양흡입요법%복소술%매박수출량%초양화물기화매
Asphyxia neonatorum%Oxygen inhalation therapy%Resuscitation%Stroke volume%Superoxide dismutase
目的:通过建立新生猪全身缺氧模型,观察空气或氧气复苏对新生猪心脏泵血功能和心肌超氧化物歧化酶活性的影响。方法32只体重1.6~2.5 kg新生猪随机分为3组,对照组8只,无缺氧损伤,机械通气下给予空气;空气组12只,机械通气下给予120 min全身性缺氧后,空气复苏240 min;氧气组12只,机械通气下给予120 min全身性缺氧后,给予纯氧复苏30 min,然后改为空气复苏210 min。记录缺氧120 min末(复苏0 min)和复苏10、30、60、120、180及240 min时的血气、血压和血流变化。复苏240 min时结束实验,冻存左心室标本,采用酶学法检测超氧化物歧化酶活性。采用单因素方差分析、重复测量的双因素方差分析及Student-Newman-Keuls检验进行统计学分析。结果缺氧造成动物显著的酸中毒、低血压和低氧血症。(1)动脉氧分压:复苏10和30 min时,对照组、空气组与氧气组3组间动脉氧分压差异均有统计学意义[10 min:(67±4)、(78±12)与(409±42) mmHg(1 mmHg=0.133 kPa),F=580.19;30 min:(68±3)、(79±15)与(342±62) mmHg,F=173.67;P均<0.01]。氧气组动脉氧分压高于对照组和空气组(10 min:q值分别为42.51和39.28;30 min:q值分别为23.17和21.67,P值均<0.05),但空气组与对照组比较差异无统计学意义。(2)心输出量:复苏240 min时,对照组、空气组与氧气组3组间心输出量差异有统计学意义[(181.6±33.8)、(150.9±70.1)与(103.6±53.6) dl/(min·kg),F=4.82, P<0.05]。氧气组心输出量低于对照组(q=4.25,P<0.05),氧气组与空气组、空气组与对照组比较,差异均无统计学意义(P>0.05)。(3)动脉氧含量:复苏10和30 min时,对照组、空气组与氧气组3组间动脉氧含量差异均有统计学意义[10 min:(87.0±16.1)、(76.9±13.2)与(102.2±15.9) ml O2/dl,F=8.64;30 min:(87.5±14.9)、(79.9±11.3)与(100.1±16.7) ml O2/dl, F=5.98;P值均<0.01]。复苏10 min时,氧气组CaO2高于对照组和空气组(q值分别为3.14和5.85, P值均<0.05);复苏30 min时,氧气组高于空气组(q=4.85,P<0.01),与对照组比较差异无统计学意义(q=2.71,P>0.05)。(4)氧运输:复苏10、30、60、120、180及240 min时,对照组、空气组与氧气组3组间氧运输的差异均无统计学意义[10 min:(16.5±3.3)、(15.7±9.9)与(16.9±4.2)L O2/(kg·min),F=0.10;30 min:(16.2±4.1)、(15.1±5.5)与(14.5±3.3)L O2/(kg·min), F=0.38;60 min:(16.1±4.2)、(14.9±4.0)与(13.3±3.8) L O2/(kg·min),F=1.28;120 min:(15.5±3.7)、(15.6±6.1)与(13.4±4.6) L O2/(kg·min),F=0.66;180 min:(15.4±3.1)、(15.3±9.3)与(11.9±5.0) L O2/(kg·min),F=0.97;240 min:(14.7±3.4)、(13.4±6.7)与(9.3±5.2) L O2/(kg·min),F=2.84;P值均>0.05]。(5)左心室超氧化物歧化酶活性:复苏240 min时,对照组(n=6)、空气组(n=8)与氧气组(n=8)左心室超氧化物歧化酶活性差异有统计学意义[(289±107)、(210±75)与(142±61)U/mg protein,F=5.75,P<0.05],氧气组低于对照组(q=4.79,P<0.01);空气组与对照组比较、氧气组与空气组比较差异均无统计学意义(q值分别为2.58和2.39,P值均>0.05)。结论尽管给予纯氧复苏新生猪的动脉氧分压显著高于空气复苏,但并不加快代谢性酸中毒的恢复。对比空气复苏,氧气复苏可显著减少心脏的每搏输出量。给予30 min的纯氧并不增加循环的氧运输,相反可能削弱心肌的抗氧化屏障。
目的:通過建立新生豬全身缺氧模型,觀察空氣或氧氣複囌對新生豬心髒泵血功能和心肌超氧化物歧化酶活性的影響。方法32隻體重1.6~2.5 kg新生豬隨機分為3組,對照組8隻,無缺氧損傷,機械通氣下給予空氣;空氣組12隻,機械通氣下給予120 min全身性缺氧後,空氣複囌240 min;氧氣組12隻,機械通氣下給予120 min全身性缺氧後,給予純氧複囌30 min,然後改為空氣複囌210 min。記錄缺氧120 min末(複囌0 min)和複囌10、30、60、120、180及240 min時的血氣、血壓和血流變化。複囌240 min時結束實驗,凍存左心室標本,採用酶學法檢測超氧化物歧化酶活性。採用單因素方差分析、重複測量的雙因素方差分析及Student-Newman-Keuls檢驗進行統計學分析。結果缺氧造成動物顯著的痠中毒、低血壓和低氧血癥。(1)動脈氧分壓:複囌10和30 min時,對照組、空氣組與氧氣組3組間動脈氧分壓差異均有統計學意義[10 min:(67±4)、(78±12)與(409±42) mmHg(1 mmHg=0.133 kPa),F=580.19;30 min:(68±3)、(79±15)與(342±62) mmHg,F=173.67;P均<0.01]。氧氣組動脈氧分壓高于對照組和空氣組(10 min:q值分彆為42.51和39.28;30 min:q值分彆為23.17和21.67,P值均<0.05),但空氣組與對照組比較差異無統計學意義。(2)心輸齣量:複囌240 min時,對照組、空氣組與氧氣組3組間心輸齣量差異有統計學意義[(181.6±33.8)、(150.9±70.1)與(103.6±53.6) dl/(min·kg),F=4.82, P<0.05]。氧氣組心輸齣量低于對照組(q=4.25,P<0.05),氧氣組與空氣組、空氣組與對照組比較,差異均無統計學意義(P>0.05)。(3)動脈氧含量:複囌10和30 min時,對照組、空氣組與氧氣組3組間動脈氧含量差異均有統計學意義[10 min:(87.0±16.1)、(76.9±13.2)與(102.2±15.9) ml O2/dl,F=8.64;30 min:(87.5±14.9)、(79.9±11.3)與(100.1±16.7) ml O2/dl, F=5.98;P值均<0.01]。複囌10 min時,氧氣組CaO2高于對照組和空氣組(q值分彆為3.14和5.85, P值均<0.05);複囌30 min時,氧氣組高于空氣組(q=4.85,P<0.01),與對照組比較差異無統計學意義(q=2.71,P>0.05)。(4)氧運輸:複囌10、30、60、120、180及240 min時,對照組、空氣組與氧氣組3組間氧運輸的差異均無統計學意義[10 min:(16.5±3.3)、(15.7±9.9)與(16.9±4.2)L O2/(kg·min),F=0.10;30 min:(16.2±4.1)、(15.1±5.5)與(14.5±3.3)L O2/(kg·min), F=0.38;60 min:(16.1±4.2)、(14.9±4.0)與(13.3±3.8) L O2/(kg·min),F=1.28;120 min:(15.5±3.7)、(15.6±6.1)與(13.4±4.6) L O2/(kg·min),F=0.66;180 min:(15.4±3.1)、(15.3±9.3)與(11.9±5.0) L O2/(kg·min),F=0.97;240 min:(14.7±3.4)、(13.4±6.7)與(9.3±5.2) L O2/(kg·min),F=2.84;P值均>0.05]。(5)左心室超氧化物歧化酶活性:複囌240 min時,對照組(n=6)、空氣組(n=8)與氧氣組(n=8)左心室超氧化物歧化酶活性差異有統計學意義[(289±107)、(210±75)與(142±61)U/mg protein,F=5.75,P<0.05],氧氣組低于對照組(q=4.79,P<0.01);空氣組與對照組比較、氧氣組與空氣組比較差異均無統計學意義(q值分彆為2.58和2.39,P值均>0.05)。結論儘管給予純氧複囌新生豬的動脈氧分壓顯著高于空氣複囌,但併不加快代謝性痠中毒的恢複。對比空氣複囌,氧氣複囌可顯著減少心髒的每搏輸齣量。給予30 min的純氧併不增加循環的氧運輸,相反可能削弱心肌的抗氧化屏障。
목적:통과건립신생저전신결양모형,관찰공기혹양기복소대신생저심장빙혈공능화심기초양화물기화매활성적영향。방법32지체중1.6~2.5 kg신생저수궤분위3조,대조조8지,무결양손상,궤계통기하급여공기;공기조12지,궤계통기하급여120 min전신성결양후,공기복소240 min;양기조12지,궤계통기하급여120 min전신성결양후,급여순양복소30 min,연후개위공기복소210 min。기록결양120 min말(복소0 min)화복소10、30、60、120、180급240 min시적혈기、혈압화혈류변화。복소240 min시결속실험,동존좌심실표본,채용매학법검측초양화물기화매활성。채용단인소방차분석、중복측량적쌍인소방차분석급Student-Newman-Keuls검험진행통계학분석。결과결양조성동물현저적산중독、저혈압화저양혈증。(1)동맥양분압:복소10화30 min시,대조조、공기조여양기조3조간동맥양분압차이균유통계학의의[10 min:(67±4)、(78±12)여(409±42) mmHg(1 mmHg=0.133 kPa),F=580.19;30 min:(68±3)、(79±15)여(342±62) mmHg,F=173.67;P균<0.01]。양기조동맥양분압고우대조조화공기조(10 min:q치분별위42.51화39.28;30 min:q치분별위23.17화21.67,P치균<0.05),단공기조여대조조비교차이무통계학의의。(2)심수출량:복소240 min시,대조조、공기조여양기조3조간심수출량차이유통계학의의[(181.6±33.8)、(150.9±70.1)여(103.6±53.6) dl/(min·kg),F=4.82, P<0.05]。양기조심수출량저우대조조(q=4.25,P<0.05),양기조여공기조、공기조여대조조비교,차이균무통계학의의(P>0.05)。(3)동맥양함량:복소10화30 min시,대조조、공기조여양기조3조간동맥양함량차이균유통계학의의[10 min:(87.0±16.1)、(76.9±13.2)여(102.2±15.9) ml O2/dl,F=8.64;30 min:(87.5±14.9)、(79.9±11.3)여(100.1±16.7) ml O2/dl, F=5.98;P치균<0.01]。복소10 min시,양기조CaO2고우대조조화공기조(q치분별위3.14화5.85, P치균<0.05);복소30 min시,양기조고우공기조(q=4.85,P<0.01),여대조조비교차이무통계학의의(q=2.71,P>0.05)。(4)양운수:복소10、30、60、120、180급240 min시,대조조、공기조여양기조3조간양운수적차이균무통계학의의[10 min:(16.5±3.3)、(15.7±9.9)여(16.9±4.2)L O2/(kg·min),F=0.10;30 min:(16.2±4.1)、(15.1±5.5)여(14.5±3.3)L O2/(kg·min), F=0.38;60 min:(16.1±4.2)、(14.9±4.0)여(13.3±3.8) L O2/(kg·min),F=1.28;120 min:(15.5±3.7)、(15.6±6.1)여(13.4±4.6) L O2/(kg·min),F=0.66;180 min:(15.4±3.1)、(15.3±9.3)여(11.9±5.0) L O2/(kg·min),F=0.97;240 min:(14.7±3.4)、(13.4±6.7)여(9.3±5.2) L O2/(kg·min),F=2.84;P치균>0.05]。(5)좌심실초양화물기화매활성:복소240 min시,대조조(n=6)、공기조(n=8)여양기조(n=8)좌심실초양화물기화매활성차이유통계학의의[(289±107)、(210±75)여(142±61)U/mg protein,F=5.75,P<0.05],양기조저우대조조(q=4.79,P<0.01);공기조여대조조비교、양기조여공기조비교차이균무통계학의의(q치분별위2.58화2.39,P치균>0.05)。결론진관급여순양복소신생저적동맥양분압현저고우공기복소,단병불가쾌대사성산중독적회복。대비공기복소,양기복소가현저감소심장적매박수출량。급여30 min적순양병불증가순배적양운수,상반가능삭약심기적항양화병장。
To assess the effects of resuscitation with oxygen or room air on the cardiac circulation and the activity of superoxide dismutase (SOD) in a hypoxic newborn piglet model. Methods Newborn piglets(1.6-2.5 kg) were randomly assigned into three groups:control group (n=8) with no hypoxic insult;room air group (n=12) resuscitated with room air for 240 min after 120 min hypoxia;and oxygen group (n=12) resuscitated with 100% oxygen for 30 min followed by 210 min with room air after 120 min hypoxia. Blood gas analysis, blood pressure and hemodynamic parameters were recorded at 0, 10, 30, 60, 120, 180 and 240 min of resuscitation. The activity of superoxide dismutase (SOD) in the left ventricle was measured at 240 min of resuscitation using enzyme method . One-way analysis of variance, two-way analysis of variance measured repeatedly and Student-Newman-Keuls test were applied as statistical methods. Results Severe metabolic acidosis, hypotension and hypoxemia were caused by hypoxia.(1)Arterial oxygen partial pressure(PaO2):At 10 min of resuscitation, PaO2 of control group, room air group and oxygen group was (67±4), (78±12) and (409±42)mmHg(1 mmHg=0.133 kPa) (F=580.19, P<0.01). At 30 min of resuscitation, PaO2 of the three group was (68±3), (79±15) and (342±62)mmHg(F=173.67;P<0.01). PaO2 of oxygen group was higher than room air group and control group (10 min:q=42.51 and 39.28, 30 min: q=23.17 and 21.67, all P<0.05). There was no statistical significance between the room air group and control group. (2)Cardiac output(CO):At 240 min of resuscitation,CO of control group, room air group and oxygen group was(181.6±33.8), (150.9±70.1) and (103.6±53.6) dl/(min·kg) (F=4.82, P<0.05). CO of oxygen group was lower than control group (q=4.25,P<0.05). There was no statistical significance between oxygen group and room air group, neither was between room air group and control group (all P>0.05). (3)Arterial oxygen content (CaO2):At 10 min of resuscitation, CaO2 of control group, room air group and oxygen group was(87.0±16.1), (76.9±13.2) and (102.2±15.9) ml O2/dl (F=8.64, P<0.01). At 30 min of resuscitation, CaO2 of the three group was(87.5±14.9), (79.9±11.3) and (100.1±16.7) ml O2/dl (F=5.98, P<0.01). At 10 min of resuscitation, CaO2 of oxygen group was higher than control group and room air group (q=3.14 and 5.85, all P<0.05). At 30 min of resuscitation, CaO2 of oxygen group was higher than room air group (q=4.85, P<0.01), but there was no statistical significance between oxygen group and control group (q=2.71, P>0.05). (4)Oxygen delivery (DO2): At 10, 30, 60, 120, 180 and 240 min of resuscitation, there were no statistical significance among DO2 of control group, room air group and oxygen group [10 min:(16.5±3.3), (15.7±9.9) and (16.9±4.2)L O2/(kg·min), F=0.10;30 min:(16.2±4.1), (15.1±5.5) and (14.5±3.3) L O2/(kg·min), F=0.38;60 min:(16.1±4.2), (14.9±4.0)and(13.3±3.8)L O2/(kg·min), F=1.28;120 min:(15.5±3.7),(15.6±6.1)and(13.4± 4.6) L O2/(kg·min), F=0.66;180 min:(15.4±3.1), (15.3±9.3) and (11.9±5.0) L O2/(kg·min), F=0.97;240 min:(14.7±3.4), (13.4±6.7) and (9.3±5.2) L O2/(kg·min), F=2.84;all P>0.05]. (5) SOD activity in the left ventricle:At 240 min of resuscitation, SOD activity of control group (n=6), room air group (n=8) and oxygen group (n=8) was (289±107), (210±75) and (142±61)U/mg protein, F=5.75, P<0.05]. SOD activity of oxygen group was lower than control group (q=4.79, P<0.01). There was no statistical significance between oxygen group and room air group, neither was between room air group and control group(q=2.58 and 2.39, all P>0.05). Conclusions Despite higher oxygen content in the blood, resuscitation with oxygen is not beneficial to recovery from metabolic acidosis in newborn hypoxic piglets. Oxygen supplementation does not increase oxygen delivery but reduces SV compared to resuscitation with room air. Resuscitation with oxygen may impair the oxidative stress defense.