Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxa...Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapar tum asphyxia. Methods: Retrospective cohort study in term infants with post-asp hyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995.Severe and moderate hyperoxaemia were defined as PaO2 > 26.6 and PaO2 > 13.3 kPa (20 0 and 100 mm Hg). Severe and moderate hypocapnia were defined as PaCO2 < 2.6 an d PaCO2 < 3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 mont hs was defined as death, severe cerebral palsy, or any cerebral palsy with blind ness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic varia bles, and factors adjusted for initial disease severity. Results: Of 244 infants , 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopm ental deficits). Multivariate analyses showed an association between adverse out come and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95%confidence interval (Cl) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% Cl 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infan ts who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95%Cl 1.4 to 14.9, p = 0.012). Conclusion s: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcom e in infantswith post-asphyxial HIE. During the first hours of life, oxygen sup plementation and ventilation should be rigorously controlled.展开更多
目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入2...目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入20-HETE阻断剂17-octadecynoic acid（17-ODYA）并过度通气致PETCO2 20 mm Hg时、加入外源性20-HETE并过度通气致PETCO2 20 mm Hg时,分别于各状态1、5、15、30、60min时测量大脑中动脉、小动脉的直径。结果整个实验过程体温和血液动力学维持稳定。与PETCO2 40 mm Hg时相比,过度通气致PETCO2 20 mm Hg时小动脉直径缩小（P＜0．05）;17-ODYA局部给药并过度通气致PETCO 20 mm Hg时小动脉直径差异无统计学意义（P＞0．05）;外源性20-HETE局部给药并过度通气时小动脉直径缩小（P＜0．05）;在上述各种状态时大脑中动脉直径均无明显变化（P＞0．05）。结论犬低碳酸血症时,20-HETE可能是诱发脑小动脉收缩的机制之一。展开更多
背景同步监测动脉血压（arterial blood pressure，ABP）和大脑中动脉血流速度可用于计算表观零流压（apparent zero flow pressure，aZFP）。压力一流速关系斜率的倒数被称为阻力面积乘积（resistance area product，RAP），是一项脑...背景同步监测动脉血压（arterial blood pressure，ABP）和大脑中动脉血流速度可用于计算表观零流压（apparent zero flow pressure，aZFP）。压力一流速关系斜率的倒数被称为阻力面积乘积（resistance area product，RAP），是一项脑血管阻力指标。关于血管活性药物，动脉血二氧化碳分压（PaCO，）和脑自动调节功能受损在全身麻醉时对aZFP和RAP影响的研究很少。我们研究了异氟醚麻醉期间低碳酸血症和输注去氧肾上腺素对aZFP和RAP的影响。方法记录11名成年受试者在异氟醚麻醉期间桡动脉有创ABP和经颅多普勒所测的大脑中动脉血流速度信号。输注去氧肾上腺素增加ABP，调整通气以控制PaCO2。分别在两个不同的平均ABP水平（大约在80mmHg和100mmHg）和PaCO2水平（正常PaCO2：38～43mmHg和低碳酸水平：27～34mmHg），比较脑血流动力学的变化。对两种aZFP分析方法进行比较：一种基于线性回归，一种基于波形的傅立叶分析。结果在较低ABP水平，血碳酸正常时，aZFP为23±11mmHg，RAP为0．76±0．97mmHg·s·cm^-1；低碳酸血症时，aZFP为30±13mmHg（均数±标准差），RAP为1．16±0．16mmHg·s·cm^-1。，P〈0．001。在较高ABP水平可见到低碳酸血症带来的类似效应。血碳酸水平正常时，异氟醚对脑自主调节功能的损害及aZFP的影响不随ABP的上升而改变。低碳酸血症时，脑血管自动调节功能无明显损害，ABP的升高会使aZFP增加（从30±13mmHg增加到35±13mmHg，P〈0．01）和RAP增加（从1．16±0．16mmHg增加到1．52±0．20mmHg·S·cm^-1，P〈0．001）。评估aZFP和RAP对脑血流动力学的相对作用显示，RAP的变化显然比aZFP的变化在其中起更重要的作用。两种分析aZFP的方法（傅里叶分析法一线性回归法）的平均差为0．5±3．6mmHg（均数±2标准差）。结论异氟醚麻醉期间，低碳酸血症和大脑对ABP升高的自主调节反应，这两个因素可增加大脑小动脉张力，与RAP和aZFP的升高相关。RAP的变化显然比aZFP的变化产生更大的影响。这些结果提示小动脉张力通过控制血管阻力和有效灌注压来影响脑血流。展开更多
文摘Background: Episodes of hyperoxaemia and hypocapnia, which may contribute to b rain injury, occur unintentionally in severely asphyxiated neonates in the first postnatal hours. Objective: To determine whether hyperoxaemia and/or hypocapnia during the first 2 hours of life add to the risk of brain injury after intrapar tum asphyxia. Methods: Retrospective cohort study in term infants with post-asp hyxial hypoxic ischaemic encephalopathy (HIE) born between 1985 and 1995.Severe and moderate hyperoxaemia were defined as PaO2 > 26.6 and PaO2 > 13.3 kPa (20 0 and 100 mm Hg). Severe and moderate hypocapnia were defined as PaCO2 < 2.6 an d PaCO2 < 3.3 kPa (20 and 25 mm Hg). Adverse outcome ascertained by age 24 mont hs was defined as death, severe cerebral palsy, or any cerebral palsy with blind ness, deafness, or developmental delay. With outcome as the dependent variable, multivariate analyses were performed including hyperoxaemic and hypocapnic varia bles, and factors adjusted for initial disease severity. Results: Of 244 infants , 218 had known outcomes, 127 of which were adverse (64 deaths, 63 neurodevelopm ental deficits). Multivariate analyses showed an association between adverse out come and episodes of severe hyperoxaemia (odds ratio (OR) 3.85, 95%confidence interval (Cl) 1.67 to 8.88, p = 0.002), and severe hypocapnia (OR 2.34, 95% Cl 1.02 to 5.37, p = 0.044). The risk of adverse outcome was highest in infan ts who had both severe hyperoxaemia and severe hypocapnia (OR 4.56, 95%Cl 1.4 to 14.9, p = 0.012). Conclusion s: Severe hyperoxaemia and severe hypocapnia were associated with adverse outcom e in infantswith post-asphyxial HIE. During the first hours of life, oxygen sup plementation and ventilation should be rigorously controlled.
文摘目的观察20-羟廿碳四烯酸（20-HETE）在低碳酸血症犬脑血管收缩中的作用,探讨低碳酸血症时脑动脉收缩的机制。方法11条健康成年杂种犬,麻醉下开颅,在PETCO2 40 mm Hg时、过度通气致PETCO2 20 mm Hg时、恢复正常通气PETCO2加mm Hg后加入20-HETE阻断剂17-octadecynoic acid（17-ODYA）并过度通气致PETCO2 20 mm Hg时、加入外源性20-HETE并过度通气致PETCO2 20 mm Hg时,分别于各状态1、5、15、30、60min时测量大脑中动脉、小动脉的直径。结果整个实验过程体温和血液动力学维持稳定。与PETCO2 40 mm Hg时相比,过度通气致PETCO2 20 mm Hg时小动脉直径缩小（P＜0．05）;17-ODYA局部给药并过度通气致PETCO 20 mm Hg时小动脉直径差异无统计学意义（P＞0．05）;外源性20-HETE局部给药并过度通气时小动脉直径缩小（P＜0．05）;在上述各种状态时大脑中动脉直径均无明显变化（P＞0．05）。结论犬低碳酸血症时,20-HETE可能是诱发脑小动脉收缩的机制之一。
文摘背景同步监测动脉血压（arterial blood pressure，ABP）和大脑中动脉血流速度可用于计算表观零流压（apparent zero flow pressure，aZFP）。压力一流速关系斜率的倒数被称为阻力面积乘积（resistance area product，RAP），是一项脑血管阻力指标。关于血管活性药物，动脉血二氧化碳分压（PaCO，）和脑自动调节功能受损在全身麻醉时对aZFP和RAP影响的研究很少。我们研究了异氟醚麻醉期间低碳酸血症和输注去氧肾上腺素对aZFP和RAP的影响。方法记录11名成年受试者在异氟醚麻醉期间桡动脉有创ABP和经颅多普勒所测的大脑中动脉血流速度信号。输注去氧肾上腺素增加ABP，调整通气以控制PaCO2。分别在两个不同的平均ABP水平（大约在80mmHg和100mmHg）和PaCO2水平（正常PaCO2：38～43mmHg和低碳酸水平：27～34mmHg），比较脑血流动力学的变化。对两种aZFP分析方法进行比较：一种基于线性回归，一种基于波形的傅立叶分析。结果在较低ABP水平，血碳酸正常时，aZFP为23±11mmHg，RAP为0．76±0．97mmHg·s·cm^-1；低碳酸血症时，aZFP为30±13mmHg（均数±标准差），RAP为1．16±0．16mmHg·s·cm^-1。，P〈0．001。在较高ABP水平可见到低碳酸血症带来的类似效应。血碳酸水平正常时，异氟醚对脑自主调节功能的损害及aZFP的影响不随ABP的上升而改变。低碳酸血症时，脑血管自动调节功能无明显损害，ABP的升高会使aZFP增加（从30±13mmHg增加到35±13mmHg，P〈0．01）和RAP增加（从1．16±0．16mmHg增加到1．52±0．20mmHg·S·cm^-1，P〈0．001）。评估aZFP和RAP对脑血流动力学的相对作用显示，RAP的变化显然比aZFP的变化在其中起更重要的作用。两种分析aZFP的方法（傅里叶分析法一线性回归法）的平均差为0．5±3．6mmHg（均数±2标准差）。结论异氟醚麻醉期间，低碳酸血症和大脑对ABP升高的自主调节反应，这两个因素可增加大脑小动脉张力，与RAP和aZFP的升高相关。RAP的变化显然比aZFP的变化产生更大的影响。这些结果提示小动脉张力通过控制血管阻力和有效灌注压来影响脑血流。
