呼气末正压对外源性肺表面活性物质功能的影响

目的 探讨PEEP对外源性肺表面活性物质（PS）功能的影响。方法 用血清将PS稀释溶解配制成4.0、24 mg/ml的实验液体。同时将PS溶解于醋酸林格液中配成相同的浓度,作为对照。实验I:设定PEEP为 0,未成熟胎兔18只随机分为2组（每组9只）:A1组,经气道内注入溶解于醋酸林格液的PS24 mg/ml;B1组,注入溶于血清的PS24 mg/ml,实验Ⅱ设定PEEP为2.5cm H2O ,未成熟胎兔24只随机分为3组（每组8只）:A2组,经气道内注入溶解于醋酸林格液的 PS4.0 mg/ml;B2组,注入溶于血清的PS4.0 mg/ml;C2组未注入任何物质。人工通气后 5、10、15、20min测定动物潮气量。结果 人工通气 20 min时,A1组动物的潮气量大于15 ml/kg,而B1组小于8.0 ml/kg（P<0.05）;A2和B2组动物的潮气量均超过20 ml/kg,而 C2组小于2.0 ml/kg。结论PEEP可以增强PS的活性,拮抗血清对PS的抑制。     

经颅多谱勒检测兔大脑中动脉微血栓栓子的研究

目的应用经颅多谱勒（TCD）动态检测兔血栓栓塞模型大脑中动脉（MCA）的微栓子信号（MES），观察栓子的负荷量与缺血性脑血管病（ICVD）发生的相关性。方法将实验动物随机分为3组，即A组含3—5个栓子，B组含6-10个栓子，C组为生理盐水对照组。采用自体动脉血微栓子建立兔局灶性脑缺血模型同时TCD监测MES。栓塞后6h进行磁共振成像（MRI）及兔脑组织病理观察。结果A、B组TCD均监测到MES；B组MRI的T1WI、T2WI及病理观察见梗死灶，而A组仅在弥散加权成像（DWI）见可疑小缺血灶。结论TCD实时、动态观察微栓子信号，能预测缺血性脑血管病发生的危险性，为临床及早干预治疗提供科学依据。     

甘露醇注射速度对留置针穿刺部位血管损伤的实验研究

目的了解在25℃环境中以不同速度静脉注射20％甘露醇对兔耳静脉损伤情况。方法选择健康成年的新西兰兔36只，随机取4只作为对照组，另32只随机分为A、B、C、D四组各8只。均于兔两耳留置静脉留置针。对照组给予生理盐水5ml／kg 30min注入；另四组给予20％甘露醇5ml／kg分别于5min（A组）、10min（B组）、20min（C组）、30min（D组）注射完毕。均8h给药1次，连续3d。最后1次给药后处死兔，在穿刺点及以上2cm处取血管组织行病理检查。结果对照组血管壁增厚、血管周围炎症、纤维组织增生及血栓形成情况与其余四组之间比较，差异有显著性意义（均P〈0．05）；实验组四组比较，差异无显著性意义（均P〉0．05），D组血管壁增厚、血管周围炎症相对较多，A组血栓形成相对较多。结论注射甘露醇对穿刺部位血管均有损伤；根据注射甘露醇时的速度、持续时间不同，穿刺部位血管的损伤特点不一。     

吡那地尔介导超极化心脏停搏液对心肌的保护作用

目的：为了提高心脏停搏液的心肌保护作用，探讨含吡那地尔（pinacidil)超极化心脏停搏液对心肌的保护作用。方法：32只新西兰兔根据体外循环中使用不同的心脏停搏液分为对照组和实验组，对照组用St Thomas Ⅱ号心脏停搏液，实验组用含吡那地尔（50μmol/L）的心脏停搏液。两组又根据主动脉阻断后是否再灌注，分别分为两组（对照组A、对照组B、实验组A、实验组B），每组8只兔。对照组A和实验组A在主动脉阻断60分钟后结束实验；对照组B和实验组B于主动脉阻断60分钟、复滞30分钟结束实验。记录心脏电机械停搏时间，复跳时的心律失常情况，测定实验结束时各组心肌三磷酸腺苷（ATP）、总腺苷酸（TAN）、Ca^2 、丙二醛（MDA）含量，对照组B和实验组B血清心肌酶含量，并观察心肌超微结构变化。结果：4组心脏均迅速发生电机械停搏，对照组B、实验组B复跳时均发生心律失常3例，未发生严重心律失常；实验组A和实验组B的ATP、TAN分别高于对照组A和对照组B（P＜0．01），而Ca^2 和MDA分别显著低于对照组A和对照组B（P＜0．05），实验组B心肌酶的漏出量显著低于对照组B（P＜0．01）。实验组B超微结构损伤轻，优于对照组B。结论：含吡那地尔的心脏停搏液对心肌保护的作用优于高K^ 心脏停搏液。     

腰椎穿刺术后垫枕与去枕对颅内压的影响

目的为腰椎穿刺术后患者提供安全、舒适的体位。方法选择脑出血行侧脑室引流的患者90例，测定颅内压后分为高颅压组、正常颅压组和低颅压组各30例；腰穿后每组均分别予以垫枕与去枕干预各15例．接受垫枕干预者腰穿后于枕下垫软枕（厚7～8cm），并每2小时翻身1次；接受去枕干预者按护理常规去枕平卧6h，每2小时将手伸至患者背部按摩皮肤。各组均在腰穿前，腰穿后30min、60min、2h、4h、6h分别监测脑室颅内压变化。结果高颅压和低颅压组患者垫枕和去枕对颅内压影响显著（均P〈0．05）；正常颅压组患者垫枕和去枕对颅内压影响无显著性意义（均P〉0．05）；接受去枕干预者皮肤反应发生率显著高于接受垫枕干预者（P〈0.01）。结论高颅压患者腰穿后采取垫枕位更合适，正常颅压患者腰穿后可以垫枕，低颅压患者腰穿后不宜垫枕。     

经颅多普勒超声在额部入路微创锥颅术后颅内压监测的应用

有研究显示动态经颅多普勒(TCD)检查所得血流动力学参数与高血压脑出血术后颅内压(ICP)的变化相关,本研究旨在分析高血压性脑出血患者血流动力学参数与ICP、脑灌注压(CPP)的关系,以指导临床应用。1资料和方法1.1一般资料:收集2010年2月～2012年1月我院神经科行额部入路锥颅血肿清除术的高血压性脑出血患者共65例(男35例,女30例),年龄为39～79岁。70岁者5例,2型     

磷脂酶A2抑制剂溴苯乙酮对大鼠急性失血性休克复苏后早期损伤？…

目的 观察磷脂酶Ａ２抑制剂４－二溴苯乙酮（４－ＢＰＢ）对大鼠急性失血性休克复苏后早期肺损伤的保护作用。方法 纯种ＳＤ大鼠３６只，随机分为假手术组（对照组）乳酸林格氏液复苏组（ＬＲ组）乳酸林格氏液＋４－ＢＰＢ复苏组（保护组）。两复苏组动物放血并维持低血压（ＭＡＰ４～５．３ｋＰａ）６０分钟，其后１０分钟内分别输入全部自体抗凝血或同时静注４－ＢＰＢ（２５μｍｏｌ）２０分钟内输入２倍放血量的乳酸林洛氏液，     

犬内毒素性休克时琥珀明胶和乳酸钠林格氏液的容量动力学

目的比较犬内毒素性休克时琥珀明胶和乳酸钠林格氏液的容量动力学。方法健康杂种犬20只,雌雄不拘,随机分为4组（n=10）,乳酸钠林格氏液组（CL组）经30min静脉输注乳酸钠林格氏液30ml/kg;琥珀明胶组（CG组）经30min静脉输注琥珀明胶10ml/kg;内毒素＋乳酸钠林格氏液组（LL组）静脉注射内毒素250μg/kg,再经30min静脉输注乳酸钠林格氏液30ml/kg;内毒素＋琥珀明胶组（LG组）静脉注射内毒素250μg/kg,再经30min静脉输注琥珀明胶10ml/kg。补液期间每隔5分钟测定血红蛋白浓度和红细胞压积;记录血液动力学指标和总尿量。应用物质守恒定律和容量动力学理论,计算血浆容量增加、外周容量增加、容量扩张效率、目标容积（V）和清除率（Kr）。结果与CL组比较,CG组V和Kr降低,LL组V升高（P〈0.05）;与CG组比较,LG组V和Kr升高（P〈0.05）;与LL组比较,LG组V和K降低（P〈0.05）。与CG组和LG组比较,CL组和LL组血浆容量增加和容量扩张效率降低,外周容量增加升高（P〈0.05）;与CL组和CG组比较,LL组和LG组血浆容量增加和容量扩张效率降低,外周容量增加升高（P〈0.05）。结论犬内毒素性休克时,乳酸钠林格氏液的扩容效率较琥珀明胶降低更为明显。     

腰大池灌注林格氏液加脑室外引流治疗脑室出血的实验研究

目的 探讨腰大池恒压灌注林格氏液加侧脑室外引流治疗脑室内出血的安全性、可行性及疗效。方法 选用纯种比格犬10条做成脑室内出血的模型，模型建立后4h开始治疗，实验组5条，以2．96kPa(1kPa＝7．5mm Hg)的压力经腰大池灌注林格氏液，同时行侧脑室外引流；对照组5条，用侧脑室外引流的方法。两组在治疗过程中均严格监测颅内压(ICP)及生命体征，记录引流量及灌注量，经12h的治疗后处死动物并收集脑室内全部残余积血，比较两组标本含铁血红蛋白的吸光度值。结果 两组动物从模型建立后至处死前生命体征平稳颅内压波动不太。经12h的治疗，实验组的引流量明显多于对照组(P＜0．05)，实验组脑内残余积血量明显少于对照组，两组差异有显著性(P＜0．05)。结论 以2．96kPa的压力恒压灌注林格氏液于腰大池内，同时行侧脑室外引流治疗脑室内出血的方法安全可行，能更快地消除脑室内积血。     

丙酮酸乙酯调节脓毒症小鼠肝细胞HSP70表达的研究

目的研究丙酮酸乙酯（EP）对脓毒症小鼠肝细胞热休克蛋白70（HSPT0）的调节作用。方法制作小鼠盲肠结扎穿孔模型（CLP），应用丙酮酸乙酯林格氏液（REPS）与乳酸钠林格氏液（RLS）对小鼠进行液体复苏，60只小鼠分3组，各20只：假手术组、CLP模型＋REPS复苏组、CLP模型＋RLS复苏组，检测肝组织丙二醛（MDA）及肝细胞HSP70的表达。结果脓毒症小鼠较假手术组MDA浓度增高，P〈0．01。EP显著提高脓毒症小鼠肝组织的抗氧化能力，REPS组肝组织MDA浓度低于RLS组【（48．18±598）μmol／g．prot vs（78．34±11．16）μmol／gprot，P〈0．01]；REPS组小鼠肝细胞HSPT0表达较RLS组增高[（28．76±5．69）vs（20．04±4．93），P〈0．051。HSP70表达与MDA值呈负相关（r=-0．733，P〈0．01）。结论EP具有的抗氧化作用能提高脓毒症小鼠肝细胞的HSPT0表达。     

Intracranial pressure during liver transplantation for fulminant hepatic failure

During orthotopic liver transplantation (OLT) for fulminant hepatic failure (FHF), some patients develop cerebral injury secondary to intracranial hypertension. We monitored intracranial pressure (ICP) and cerebral perfusion pressure (CPP) before and during OLT in 12 FHF patients undergoing transplantation. All four patients who had normal ICP preoperatively maintained normal ICP/CPP throughout OLT. During OLT, four of the eight patients with pretransplant intracranial hypertension had six episodes of ICP increase. These episodes of intracranial hypertension occurred during failing liver dissection (n=3) and graft reperfusion (n=3). At the end of the anhepatic phase, the ICP was lower than the preoperative ICP in all patients, and was below 15 mmHg in all but one patient. These data suggest that in FHF patients who develop intracranial hypertension before OLT, dissection of the native liver and graft reperfusion are associated with a risk of brain injury resulting from intracranial hypertension and cerebral hypoperfusion.     

Management morbidity and mortality in grade IV and V patients with aneurysmal subarachnoid haemorrhage

Summary Intracranial haemodynamics were studied in 20 patients with diffuse and focal brain injury and experimental animals with acute intracranial hypertension by the use of TCD ultrasound. The mean flow velocity in the middle cerebral artery (MCA) commonly decreased on the side of the haematoma depending on intracranial pressure (ICP) elevation and cerebral perfusion pressure (CPP) reduction in focal injury. The decrease of the MCA flow velocity returned to normal after treatment. The flow velocities decreased bilaterally and there was no difference between the right and left side in diffuse injury. But the velocities increased in spite of ICP elevation when diffuse cerebral swelling developed. Cerebrovascular CO₂ reactivity was impaired in two groups of patients with low Glasgow Coma Scale (GCS) scores. The mean velocity of the MCA and blood flow in the internal carotid artery exhibited flow patterns which changed correlatively depending on CPP reduction in experimental animals. Noninvasive study by use of TCD ultrasound can provide valuable information on variant haemodynamic phenomena in patients with diffuse and focal brain injury.     

The effect of changes in cerebral perfusion pressure upon middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation after severe brain injury.

Middle cerebral artery blood flow velocity and jugular bulb venous oxygen saturation (SJO2) were measured by transcranial Doppler (TCD) ultrasonography and continuous venous oximetry, respectively, in 41 severely brain-injured patients. The purpose of the study was to examine the relationships between TCD flow velocity, SJO2, and alterations in blood pressure (BP), intracranial pressure (ICP), and cerebral perfusion pressure (CPP). In these patients, CPP was reduced either by rising ICP or by falling BP. Both forms of reduction of CPP resulted in a greater fall in diastolic flow velocity than other flow parameters. As CPP decreased below a critical value of 70 mm Hg, a progressive increase in TCD pulsatility index (PI) was observed (r = -0.942, p less than 0.0001), accompanied by a fall in SJO2 (r = 0.78, p less than 0.0001). At pressures above 70 mm Hg, there was no correlation of either PI or SJO2 with CPP. The relationship between PI and CPP held true in patients with both focal and diffuse pathologies and was the same whether changes in CPP resulted from alterations in ICP or BP. The PI and SJO2 correlated better with CPP than with ICP or BP. Transcranial Doppler ultrasonography can identify states of reduced CPP. Decreases in SJO2 with falling CPP suggested progressive failure of cerebral blood flow to meet metabolic demands. Monitoring of TCD and SJO2 may be used to define the optimum CPP level for management of severely brain-injured patients.     

近红外光谱技术在高血压脑出血术中监测运用的探讨

目的 探讨近红外光谱技术（NIRs）在术前、术中、术后对高血压脑出血病人颅内压（ICP）、脑灌注压（CPP）和生命体征的影响。方法 将高血压脑出血病人20例按健侧及患侧术前、术中、术后监测病人ICP、CPP、脑组织血氧饱和度（rScO2）和生命体征变化,并进行相关性分析。结果 随着手术的进程,患者的CPP值逐渐升高,ICP值逐渐降低,组间差异具有统计学意义（P<0.05）。患侧术前、术中、术后两两比较显示,患侧术前、术中、术后患者的ICP较健侧降低（P<0.05）,ICP在术中、术后亦均低于术前（P<0.05）;术后病人CPP高于健侧（P<0.05）。术前、术中、术后病人的rScO2、脉搏血氧饱和度、心率、收缩压、舒张压、平均动脉压和体温差异均无统计学意义（P>0.05）。术前、术中、术后高血压脑出血患者rScO2水平与CPP呈负相关（P<0.05）,与ICP、平均动脉压呈正相关关系（P<0.05）。结论 NIRs在高血压脑出血病人术前、术中、术后监测可及时获得出血的情况,有助于临床早期诊断和治疗。     

近红外光谱技术在高血压脑出血术中监测运用的探讨

目的 探讨近红外光谱技术（NIRs）在术前、术中、术后对高血压脑出血病人颅内压（ICP）、脑灌注压（CPP）和生命体征的影响。方法 将高血压脑出血病人20例按健侧及患侧术前、术中、术后监测病人ICP、CPP、脑组织血氧饱和度（rScO2）和生命体征变化,并进行相关性分析。结果 随着手术的进程,患者的CPP值逐渐升高,ICP值逐渐降低,组间差异具有统计学意义（P<0.05）。患侧术前、术中、术后两两比较显示,患侧术前、术中、术后患者的ICP较健侧降低（P<0.05）,ICP在术中、术后亦均低于术前（P<0.05）;术后病人CPP高于健侧（P<0.05）。术前、术中、术后病人的rScO2、脉搏血氧饱和度、心率、收缩压、舒张压、平均动脉压和体温差异均无统计学意义（P>0.05）。术前、术中、术后高血压脑出血患者rScO2水平与CPP呈负相关（P<0.05）,与ICP、平均动脉压呈正相关关系（P<0.05）。结论 NIRs在高血压脑出血病人术前、术中、术后监测可及时获得出血的情况,有助于临床早期诊断和治疗。     

Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury. The Executive Committee of the International Selfotel Trial

OBJECT: Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate. METHODS: The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-D-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP > or = 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg. CONCLUSIONS: Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.     

Intracranial pressure changes following traumatic brain injury in rats: lack of significant change in the absence of mass lesions or hypoxia

Traumatic brain injury (TBI) often causes raised intracranial pressure (ICP), with >50% of all TBI- related deaths being associated with this increase in ICP. To date, there is no effective pharmacological treatment for TBI, partly because widely used animal models of TBI may not replicate many of the pathophysiological responses observed in humans, and particularly the ICP response. Generally, rodents are the animal of choice in neurotrauma research, and edema formation has been demonstrated in rat models; however, few studies in rats have specifically explored the effects of TBI on ICP. The aim of the current study was to investigate the ICP response of rats in two different, focal and diffuse, injury models of TBI. Adult male Sprague-Dawley rats were subjected to brain trauma by either lateral fluid percussion or impact-acceleration induced injury, in the presence or absence of secondary hypoxia. ICP, mean arterial blood pressure (MABP), and cerebral perfusion pressure (CPP) were monitored for 4?h after TBI. TBI alone or coupled with hypoxia did not result in any significant increase of ICP in rats unless there was an intracranial hemorrhage. At all other times, changes in CPP were the result of changes in MABP and not ICP. Our results suggest that rats may be able to compensate for the intracranial expansion associated with cerebral edema after TBI, and that they only develop a consistent post-traumatic increase in ICP in the presence of a mass lesion. Therefore, they are an inappropriate model for the investigation of ICP changes after TBI, and for the development of therapies targeting ICP.     

体位变化对脑室引流术患者颅内压和平均动脉压及脑灌注压的影响

目的 探讨脑室引流患者的体位变化对平均动脉压、颅内压和脑灌注压的影响.方法 对60例接受过脑室穿刺术并留置脑室引流管患者,监测其抬高床头0°、15°、30°、45°时的颅内压(ICP)和平均动脉压(MAP),再计算出脑灌注压(CPP),比较不同体位状态下患者的MAP、ICP和CPP.结果 ICP随着床头的抬高而显著降低...     

Cerebral autoregulation following head injury.

OBJECT: The goal of this study was to examine the relationship between cerebral autoregulation, intracranial pressure (ICP), arterial blood pressure (ABP), and cerebral perfusion pressure (CPP) after head injury by using transcranial Doppler (TCD) ultrasonography. METHODS: Using ICP monitoring and TCD ultrasonography, the authors previously investigated whether the response of flow velocity (FV) in the middle cerebral artery to spontaneous variations in ABP or CPP provides reliable information about cerebral autoregulatory reserve. In the present study, this method was validated in 187 head-injured patients who were sedated and receiving mechanical ventilation. Waveforms of ICP, ABP, and FV were recorded over intervals lasting 20 to 120 minutes. Time-averaged mean FV and CPP were determined. The correlation coefficient index between FV and CPP (the mean index of autoregulation [Mx]) was calculated over 4-minute epochs and averaged for each investigation. The distribution of averaged mean FV values converged with the shape of the autoregulatory curve, indicating lower (CPP < 55 mm Hg) and upper (CPP > 105 mm Hg) thresholds of autoregulation. The relationship between the Mx and either the CPP or ABP was depicted as a U-shaped curve. Autoregulation was disturbed in the presence of intracranial hypertension (ICP > or = 25 mm Hg) and when mean ABP was too low (ABP < 75 mm Hg) or too high (ABP > 125 mm Hg). Disturbed autoregulation (p < 0.005) and higher ICP (p < 0.005) occurred more often in patients with unfavorable outcomes than in those with favorable outcomes. CONCLUSIONS: Autoregulation not only is impaired when associated with a high ICP or low ABP, but it can also be disturbed by too high a CPP. The Mx can be used to guide intensive care therapy when CPP-oriented protocols are used.     

Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.