开颅术中脑组织氧代谢监测的初步探讨

一、临床资料与方法1.临床病例:男12例,女8例年龄16～65岁,平均36.5岁。其中外伤性颅内血肿12例动脉瘤8例,均在全麻下行开颅手术治疗。所有病例麻醉用药完全一致,并由同一麻醉师操作。2.研究方法:采用Codman公司Neurotrend-7连续动态监测脑组织氧分压(PbtO2)、二氧化碳分压(PbtCO2)和pH值(pHbt)和脑温(BT)。动脉瘤患者是在载瘤动脉供血区植入Neurotrend-7探头;脑外伤患者,在骨窗缘(下面为正常脑组织)插入校准好的探头;插入深度为皮层下4cm。载瘤动脉临时阻断过程中平均动脉血压(MAP)、指端血氧饱和度SpO2、呼气末CO2分压(ETCO2)、…     

动脉瘤术中脑组织氧代谢监测的初步探讨

目的 为探讨动脉瘤术中进行脑组织氧代谢监测的临床意义。方法 20例颅内动脉瘤夹闭术中,对载瘤动脉暂时阻断,并对被阻断动脉供血区脑组织持续进行氧代谢监测,比较阻断前后P_(bt)O_2、P_(bt)CO_2和pH的变化。结果 载瘤动脉阻断后,P_(bt)O_2从阻断前(22±3)mmHg下降到(14±2)mmHg(P<0.01),P_(bt)CO_2从(46±2)mmHg升高到(54±3)mmHg(P<0.01),pH从7.10±0.03下降到7.02±0.02(P<0.01);被阻断动脉供血区出现脑梗塞者3例。结论 脑组织氧代谢监测可及时准确地发现载瘤动脉阻断后而引起的脑组织缺血缺氧,并有助于术者调整阻断时间,从而防止阻断动脉造成医源性脑缺血损害。     

颅内动脉瘤术中脑组织氧代谢监测的临床研究

目的　探讨颅内动脉瘤术中进行脑组织氧代谢监测临床意义。方法　 2 0 0 0年 10月至 2 0 0 2年 7月间对 2 0例颅内动脉瘤夹闭术中载瘤动脉临时阻断的患者进行被阻断动脉供血区持续脑组织氧代谢监测 ,比较临时阻断载瘤动脉前后PbtO2 、PbtCO2 和pHbt的变化。结果　载瘤动脉临时阻断后 ,PbtO2 、pHbt分别从 (2 2± 3 )mmHg及 7 10± 0 0 3下降到 (14± 2 )mmHg及 7 0 2± 0 0 2 (P <0 0 1) ,PbtCO2 从 (4 6± 2 )mmHg升高到 (5 4± 3 )mmHg(P <0 0 1)。而且 ,上述指标均在临时夹闭后 3 0s内就发生明显的变化。结论　脑组织氧代谢监测是一种安全、可靠、灵敏的监测手段 ,可及时准确地发现因载瘤动脉被阻断而引起的脑组织缺血缺氧 ,并有助于术者调整临时阻断时间 ,从而防止临时阻断动脉造成医源性脑缺血损害。     

脑组织氧分压监测在颅脑外伤中的应用

脑组织氧分压监测与以往传统的监测方法相比,有较大的优越性。其意义在于不仅能早期发现脑缺血缺氧,准确判断预后;还能及时根据病情变化调整治疗方案,合理评价治疗措施,改善病人预后。     

多参数系统生物传感器Neurotrend-7监测移植早期肝细胞的代谢

背景：目前,各种监测设备已经用于移植肝的早期监测,但没有一种方法能够持续不断的监测移植肝细胞的代谢变化来反映移植肝内部环境的变化情况。 目的：探讨应用多参数系统生物传感器Neurotrend-7持续监测肝细胞代谢,为早期发现移植后肝脏功能不良提供依据。 方法：健康成年雄性日本大耳白兔24只分为3组,对照组(n=4)：开腹仅行肝组织埋入氧代谢监测传感器及标本取材后关腹。两个实验组完成兔肝移植后肝内置入多参数监测仪传感器探针,实验1组(n=10)供肝保存时间< 2 h;实验2组(n=4)供肝保存时间> 4 h。移植前及移植后1,3,5 d连续监测肝组织的pH、氧分压、二氧化碳分压变化并测量动脉血PaO2、PaCO2、动脉血气pH值。同时,切取同位点的肝组织行光镜和电镜检查。 结果与结论：实验2组肝组织氧分压显著低于实验1组(P < 0.05),且随时间逐渐下降;肝组织二氧化碳分压各时段高于实验1组(P < 0.05),并且随时间逐渐增高;肝组织pH值较实验1组各时间段更低(P < 0.05),提示肝功能严重不良或移植肝无功能。肝组织氧分压与动脉血PaO2呈正相关,肝组织二氧化碳分压与动脉血PaCO2无明显相关性;肝组织pH与动脉血气pH值也无明显相关性。变化与组织学检查相似。提示,多参数系统生物传感器Neurotrend-7可为早期发现移植后肝脏功能不良,观察其演变规律,指导临床早期预防和治疗,为其在肝脏外科和器官移植领域临床应用提供准确的数据支持。     

脑组织氧代谢监测仪在重型脑损伤中的应用现状

脑组织氧代谢监测仪能长期连续监测脑组织氧分压、二氧化碳分压、pH值和脑温,直接、动态地观察脑组织的病理生理变化。用于急性重型脑损伤患者,可直接发现重型脑损伤患者脑组织的缺血缺氧状况,以评估预后和指导治疗。     

多参数脑组织代谢监测在神经外科中的应用

正常脑组织有精密的自动调节功能对脑血流进行调节。但在颅脑外伤、各种神经外科手术或病理状况下脑血流的自动调节功能容易受损,极易发生脑缺血缺氧。脑组织的缺血缺氧是造成外伤或手术后继发性脑损害的一个主要原因。因而准确有效地监测脑组织氧合情况,有助于早期发现和治疗脑缺血缺氧,减轻继发性脑损害,改善病人的预后。一、多参数脑组织代谢监测多参数脑组织代谢(Neurotrend系统)监测是随着电子和光纤技术的发展而新近涌现的有创脑氧监测技术。Neurotrend系统是采用原用于血管内血气监测的Paratrend7探头技术,在直径0.5mm,长约25mm的…     

重型颅脑创伤亚低温治疗中脑组织氧分压持续监测的应用

目的 研究亚低温治疗状态下重型颅脑创伤( sTBI)患者伤后早期脑组织氧分压(PbtO2)的动态变化及临床意义.方法 38例sTBI患者进行亚低温治疗,连续监测PbtO2、颈静脉血氧饱和度(SjvO2)、颅内压(ICP)、和脑灌注压(CPP)等指标,对监测结果以及PbtO2和其他指标相关性进行分析,并记录患者伤后3个月的格拉斯哥预后评分.结果 在亚低温治疗初期,患者PbtO2、SjvO2和CPP明显上升,ICP明显下降,而治疗36 h和48 h后PbtO2及SjvO2无明显变化.亚低温治疗后ICP较治疗前明显下降,低PbtO2情况明显改善,ICP和PbtO2之间呈负相关;PbtO2及SjvO2水平明显上升,PbtO2与SjvO2呈直线正相关;PbtO2与CPP呈直线正相关.监测过程中,在SjvO2和CPP水平正常的情况下,仍有较大比例的患者出现低PbtO2情况.治疗过程中没有出现过低PbtO2水平的患者预后良好.结论 PbtO2是监测sTBI患者局部脑组织氧合的一项重要指标,具有很高敏感性,对于指导治疗和判断预后具有重要意义,而亚低温能够明显改善PbtO2降低的情况.     

第3届国际脑组织氧及代谢学术会议纪要

第3届国际脑组织氧(PbrO_2)及代谢学术会议于1999年4月29～30日在德国柏林召开,与会200多名代表就脑组织氧含量监测在颅脑创伤、脑缺血等疾病中价值及前景进行交流和讨论。本文作者参加了这次学术会议,作简要介绍。1 脑组织氧监测仪器种类 目前国际上有两种脑组织氧含量监测仪器,一种是德国Licox生产的脑组织氧含量监测仪,另一种是英国Diametric公司生产的脑组织气体分析仪。     

重型颅脑损伤中脑温脑组织氧分压持续监测

目的研究重型颅脑损伤中脑温(BT)、脑组织氧分压(PbtO2)的持续变化及其意义.方法应用脑温、脑组织氧分压(PbtO2)探针脑白质温度、脑组织内物理性溶解的氧的压力.结果通过对10例重型闭合性颅脑损伤患者研究分析发现(1)在诱导低温后,直肠温度(RT)与BT的差异比正常体温时明显.(2)在重型颅脑伤后,PbtO2值降低,PbtO2＜10mmHg时,可认为是脑缺氧的阈值.(3)伤后24小时内PbtO2＜5mmHg预示病人预后不良.(4)脑组织氧分压测定技术可指导过度换气的应用.结论在低温状态下,RT与BT的差异加大,因此,在研究低温对脑外伤的影响时,最好能直接测量脑温.脑组织氧分压监测安全可靠,是脑组织氧合程度的一种灵敏的监测方法,它可以提示预后,并且对临床治疗具有重要的指导作用.     

Brain tissue oxygen monitoring in intracerebral hemorrhage

Introduction: Brain tissue oxygen (P_brO₂) monitoring is an emerging technique for detection of secondary brain injury in neurocritical care. Although it has been extensively reported in traumatic brain injury and aneurysmal subarachnoid hemorrhage, its use in nontraumatic intracerebral hemorrhage (ICH) has not been well described. We report complementary preliminary studies in a large animal model and in patients that demonstrate the feasibility of P_brO₂ monitoring after ICH. Methods: To assess early events after ICH, Licox Clark-type oxygen probes were inserted in the bilateral frontal white matter of four anesthetized swine that subsequently underwent right parietal hematoma formation in an experimental model of ICH. Intracranial pressure (ICP) was monitored as well. Seven patients with acute ICH, who were undergoing ICP monitoring as part of standard neurocritical care, had placement of a frontal oxygen probe, with subsequent monitoring for up to 7 days. Results: In the swine ICH model, a rise in ICP early after hematoma formation was accompanied by a decrease in ipsilateral and contralateral P_brO₂. Secondary increases in hematoma volume resulted in further decreases in P_brO₂ over the first hour after ICH. In patients undergoing oxygen monitoring, low P_brO₂ (<15 mmHg) was common. In these patients, changes in F_iO₂, mean arterial pressure, and cerebral perfusion pressure (but not ICP) predicted subsequent change in P_brO₂. Conclusion: Brain tissue oxygen monitoring is feasible in ICH patients, as well as in a swine model of ICH. Translational research that emphasizes complementary information derived from human and animal studies may yield additional insights not available from either alone.     

A fully implantable telemetry system for the chronic monitoring of brain tissue oxygen in freely moving rats

The ability to monitor tissue oxygen concentration in a specific region of the brain in a freely moving animal could provide a new paradigm in neuroscience research. We have developed a fully implantable telemetry system for the continuous and chronic recording of brain tissue oxygen (PO_2,BR) in conscious animals. A telemetry system with a sampling rate of 2 kHz was combined with a miniaturized potentiostat to amperiometrically detect oxygen concentration with carbon paste electrodes. Wireless power was employed to recharge the telemeter battery transcutaneously for potential lifetime monitoring. Rats were implanted with the telemeter in the peritoneal cavity and electrodes stereotaxically implanted into the brain (striatum or medulla oblongata). While the animals were living in their home cages the sensitivity to changes in oxygen was validated by repeatedly altering the inspired oxygen (10%, 100%, respectively) or a pharmacological stimulus (carbonic anhydrase inhibitor: acetazolamide 50 mg/kg IP). Basal level of PO_2,BR was monitored for 3 weeks and showed good overall stability and good correlation to movement such as grooming. During hypoxia, PO_2,BR decreased significantly by -51% ± 2% from baseline, whereas it increased by 34% ± 3% during hyperoxia. Following the systemic administration of acetazolamide, PO_2,BR increased by 38% ± 4%. We propose this new technology provides a robust method to measure changes in oxygen concentration in specific areas of the brain, in conscious freely moving rats. The ability to track long term changes with disease progression or drug treatment may be enabled.     

过度通气对重型颅脑创伤病人的脑血流和脑组织氧分压的影响

目的研究过度通气(HV)对重型颅脑创伤(sTBI)病人的颅内压(ICP)、脑血流(CBF)和脑组织氧分压(PbtO2)的影响。方法20例sTBI(GCS3～8分)病人,伤后2～5dICP超过20mmHg时,应用机械通气法使呼气末二氧化碳分压(PetCO2)维持在27～32mmHg之间30min,同时连续监测ICP、CBF和PbtO2。结果所有病人共进行了46次HV,HV可使ICP明显下降(43/46),而CBF和PbtO2对CO2的反应差异较大,其中大部分试验(38/46)CBF和PbtO2明显下降,但仍然保持在各自的缺血阈值(50AU和10mmHg)之上;5次试验CBF和PbtO2下降低于各自的缺血阈值;3次试验ICP无明显变化,CBF轻度升高,而PbtO2下降。结论HV可降低ICP,但有导致或加重脑缺血的危险,应尽量避免早期长时程应用。HV应在CBF持续监测下应用。     

动脉瘤性蛛网膜下腔出血病人Lindegaard比值与脑组织氧分压的相关性

目的 探讨动脉瘤性蛛网膜下腔出血（a SAH）病人经颅多普勒超声（TCD）检测Lindegaard比值（LR）与脑组织氧分压（PbtO2）的相关性。方法 2019年8月至2022年2月前瞻性收集a SAH共46例。使用LICOX-Ⅱ型脑组织氧分压监测系统,采用氧分压探针（Clark型微型电极）记录大脑中动脉供血脑组织PbtO2,其中PbtO2<20 mmHg且持续时间≥10 min定义为局部组织缺氧。TCD检测PbtO2探针同侧MCA和颈内动脉（ICA）颅外段,LR指同侧MCA与ICA颅外段平均血流速度比值,LR≥3存在脑血管痉挛。结果 根据PbtO2监测结果,16例出现脑组织缺氧（缺氧组）,30例无脑组织缺氧（非缺氧组）;与非缺氧组相比,缺氧组入院GCS评分较低（P=0.041）,脑血管痉挛发生率呈增高趋势（P=0.057）。LR判断存在脑血管痉挛37例,无脑血管痉挛9例。LR与PbtO2呈显著负相关（r=-0.305,P=0.039）。LR≥3预测脑组织缺氧的特异性很高（93.3%）,但敏感性较低（56.3%）;LR对脑组织缺氧的阳性预测值和阴性预测值分别为81.8%和80....     

Initial clinical experience with near-infrared spectroscopy in assessing cerebral tissue oxygen saturation in cerebral vasospasm before and after intra-arterial verapamil injection

Cerebral vasospasm is a devastating complication after subarachnoid hemorrhage. The use of cerebral tissue oxygen saturation (SctO₂) to non-invasively assess changes in cerebral tissue perfusion induced by intra-arterial (IA) verapamil treatment has not been described to our knowledge. A total of 21 consecutive post-craniotomy patients scheduled for possible IA verapamil treatment of cerebral vasospasm were recruited. The effect of IA verapamil injection on SctO₂ being continuously monitored on both the left and right forehead was investigated. Comparisons between changes in SctO₂ monitored on the ipsilateral and contralateral forehead in relationship to the side of internal carotid artery (ICA) injection were performed. A total of 47 IA verapamil injections (15 left ICA, 18 right ICA, and 14 vertebral artery injections) during 18 neurointerventional procedures in 13 patients were analyzed. IA verapamil administration led to both increases and decreases in SctO₂. Changes in SctO₂ ipsilateral to the ICA injection side were more pronounced (p = 0.02 and 0.07 for left and right ICA injections, respectively) and favored compared to contralateral SctO₂ changes. We were unable to obtain reliable measurements on the side ipsilateral to the craniotomy during four procedures in three patients, presumably secondary to pneumocephalus. The local cerebral vasodilating effect of IA verapamil injection is suggested by the differential changes in SctO₂ ipsilateral and contralateral to the ICA injection side. The inconsistent changes in SctO₂ and the limitations of applying cerebral oximetry in this patient population needs to be recognized.     

Effect of hyperventilation on brain tissue oxygenation and cerebrovenous PO2 in rats

Previous studies have shown that cortical tissue oxygenation is impaired during hyperventilation. However, it is important to quantify the effect of hyperventilation on brain tissue PO(2) and cerebrovenous PO(2) simultaneously especially since cerebral venous oxygenation is often used to assess brain tissue oxygenation. The present study was designed to measure the sagittal sinus PO(2) (PvO(2)), brain tissue PO(2) in the thalamus (PtO(2)), and brain temperature (Bt) simultaneously during acute hyperventilation. Isoflurane-anesthetized rats were hyperventilated for 10 min during which time the arterial carbon dioxide tension (PaCO(2)) dropped from 40.3+4.9 mmHg to 23.5+2.8 mmHg. PtO(2) declined from 26.0+/-4.2 mmHg to 14.8+/-5.2 mmHg (P=0.004) while brain temperature decreased from 36.5+0.3 degrees C to 36.2+0.3 degrees C (P=0.02). However, PvO(2) and arterial blood pressure (BP) did not change during hyperventilation. The maintenance of PvO(2) when perfusion is thought to decline and PtO(2) decreases suggests that there may be a diffusion limitation, possibly due to selective perfusion. Therefore, cerebrovenous PO(2) may not give a good assessment of brain tissue oxygenation especially in conditions of acute hyperventilation, and deeper brain regions other than the cortex also show impaired tissue oxygenation following hyperventilation.     

Brain oxygen tension monitoring following penetrating ballistic-like brain injury in rats

While brain oxygen tension (PbtO₂) monitoring is an important parameter for evaluating injury severity and therapeutic efficiency in severe traumatic brain injury (TBI) patients, many factors affect the monitoring. The goal of this study was to identify the effects of FiO₂ (fraction of inspired oxygen) on PbtO₂ in uninjured anesthetized rats and measure the changes in PbtO₂ following penetrating ballistic-like brain injury (PBBI). Continuous PbtO₂ monitoring in uninjured anesthetized rats showed that PbtO₂ response was positively correlated with FiO₂ (0.21-0.35) but PbtO₂ remained stable when FiO₂ was maintained at ∼0.26. Importantly, although increasing FiO₂ from 0.21 to 0.35 improved P_aO₂, it concomitantly reduced pH levels and elevated P_aCO₂ values out of the normal range. However, when the FiO₂ was maintained between 0.26 and 0.30, the pH and P_aO₂ levels remained within the normal or clinically acceptable range. In PBBI rats, PbtO₂ was significantly reduced by ∼40% (16.9 ± 1.2 mmHg) in the peri-lesional region immediately following unilateral, frontal 10% PBBI compared to sham rats (28.6 ± 1.7 mmHg; mean ± SEM, p < 0.05) and the PBBI-induced reductions in PbtO₂ were sustained for at least 150 min post-PBBI. Collectively, these results demonstrate that FiO₂ affects PbtO₂ and that PBBI produces acute and sustained hypoxia in the peri-lesional region of the brain injury. This study provides important information for the management of PbtO₂ monitoring in this brain injury model and may offer insight for therapeutic strategies targeted to improve the hypoxia/ischemia state in the penetrating-type brain injury.     

胎脑组织移植免疫排斥反应的实验研究

以Ｗｉｓｔｅｒ大鼠作为受体动物进行同种及异种胎脑皮质组织移植。移植后应用光镜与电镜技术及免疫组化技术在不同时间内对移植物的存活及排斥反应进行了探讨。同时对移植区血脑屏障开放情况进行了研究。结果表明胞组织移植后存在排斥反应，应用免疫抑制剂可有效增加移植物存活率。