醒脑静对家兔脑缺血再灌流时TNF,IL—1β,IL—6水平及脑超微 …

目的 探讨脑缺血再灌流损伤中机体肿瘤坏死因子（ＴＮＦ）、白细胞介素－１β（ＩＬ－１β）、白细胞介素－６（ＩＬ－６）水平和脑超微结构的变化及醒脑静（ＸＮＪ）对其的影响。方法 建立家兔急性全脑缺血及缺血再灌流动物模型。于缺血前和再灌流前对照组（Ａ组）静脉注射生理盐水１ｍｌ／ｋｇ,醒脑静保护组（Ｂ组）静脉注射ＸＮＪ１ｍｇ／ｋｇ,观察血、脑组织中ＴＮＦ、ＩＬ－１β、ＩＬ－６水平及脑组织超微结构。结果 缺血     

大鼠脑创伤后白细胞介素—1β和肿瘤坏死因子—αmRNA在脑组？…

目的：研究大鼠实验性脑创伤脑组织中白细胞介素－１β（ＩＬ－１β）及肿瘤坏死因子－α（ＴＮＦ－α）ｍＲＮＡ表达水平的变化。方法：由液压型创伤装置致大鼠一侧脑挫伤，利用地高辛标记的寡核苷酸探针原位杂交技术观测ＩＬ－１β和ＴＮＦ－α的基因表达。结果：鼠脑创伤后上述两种细胞因子的基因表达水平迅速增高，在伤后１小时即可达取最高水平，并持续至伤后６小时，伤后２４小时后基本恢复到正常水平，两种细胞因子在脑组织中     

癫痫患儿血白细胞介素—1β,可溶性白细胞介素—2受体和？…

目的：探讨癫痫的免疫学发病机制。方法：选择原发性全身型癫痫呈强直和（或）阵挛发作患儿６０例为研究对象，分为服用苯巴比妥、卡马西平及未服药３组，测定其外周血单核细胞（ＰＢＭＣ）在植物血凝素（ＰＨＡ）的作用下释放白细胞介素－１β（ＩＬ－１β）、肿瘤坏死因子－α（ＴＮＦ－α）的量及血清ＴＮＦ－α、可溶性白细胞介素－２受体（ＳＩＬ－２Ｒ）的含量，并与对照组比较。结果：３组癫痫患儿间各指标含量均无显著性差异     

川芎嗪注射液对脑缺血-再灌注损伤家兔血清白细胞介素-8的影响

目的：观察川芎嗪注射液（ＴＭＲＩ）对脑缺血－再灌注损伤（ＣＩＲＩ）家兔血清白细胞介素－８（ＩＬ－８）的合成和释放的影响,并探讨其脑保护机制。方法：制备家兔ＣＩＲＩ模型,随机分为假手术对照组、缺血－再灌注组和ＴＭＲＩ组,分别在缺血前、缺血３０分钟、再灌注３０、６０、１２０分钟取静脉血,测定血清ＩＬ－８浓度,实验结束取脑皮质ＨＥ染色,光镜观察脑组织病理学改变。结果：缺血－再灌注组在脑缺血－再灌注时间不同时间点血清ＩＬ－８水平随脑缺血－再灌注时间延长呈进行性升高,分别为缺血前的１．３８、１．６２、１．９３和２．２９倍,明显高于假手术组,光镜下白细胞大量浸润、神经元明显损伤;ＴＭＲＩ组不同时间点血清ＩＬ－８浓度显著低于缺血－再灌注组,光镜下白细胞浸润、神经元损伤程度较缺血－再灌注组明显减轻,而与假手术组比较均无显著性差     

肿瘤坏死因子α,白细胞介素—1β和巨噬细胞炎性蛋白—1α…

首先用全血内毒素血症动物模型，以内毒素刺激全血，显示动物上清液肿瘤坏死因子（ＴＮＦα）浓度随内毒素剂量增加而增加，地塞米松明显抑制其释放，布洛芬对。ＴＮＦα释放为双向效应。腹腔注射内毒素复制大鼠生肺损伤模型，显示肺毛细血管通和随内毒素剂量增大而增加，提前１小时注射地塞米松、布洛芬能防止血管通透性增加；同时观察到肺组织中ＴＮＦα、白细胞介素－１β（ＩＬ－１β）、巨噬细胞炎性蛋白－１α（ＭＩＰ－１α）     

肾综合征出血热患者尿液中TNF,IL—6,IL—8的检测及意义

采用双抗体夹以ＥＬＩＳＡ法对４８例ＨＦＲＳ患者１５６份系列尿液中ＴＮＦ，ＩＬ－６，ＩＬ－８进行了动态检测，结果发现：ＨＦＲＳ患者尿液中ＴＮＦ，ＩＬ－６，ＩＬ－８含量较对照组明显增高（Ｐ〈０．００１），且病程前三期平均含量较全病中明显高，ＴＮＦ与ＩＬ－６呈显著正要关（γ＝０．５６２１，Ｐ〈０．００５），ＩＬ－６与ＩＬ－８呈显著正相关（γ＝０．３８４５，Ｐ〈０．０１）；ＴＮＦ含量发热期明显升高，低血压     

脂多糖致肺血管内巨噬细胞释放几种细胞因子的改变

目的 探讨肺血管内巨噬细胞（ＰＩＭ）释放的细胞因子在感染性急性肺损伤（ＡＬＩ）发病中的作用。方法 仿Ｍｏｒｔｏｎ法灌洗肺血管床,贴壁法分离猪ＰＩＭ,培养于ＰＩＭ１６４０培养基,予１０μｇ／ｍｌ脂多糖（ＬＰＳ）刺激,胸腺细胞增殖法测ＰＩＭ培养上清白细胞介素１β（ＩＬ－１β）活性,酶联免疫吸附试验（ＥＬＩＳＡ）法测肿瘤坏死因子α（ＴＮＦα）、白细胞介素６（ＩＬ－６）、白细胞介素８（ＩＬ－８）含量。结果     

支气管哮喘一氧化氮,细胞因子与气道反应性相关性研究

目的：了解哮喘患者一氧化氮（ＮＯ）及细胞因子白细胞介素６（ＩＬ－６）、白细胞介素（ＩＬ－８）、肿瘤坏死因子－α（ＴＮＦα）、干扰素－γ（ＩＦＮγ）与气道高反应性（ＡＨＲ）的相互关系，探讨ＮＯ和细胞因子在哮喘发病中的作用。方法：测定１７名哮喘缓解期患者和１０名健康人血清ＮＯ２＾－、ＩＬ－６、ＩＬ－８、ＩＮＦα、ＩＦＮγ水平，并对哮喘患者及健康人进行组胺激发试验，得出ＰＤ２０ＦＥＶ１值。结果：哮喘患者     

大黄对SIRS和MODS患者肿瘤坏死因子α及白介素的影响

目的：探讨大黄粉对全身炎性反应综合征和多器官功能障碍综合征（ＭＯＤＳ）患者肿瘤坏死因子－α（ＴＮＦ－α）,白介素－１（ＩＬ－１）,ＩＬ－６的拮抗作用。方法：４０例虱在综合治疗的基础上经胃管给予大黄粉治疗,治疗前后检测血清ＴＮＦ－α,ＩＬ－１,ＩＬ－６的含量,并与正常对照组４０例结果进行比较。结果;在应激状态下,ＳＩＲＳ和ＭＯＤＳ患者的ＴＮＦα,ＩＬ－１和ＩＬ－６水平均明显高于正常对照组;应用大黄粉     

大鼠脑创伤后白细胞介素-1β和肿瘤坏死因子-αmRNA在脑组织中的表达

目的：研究大鼠实验性脑创伤后脑组织中白细胞介素１β（ＩＬ１β）及肿瘤坏死因子α（ＴＮＦα）ｍＲＮＡ表达水平的变化。方法：由液压型创伤装置致大鼠一侧脑挫伤，利用地高辛标记的寡核苷酸探针原位杂交技术观测ＩＬ１β和ＴＮＦα的基因表达。结果：鼠脑创伤后上述两种细胞因子的基因表达水平迅速增高，在伤后１小时即可达到最高水平，并持续至伤后６小时，伤后２４小时后基本恢复至正常水平。两种细胞因子在脑组织中的表达区域很类似，主要出现于创伤侧及对侧脑皮质、海马、胼胝体、脉络丛等部位。结论：脑创伤后炎性细胞因子主要由中枢神经系统内部产生，ＩＬ１β及ＴＮＦα可能对脑创伤后继发性神经损害有直接的作用     

Effect of brain cooling on brain ischemia and damage markers after fluid percussion brain injury in rats

Although systemic cooling had recently been reported as effective in improving the neurological outcome after traumatic brain injury, several problems are associated with whole-body cooling. The present study was conducted to test the effectiveness of brain cooling without interference with the core temperature in rats after fluid percussion traumatic brain injury (TBI). Brain dialysates ischemia (e.g., glutamate and lactate-to-pyruvate ratio) and injury (e.g., glycerol) markers before and after TBI were measured in rats with mild brain cooling (33 degrees C) and in the sham control group. Brain cooling was accomplished by infusion of 5 mL cold saline via the external jugular vein under general anesthesia. The weight loss was determined by the difference between the first and third day of body weight after TBI. The maximum grip angle in an inclined plane was measured to determine motor performance, whereas the percentage of maximal possible effect was used to measure blockade of proprioception. The triphenyltetrazolium chloride staining procedures were used for cerebral infarction assay. As compared with those of the sham-operated controls, the animals with TBI had higher values of extracellular levels of glutamate, lactate-to-pyruvate ratio, and glycerol in brain and intracranial pressure, but lower values of cerebral perfusion pressure. Brain cooling adopted immediately after TBI significantly attenuated the TBI-induced increased cerebral ischemia and injury markers, intracranial hypertension, and cerebral hypoperfusion. In addition, the TBI-induced cerebral infarction, motor and proprioception deficits, and body weight loss evaluated 3 days after TBI were significantly attenuated by brain cooling. We successfully demonstrate that brain cooling causes attenuation of TBI in rats by reducing cerebral ischemia and injury resulting from intracranial hypertension and cerebral hypoperfusion. Because jugular venipuncture is an easy procedure frequently used in the emergency department, for preservation of brain function, jugular infusion of cold saline may be useful in resuscitation for trauma patients.     

Severity and correlates of brain fog in people with traumatic brain injury

Brain fog is one symptom that has been underexplored in traumatic brain injury (TBI). We explored the cognitive and affective correlates of brain fog in people with symptomatic mild TBI (n = 15), moderate-to-severe TBI (n = 15), and a healthy control group (n = 16). Measures across the studies assessed “brain fog” (Mental Clutter Scale), objective cognition (Useful Field of View® and Cogstate Brief Battery®), post-concussive symptoms (Post-Concussion Symptom Scale), and depressive symptoms (Profile of Moods Scale). Brain fog was higher in symptomatic mild TBI and moderate-to-severe TBI compared with healthy controls. Greater brain fog corresponded to greater depressive symptoms in symptomatic mild TBI. Greater brain fog corresponded to poorer episodic memory and working memory in moderate-to-severe TBI. Brain fog appears to reflect challenges in recovery, including depressive symptoms and worse cognitive function. Screening for brain fog might be worthwhile in people with brain injuries.     

子痫前期对足月新生儿脑损伤及脑发育的影响

目的研究母亲妊娠合并子痫前期对足月新生儿脑损伤及脑发育的影响。方法通过临床观察,并予颅脑超声检查（动态）,观察孕母合并子痫前期所生96例足月儿脑损伤及脑发育情况,并分析与妊娠合并子痫前期程度的关系。结果本组足月儿轻度脑损伤占32.3%,重度脑损伤占6.3%,损伤类型主要是新生儿缺血缺氧性脑病（H IE）,子痫前期程度越重,重度脑损伤发生率越高;早发型子痫前期母亲所生新生儿重度脑损伤发生率明显高于晚发型;严重的妊娠高血压疾病,新生儿脑发育落后的比例高。结论母亲妊娠合并子痫前期的程度越重,其新生儿脑损伤、脑发育迟缓的发生率越高,早发型高于晚发型,因此对妊娠高血压疾病母亲所生新生儿要加强监测,改善预后。     

Association between brain tissue pH and brain injury during asphyxia in piglets

BACKGROUND: Acidosis may contribute to brain injury from asphyxia, but its role is unclear. In order to evaluate the association between brain acidosis and cerebral injury, we subjected piglets to hypoxia and hypotension (HYP-HOTN) or hypoxia alone (HYP) to inflict varying amounts of brain damage. We hypothesized that piglets with a more severe brain injury would have a lower brain pH. METHODS: Piglets had a pH microprobe inserted into the cerebral cortex. HYP animals breathed 5-8% O(2)/7% CO(2) for 30 min with mean arterial pressure (MAP) maintained at >40 mmHg. HYP-HOTN animals breathed the same gas for 30 min, but during the last 15 min, MAP was reduced to 25-30 mmHg by withdrawing blood. After 4 h of recovery, the animals were perfusion-fixed and pathology assessed. Somatosensory-evoked potentials (SEP) were also monitored. RESULTS: HYP-HOTN piglets had more neuropathology than HYP animals. During the last 15 min of injury, brain pH in the HYP-HOTN group was significantly higher than that in HYP. However, recovery of brain pH was prolonged in the HYP-HOTN animals. The amount of time for brain pH to recover to > or =7.00 correlated very well with both the degree of neuropathology and SEP recovery. The reduction in brain pH, either absolute or relative to baseline, was not associated with the severity of damage. CONCLUSIONS: The time needed for brain pH to recover after asphyxia, but not its severity, was associated with the amount of brain injury. Further study is warranted to determine whether immediate restoration of brain pH will reduce brain damage.     

Mediators of brain edema and secondary brain damage

Progress is our understanding of the roles of vasogenic and cytotoxic brain edema in secondary brain damage can be expected from studies of the ability of biochemical factors to open the blood-brain barrier, derange the microcirculation, and cause cell swelling and necrosis. Mediator compounds are considered to form or to become released in an area of primarily damaged brain (necrosis) and to enter the cerebral parenchyma through the broken blood-brain barrier from the intravascular space. Many biochemical factors must be considered. We suggested three criteria for determining the roles of mediators: a) they must inflict brain tissue damage, b) they must occur in pathologic concentrations or in compartments not normally present, and c) specific inhibition should attenuate secondary brain damage. These requirements are met by the kallikrein-kinin system and by glutamate. In the case of arachidonic acid and its many metabolites, the concept is difficult to test because fatty acids may be active only if not bound to proteins, and therapeutic inhibition might be difficult. A variety of mediators may enhance each other in a cascade manner by various initiating reactions that might be amenable for pharmacologic inhibition.