CT检查对新生儿缺氧缺血性脑病预后判断的价值

目的　探讨CT检查对判断新生儿缺氧缺血性脑病 (HIE)预后的价值。方法　对 85例HIE患儿分别在生后 1周内、2周～ 2个月、3～ 6个月、1～ 1 5岁进行CT检查 ;同时在生后12～ 14d进行新生儿行为神经测定 ;在 1～ 1 5岁测定发育商判断预后。结果　生后 1周内CT结果分度为重度者预后不良率为 4 0 9% (9/ 2 2 ) ,为中度者预后不良率为 5 7% (3/ 5 2 ) ;2个月时CT随访结果异常者预后不良率为 6 0 0 % (6 / 10 ) ;CT结果中度且 12～ 14d的NBNA评分≥ 35分与 <35分者的预后差异无显著性 ,CT结果重度且 12～ 14d的NBNA评分 <35分者有 72 7% (8/ 11)预后不良。结论　生后 1周内CT分度及生后 1个月左右随访结果 ,同时结合临床、生后 12～ 14dNBNA评分对判断HIE患儿的预后、制定治疗方案及疗程有重要意义。     

Acute cerebral infarction: pathophysiology and modern treatment concepts

Summary This review focuses on the pathophysiological changes in acute cerebral ischemia, with special emphasis on disturbances of the cerebral blood flow (CBF) and the associated penumbra concept. Alternatively, the model of peri-infarct depolarization is demonstrated. Metabolic and molecular changes caused by cerebral ischemia and reperfusion are discussed, namely energy failure, release of glutamate with an excitatoric burst, calcium influx in neurons, generation of free radicals, activation of different proteases, disturbances of protein synthesis, induction of gene expression and apoptosis, loss of membrane integrity, edema formation and microvascular disturbances. In summary, the pathophysiological changes after focal cerebral ischemia and reperfusion are most adequately described by a network of interacting different mechanisms of tissue alterations. The simple concept of a cascade of ischemic effects which would be easy to block seems to be less applicable. A time window of approximately 6 h for the acute stroke therapy is postulated on the base of the above mentioned pathophysiological changes. The recently introduced treatment regimen with optimized basic treatment, recanalization using thrombolysis and neuroprotection by different agents is presented. Different modes of a possible intervention are discussed. Modern concepts of stroke therapy including stroke-unit care and thrombolysis with add-on neuroprotection seem to have potential for improving the outcome of acute stroke patients.      

低血流期间缺钠对心肌缺血再灌注损伤的影响

目的探讨低血流期间无销对再灌注心脏功能恢复的影响。方法采用等客收缩大鼠灌流心脏模型，低血流期以无钠的Krebs-Henseleit（K-H）液灌注．San-ei362型多道重理记录仪，测定再灌注不同时刻左心宝功能及乳酸脱氨酶活性．结果再灌注30min.在各相应时刻，缺钠组左心室收缩压（LVSP）、心率（HR）、左心室内压最大上升速率（dp／dtmax）的恢复均显著高于对照组（P＜0．001），左心室舒张期末压（LVEDP）显著低于对照组（P＜0.001），乳酸脱氢酶数据低于对照组。结论低血流缺血间无销减轻了心脏血液动力学的损害，心肌乳酸脱氢酶的漏出减少，这可能与因低血流期间无销细胞内钠超负荷减轻有关。     

Early Stroke Recognition: Developing an Out-of-hospital NIH Stroke Scale

Objective : To develop an abbreviated and practical neurologic scale that could assist emergency medical services or triage personnel in identifying patients with stroke.
Methods : A prospective, observational, cohort study was performed at university-based EDs. Participants were 74 patients treated in a thrombolytic stroke trial and 225 consecutive non-stroke patients evaluated during 4 random 12-hour shifts in the ED. Scores on the NIH Stroke Scale were obtained for all patients by physicians. Items of this scale were modified and recoded to a binomial (normal or abnormal) scale. Serial univariate analyses using χ² were performed to rank items. Recursive partitioning was then performed to develop the decision rule for predicting the presence of stroke.
Results : Three items identified 100% of patients with stroke: facial palsy, motor arm, and dysarthria. An Abbreviated NIH Stroke Scale based on these items had a sensitivity of 100% and a specificity of 92%. A proposed Out-of-hospital NIH Stroke Scale consisting of facial palsy, motor arm, and a combination of dysarthria and best language items (abnormal speech) had a sensitivity of 100% and a specificity of 88%.
Conclusion : Using the derivation data set, a proposed Out-of-hospital NIH Stroke Scale had a high sensitivity and specificity for identifying patients with stroke when performed by physicians in this group of 299 ED patients. Prospective studies of other health care professionals using the scale in the out-of-hospital arena are needed.     

ISCHAEMIA-REPERFUSION INJURY TO THE INTESTINE

Ischaemia-reperfusion injury (IRI) is of obvious relevance in situations where there is an interruption of blood supply to the gut, as in vascular surgery, or in the construction of free intestinal grafts. It is now appreciated that IRI also underlies the gut dysfunction that occurs in early shock, sepsis, and trauma. The events that occur during IRI are complex. However, recent advances in cellular biology have started to unravel these underlying processes. The aim of this review is to provide an outline of current knowledge on the mechanisms and consequences of IRI. Initially, IRI appears to be mediated by reactive oxygen metabolites and, at a later stage, by the priming and activation of polymorphonuclear neutrophils (PMN). Ischaemia-reperfusion injury can diminish the barrier function of the gut, and can promote an increase in the leakage of molecules (intestinal permeability) or the passage of microbes across the wall of the bowel (bacterial trans-location). Ischaemia-reperfusion injury to the gut can result in the generation of molecules that may also harm distant tissues.     

不同脑缺血和再灌流过程中大鼠脑组织NO含量的动态变化

采用线栓法制成大鼠大脑中动脉梗塞 ( MCAO)模型 ,依 Hb O2 - NO法测定持续性脑缺血和缺血 /再灌流脑组织内 NO含量的变化 ,以探讨不同脑缺血和再灌流过程中 NO的变化规律及其意义。结果 :缺血 3小时受损脑组织 NO水平即增高 ,再灌流后 NO逐步升高 ,而持续性缺血状态下 NO则表现降低后再升高的变化。虽然两组 NO在 7天时均有明显降低 ,但仍高于缺血前水平。认为持续性脑缺血和缺血 /再灌流情况下 NO的变化规律有所不同 ,与缺血脑组织的缺氧及产生 NO所需底物供应缺乏有关 ,且可能与脑组织的损害密切相关     

Protein kinase C in focal ischemic rat brain: dual autoradiographic analysis of [C]iodoantipyrine (IAP) and [H]phorbol-12,13-dibutyrate (PDBu)

Protein kinase C (PKC) activity was measured in rat brain with 2 h of middle cerebral artery (MCA) and common carotid artery (CCA) occlusion, using dual autoradiography of [¹⁴C]iodoantipyrine (IAP) and [³H]phorbol-12,13-dibutyrate (PDBu). In the ischemic brain, it required more than 120 min of incubation to obtain a plateau in PDBu binding. In contrast, the binding of PDBu in non-ischemic brain reached a plateau with incubation for 60 min. This delay of PDBu binding in the ischemic brain suggests that the affinity of this ligand is reduced due to a change in structure of the cell membrane caused by ischemia. PDBu binding in the ischemic brain increased significantly compared to the non-ischemic brain. This finding provides further evidence that excessive activation of PKC in the ischemic brain may play an important role in ischemic neuronal damage. ©1997 Elsevier Science B.V. All rights reserved.     

大鼠脊髓缺血再灌流时脊髓神经元对躯体和内脏传入刺激的反应

５０只大鼠用乌拉坦麻醉，箭毒制动。通过阻断腹主动脉血流以模拟腰段脊髓的局部缺血和再灌流损伤，玻璃微电极记录Ｌ２节段脊髓单位放电（ＳＣＵＤｓ），观察缺血再灌流时脊髓神经元对腓神经刺激（ＰＮＶ），内脏大神经刺激（ＶＬＮＶ）及两者同时刺激（ＳＶ）的反应。结果在缺血前所记录的１３３个自发放电单位中，对３种刺激均产生兴奋（Ｅ）、抑制（Ｉ）及无反应（ＮＲ）３种形式的反应，表明大鼠Ｌ２节段脊髓存在躯体、内脏和躯体内脏反应性神经元，并有会聚和阻塞现象。在脊髓缺血再灌流时，神经元对ＰＮＶ、ＶＬＮＶ、ＳＶ也产生Ｅ、Ｉ、ＮＲ３种形式的反应，提示脊髓缺血再灌流时神经元对躯体和内脏传入刺激的反应形式不受影响；但缺血时ＳＣＵＤｓ对ＰＮＶ、ＶＬＮＶ产生反应的单位数减少，这表明脊髓缺血损伤时神经元对躯体和内脏传入刺激的反应性减弱，随着缺血损伤加重，脊髓神经元对躯体内脏信号的整合功能下降     

Semipermeable Hollow Fiber Membranes in Hepatocyte Bioreactors: A Prerequisite for a Successful Bioartificial Liver?

Abstract: Recent studies have shown that liver support systems based on viable hepatocytes can prolong life in animal models of acute liver failure. Now the time has come to elucidate the design characteristics that are essential to construct an efficient bioreactor. The gold standard remains the intact liver. Despite the very high cell density in this organ, individual cell perfusion is guaranteed resulting in low diffusional gradients which are essential for optimal mass transfer. These conditions are not met in bioreactors based on hollow fiber membranes. Moreover, the semipermeable membranes can foul and act as a diffusional barrier between the hepatocytes and the blood or plasma of the recipient. We devised a novel bioreactor for use as a bioartificial liver that does not include hollow fiber membranes for blood or plasma perfusion. The device is based on an integral oxygenator and a nonwoven polyester matrix material for hepatocyte culture as small aggregates. The efficacy of this original design was tested in rats with liver ischemia. Preliminary results show statistically significantly improved survival; life was prolonged 100% compared to the control experiments.     

电针对沙鼠急性脑缺血再灌注后神经原损伤的保护作用

本实验利用沙鼠急性脑缺血再灌注模型，研究电针对脑缺血及再灌注各期脑电活动的影响及组织病理学的改变。结果表明：缺血１０ｍｌｎ，脑电幅度受到严重抑制，甚至变平坦，总功率大大下降，再灌注后总功率难以恢复，在１２０ｍｉｎ时仅恢复到缺血前的２７．３９±１１．３１％，以后即不再进一步恢复，电针组动物缺血１０ｍｉｎ再灌注后，脑电的恢复明显比对照组快，１２０ｍｉｎ时恢复至缺血前的７１．４５±１６．４６％（Ｐ＜０．０１），２４０ｍｉｎ时继续恢复至缺血前的７５．２７±１８．４３％。同时电针能明显减轻缺血１０ｍｉｎ后再灌注２４小时的神经原缺血性损伤。结果提示：电针对急性脑缺血引起的神经原损伤具有保护作用，并能促进脑功能的恢复。