内毒素性休克大鼠脑组织和血浆神经球蛋白水平的变化

Objective To investigate the changes in the expression of neuroglobin (Ngb) in the frontal lobe cortex, hippocampus, cerebro-spinal fluid (CSF) and plasma in a rat model of endotoxie shock. Methods Seventy SD rats of both sexes aged 7 weeks weighing 250-300 g were randomly divided into control group (group C, n = 10) and endotoxic shock group (group ES, n =60). LPS 16 mg/kg was injected via the vein in the tail in group ES. In group C, equal volume of normal saline was administered iv instead of LPS. Blood and CSF samples were taken and frontal lobe cortex and hippocampua were removed at 3, 6, 12, 24, 48, and 72 h after LPS administration for determination of Ngb expression by ELISA and Western blotting. Cerebral water content was measured --brain water content = (wet weight- dry weight) ÷ wet weight x 100%.Results The brain water content was significantly increased after LPS administration and peaked at 48 h after LPS. The expression of Ngh was significantly higher in group ES than in group C and peaked at 48 h after LPS (P < 0.01). Conclusion The up-regulation of Ngb induced by endotoxic shock is time-dependent and is one of the endogenous neuron-protective mechanisms of endotoxie shock.     

Structural changes of neurons in hippocampus from infantile rats exposed to hyperbaric oxygen

Objective:To investigate if hyperbaric oxygen (HBO) may induce structural changes of neurons in hippocampus from infactile rats and if the changes are reversible.Methods:All 27 healthy SD infantile rats were exposed to HBO(0.25MPa) or hyperbaric air(HBA) for 1 to 3 courses(10 days as 1 course).The hippocampus was taken at the end of each course to observe its morphology by light microscope and electron microscope.Results:HBO exposure induced capillary dilation,nuclear membrane winding or blurring and some mitochondria swelling with its crista blurring in neurons.The changes occurred after 1 course exposure and became significant with time.Most of the changes recovered 20 days after stopping exposure.No change was found after HBA exposure.Conclusions:Long-term HBO exposure can cause capillary dilation and ultrastructural injury of neurons in hippocampus from infantile rats.The damage is not serious,but reversible.     

计算机图像分析在评价大鼠急性胰腺炎模型病理变化中的应用

Objective To apply computer digital image analysis to evaluate pathologic changes in rat model with acute pancreatitis, and explore digitalization of the evaluating process. Methods The model was established by injection of 5% sodium taurocholate into the pancreatic duct of Sprague-Dawley rats. Rats were killed 3, 6, 12, 24, and 48 h after the surgery respectively. Paraffin-embedded sections were made and scanned by Virtual Microscopy system. Digital image analysis was applied to analyze necrosis, edema,hemorrhage and infiltration of inflammatory cells in pancreatic tissues. Results As compared with other groups, the pathologic changes of pancreatitis were significantly more severe in 48-h group [inflammatory cell number: (67.00 ±49.49)/200 × field;necrosis: (49.86±21.74)%;hemorrhage: (14 445. 60 ±6940. 35) μm2;edema: 9.58 ±0. 81;P<0. 05];Cohen's kappa statistics showed that digital image analysis had better inter-rater agreement than Schmidt' s evaluation (Kappa coefficient;0. 7vs0. 3). Conclusion Digital image analysis could improve the objectivity, accuracy, and inter-rater agreement in evaluating pathologic changes in rat model with acute pancreatitis.     

计算机图像分析在评价大鼠急性胰腺炎模型病理变化中的应用

Objective To apply computer digital image analysis to evaluate pathologic changes in rat model with acute pancreatitis, and explore digitalization of the evaluating process. Methods The model was established by injection of 5% sodium taurocholate into the pancreatic duct of Sprague-Dawley rats. Rats were killed 3, 6, 12, 24, and 48 h after the surgery respectively. Paraffin-embedded sections were made and scanned by Virtual Microscopy system. Digital image analysis was applied to analyze necrosis, edema,hemorrhage and infiltration of inflammatory cells in pancreatic tissues. Results As compared with other groups, the pathologic changes of pancreatitis were significantly more severe in 48-h group [inflammatory cell number: (67.00 ±49.49)/200 × field;necrosis: (49.86±21.74)%;hemorrhage: (14 445. 60 ±6940. 35) μm2;edema: 9.58 ±0. 81;P<0. 05];Cohen's kappa statistics showed that digital image analysis had better inter-rater agreement than Schmidt' s evaluation (Kappa coefficient;0. 7vs0. 3). Conclusion Digital image analysis could improve the objectivity, accuracy, and inter-rater agreement in evaluating pathologic changes in rat model with acute pancreatitis.     

The effects of stress- relaxation plate on disorganization and repair of regional bone structure: an experimental study

Objective:To study the influence of stress-relaxation plate on disorganization and repair of the cortex beneath the plate.Methods:A washer made of viscoelastic polyethylene was placed between the screw and the screw hole of conventional stainless rigid plate (RP) to produce a stressrelaxation plate (SRP).Both SRP and RP were applied to osteotomized tibia in 48 New Zealand rabbits.Healing process of the fracture with either SRP or RP fixation (control) was comparatively studied with polarized light microscopy,in situ hybridization of collagen mRNA and immunohistochemical technique from 2 to 36 weeks postoperatively.Results:The study of plated bone remodeling showed that the degree of cortex osteoporosis beneath the plate was similar between the SRP and RP group within 12 weeks postoperatively.In comparison,the disorganization of bone structure in SRP group happened later and milder than that of RP group,and the repair process began at 12 weeks after implantation.As a consequence,the absorption cavities became smaller and the structure of collagen fibers became well oriented along with these changes by polarized light microscopy.In addition to these,the in situ hybridization analysis of collagen genes and the immunohistochemical study of type I,Ⅲ collagen at 8 to 12 weeks after implantation.from this time on ,the changes above became more evident significantly before most of cavities were repaired by 36 weeks.In contrast to the changes in the SRP group,no expression and synthesis of any kind of collagen could be observed during 12 to 36 weeks after implantation in RP group.Conclusions:Without removal of the bone plate,the SRP fixation not only reduces the degree of plated bone osteoporosis,but also makes the disorganized bone structure restored to normal in terms of the expression and synthesis of type I collagen mRNA of osteoblasts lying on the surface of absorption cavities.     

Establishment of a mechanical injury model of rat hippocampal neurons in vitro

Objective： To establish a simple, reproducible, and practical mechanical injury model of hippocampal neurons of Sprague-Dawley rats in vitro. Methods ： Hippocampal neurons isolated from 1-2-day old rats were cultured in vitro. Mild, moderate and severe mechanical injuries were delivered to the neurons by syringe needle tearing, respectively. The control neurons were treated identically with the exception of trauma. Cell damage was assessed by measuring the Propidium Iodide （PI） uptaking at different time points （0.5, 1, 6, 12 and 24 hours） after injury. The concentration of neuron specific enolase was also measured at some time points. Results ： Pathological examination showed that degeneration, degradation and necrosis occurred in the injured cultured neurons. Compared with the control group, the ratio of PI-positive cells in the injured groups increased significantly after 30 minutes of injury （P 〈 0.05）. More severe the damage was, more PI-positive neurons were detected. Compared with the control group, the concentration of neuron specific enolase in the injured culture increased significantly after 1 hour of injury （ P 〈 0.05）. Conclusions： The established model of hippocampal neuron injury in vitro can be repeated easily and can simulate the damage mechanism of traumatic brain injury, which can be used in the future research of traumatic brain injury.     

Influence of acute ethanol intoxication on neuronal apoptosis and Bcl-2 protein expression after severe traumatic brain injury in rats

Objective: To study the influence and mechanism of acute ethanol intoxication (AEI) on rat neuronal apoptosis after severe traumatic brain injury (TBI). Methods: Ninety-six Sprague-Dawley rats were randomly divided into four groups: normal control, AEI-only, TBI-only and TBI+AEI (n=24 for each). Severe TBI model was developed according to Feeney’s method. Rats in TBI+AEI group were firstly subjected to AEI, and then suffered head trauma. In each group, animals were sacrificed at 6 h, 24 h, 72 h, and 168 h after TBI. The level of neuronal apoptosis and the expression of Bcl-2 protein were determined by TUNEL assayand immunohistochemical method, respectively. Results: Apoptotic cells mainly distributed in the cortex and white matter around the damaged area. Neuronal apoptosis significantly increased at 6 h after trauma and peaked at 72 h. Both the level of neuronal apoptosis and expression of Bcl-2 protein in TBI-only group and TBI+AEI group were higher than those in control group (P<0.05). Compared with TBI-only group, the two indexes were much higher in TBI+AEI group at all time points (P<0.05).Conclusion: Our findings suggest that AEI can increase neuronal apoptosis after severe TBI.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

地塞米松对布比卡因诱导小鼠神经元毒性的影响

Objective To investigate the effect of dexamethasone on the toxicity of bupivacaine in murine neurons.Methods Murine neuroblastoma cell line N2a was obtained from ATCC cell bank (USA). The cells were cultured in 10% fetal cow serum/MEM culture medium and divided into 4 groups voup I control (Con); group II bupivacaine ( Bup); group Ⅲ dexamethasone (Dex) and group IV Dex + Bup. The culture medium contained bupivacaine 900 μmol/L in group Bup and dexamethasone 1 μmol/L in group Dex respectively. In group Dex + Bup ( IV ) Bup was added to the culture medium with a final concentration of 900 μmol/L at 12 h after pretreatment with Dex 1 μmol/L. The cells were inoculated in 24 well plates (0.5 ml in each well, 24 wells in each group) and 10 cm culture dishes (7 ml in each dish, 4 dishes in each group). The release rate of LDH was calculated and the morphology of the cells and nucleus condensation (by Hoechst 3334224 fluorescent staining) was detected at 9 h of incubation in 24 well plates. The mitochondrial transmembrane potential (by JC-1 assay) and phosphorylation of Akt and ERKs (by Western blot) were measured at 5 h of incubation in 24 well plates and in culture dishes respectively. ResultsBupivacaine caused severe damage to the N2a cells as evidenced by increase in LDH release and nucleus condensation (apoptosis), dephosphorylation of Akt and ERKs, decrease in mitochondrial transmembrane potential and severe morphological changes. Dexamethasone pretreatment significantly attenuated bupivacaine-induced neurotoxicity. Conclusion Dexamethasone can protect N2a cells from bupivacaine-induced neurotoxicity through stabilization of mitochondrial transmembrane potential and inhibition of dephosphorylation of Akt and ERKs.     

改良血管穿刺法大鼠蛛网膜下腔出血模型的制作及评价

目的 探讨改良血管内穿刺法制作大鼠蛛网膜下腔出血(SAH)模型的制作方法,以及此模型蛛网膜下腔积血分布、吸收与神经元损伤病理特征的动态变化规律.方法 SD大鼠随机分为正常、假手术和手术组,采用改良血管内穿刺法制作SAH模型,观察各组脑组织的大体形态,以及手术组各个时间点蛛网膜下腔内血液分布情况;通过苏木素-伊红(HE)染色,观察神经组织的病理学变化.结果 3～24 h蛛网膜下腔的积血由穿刺的局部脑底面逐渐向大脑凸面蛛网膜下腔弥散;48 h第四脑室可见明显积血;大脑皮层神经元水肿随时间的增加逐渐加重,24 h达到水肿高峰,并持续到48 h;7 d时神经元水肿基本恢复.结论 改良血管穿刺是制作SAH模型较为理想的方法,蛛网膜下腔内血液的吸收再分布规律及神经元的动态损伤过程为SAH模型构建的评价提供了更完备的实验数据.     

Limited role of inducible nitric oxide synthase in blood-brain barrier function after experimental subarachnoid hemorrhage

Excessive nitric oxide (NO) produced by inducible nitric oxide synthase (iNOS) may play a pivotal role in blood-brain barrier (BBB) breakdown following subarachnoid hemorrhage (SAH). We investigated if the inhibition of iNOS could reduce BBB breakdown and cerebral edema, thereby leading to improved outcome 24 h after SAH. Forty male rats were assigned to three groups: control, SAH, and treatment groups. SAH was induced by perforating the bifurcation of the internal carotid artery. The neurological score and the mortality were evaluated 24 h after the surgery. The expression of iNOS, the concentration of NO metabolites, morphological changes in neuronal cells, water content, and IgG leakage were also evaluated. The expression of iNOS, as well as the concentration of NO metabolites, was elevated after SAH. Treatment with p-Toluenesulfonate decreased both the expression of iNOS and the concentration of NO metabolites. However, there was no significant change in water content, BBB disruption, or morphological findings between the SAH group and the treatment group. Furthermore no significant differences in neurological score or mortality were observed. The iNOS inhibitor failed to reduce BBB breakdown, brain edema, and neuronal cell death and failed to improve the neurological score and the mortality 24 h after SAH.     

SAH大鼠抗脑血管细胞增殖研究

目的 探讨大鼠SAH后脑血管细胞增殖变化,观察大鼠SAH后早期阻断VEGF的作用是否能减轻脑血管细胞增殖. 方法 72只Sprague-Dawley大鼠随机分为3组,假手术组枕大池注入NS,模型组采用枕大池二次注血法制作SAH模型,干预组在制作SAH模型的同时通过枕大池注入抗VEGF多克隆抗体.于SAH（或NS）后1、3、5、7天时处死动物,分离脑干（包含基底动脉）做形态学和PCNA免疫组化检查,观测三组大鼠基底动脉的形态学改变、基底动脉壁PCNA表达. 结果 在SAH后第1天基底动脉即出现明显血管痉挛,第3、5天达到高峰,第7天逐渐缓解.SAH模型组大鼠基底动脉壁PCNA表达第1天即开始升高,第3、5天达到顶峰,第7天后逐渐下降;NS假手术组基底动脉壁PCNA呈阴性表达;抗VEGF抗体干预组基底动脉壁PCNA呈低水平表达.枕大池注射抗VEGF抗体能缓解SAH后脑血管肌内膜增殖,减轻脑血管壁的增厚程度. 结论 VEGF介导的血管内膜增殖反应和脑血管壁增厚可能在脑血管痉挛的发生发展过程中起促进作用,SAH后早期应用VEGF拮抗剂能缓解脑血管细胞增殖.     

Impaired capillary perfusion and brain edema following experimental subarachnoid hemorrhage: a morphometric study

To evaluate microcirculatory disturbance and cerebral edema associated with subarachnoid hemorrhage (SAH), both stereological morphometry on the intraparenchymal capillary network and microgravimetry were performed on a rabbit SAH model. Autologous arterial blood (5 ml) was injected into the cisterna magna, and the animals were sacrificed at intervals of 6 hours, 1 day, 2 days, or 6 days after SAH. Capillaries in the piriform cortex, parasagittal cortex, and ventral brain stem of the midline-hemisectioned brain were injected with Evans blue dye 1 minute before sacrifice, and were planimetrically evaluated under a fluorescence microscope connected to an image analysis system. Stereological and morphological parameters including the volume density, surface density, numerical density, minimum intercapillary distance, and the diameter of Evans blue-perfused capillaries were also computed. In the piriform cortex and ventral brain stem, the volume and surface densities were significantly reduced and the minimum intercapillary distance was significantly increased 1 to 2 days after SAH. In the parasagittal cortex far from the cisternal clot, changes in the parameters were minimal. Cerebral blood volume (CBV) in the normal condition and edema formation associated with SAH were studied by the microgravimetric technique. The mean CBV in the parasagittal cortex, piriform cortex, and brain stem was 6.9%, 6.8%, and 5.6%, respectively. Following SAH, specific gravity in the piriform cortex and the ventral brain stem of the other side of the hemisectioned brain was significantly decreased at 1 to 2 days, showing a change parallel to that of the stereological parameters. The results obtained from the morphometric technique indicated the occurrence of impaired capillary perfusion and reduced capillary blood volume following SAH, while microgravimetry suggested the formation of brain edema during this period. These changes in the intraparenchymal vessels may play an important role in the pathophysiology of SAH.     

Changes in the Coagulation and Fibrinolytic System of Patients with Subarachnoid Hemorrhage

The aim of this study was to investigate the dynamic changes in the coagulation and fibrinolytic system with subarachnoid hemorrhage. The blood coagulation enzyme-AT complex (TAT), anticoagulant enzyme (AT), tissue plasminogen activator (tPA), plasminogen activin inhibitor (PAI-1), and mean blood flow velocity were measured. The TAT level was significantly higher 6 h after subarachnoid hemorrhage (SAH), whereas AT was significantly lower. These changes were maintained at 12 h to 1 d after SAH, returned to normal at 3 d, significantly changed again at 7 d to 14 d. The tPA level gradually increased after SAH and peaked at 14 d, and then returned to normal at 21 d. The PAI-1 levels were significantly lower than those in the control group 1 d after SAH gradually increased, and returned to normal at 21 d. In the cerebral vasospasm (CVS) groups, the levels of TAT, and AT significantly changed compared to the non-CVS groups after SAH. The PAI-1 levels were higher at 7 d and 14 d, but the changes were not significant. In groups Fisher III and IV as well as Hunt III to V, the TAT, AT, tPA, and PAI-1 levels were significantly higher than those in both Fisher and Hunt I and II 6 h, 12 h, 1 d, 7 d, and 14 d after SAH. The changes in the coagulation and fibrinolytic system of patients with SAH are correlated with the progress and symptoms of SAH as well as the blood content and CVS.     

广痛消泡沫气雾剂对大鼠肛门水肿的作用

目的：观察大鼠肛门水肿组织病理改变和广痛消泡沫气雾剂的干预作用。方法：SD大鼠用0.16 mL巴豆油混合液致肛门肿胀,治疗组肛门内给予广痛消泡沫气雾剂,分别于给药后24 h、48 h、72 h全部处死,取肛周组织进行染色处理,显微观察空白组、模型组、治疗组及对照组病理改变。结果：空白组直肠黏膜正常;模型组直肠黏膜呈急性炎症改变;治疗组随着给药天数的增加,黏膜层溃疡逐渐好转,黏膜下层充血、水肿明显改善,血管充血、扩张消失,对照组炎症改变不明显。结论：巴豆油注射可致SD大鼠肛门水肿炎性改变;广痛消泡沫气雾剂对大鼠肛门肿胀具有抗炎、消肿的作用。     

门静脉部分动脉化对大鼠肝部分切除后肝脏的影响

目的探讨门静脉部分动脉化对部分肝切除大鼠肝脏的影响。方法将48只SD大鼠分为肝部分切除术后非门静脉动脉化组及门静脉动脉化组。动态观察术后2，6，12h血清ALT，AST，以及肝组织中ATP，ADP，AMP含量的变化，并计算EC值；同时取肝组织行病理组织学检查。结果（1）与非动脉化组比较，动脉化组血清AST和ALT在术后2h无差异（P〉0．05），术后l2h动脉化组血清AST和ALT动脉化组明显降低（分别为P〈0.01及P〈0.05）。（2）动脉化组较非动脉化组术后各时点肝组织ATP和Ec均有明显增加（分别为P〈0.01及P〈0．05）。（3）非动脉化组肝组织病理变化随着缺血时间延长而加重；动脉化组病理变化较轻。结论门静脉部分动脉化在一定程度上可以减轻大鼠部分肝切除并肝动脉离断后的肝损害，改善肝细胞的能量代谢。     

大鼠胰腺炎模型中腺泡细胞凋亡的观察

目的: 探讨胰腺腺泡细胞凋亡在胰腺炎发病机制中作用.方法: 复制大鼠胰腺炎模型,将45只SD大鼠分成3组,即重症胰腺炎组18只,轻型胰腺炎组18只和正常对照组9只.在术后第6,12,24小时3个时相点行胰腺组织病理学检测评分和腺泡细胞TUNEL法凋亡检测.结果: 重症胰腺炎组凋亡少见,以细胞坏死为主,且随时间凋亡趋减少,各时相点凋亡指数与轻型组和正常相比差异有显著性意义.轻型组以细胞凋亡为主,随着炎症减轻凋亡增多,术后第24小时达高峰.正常组为正常胰腺组织,少见凋亡.结论: 胰腺炎腺泡细胞中存在细胞凋亡现象,细胞凋亡与坏死呈反相关,细胞凋亡有减轻胰腺炎严重程度的作用.     

Effect of propofol on pathologic time-course and apoptosis after cerebral ischemia-reperfusion injury

Background: Propofol has been demonstrated to ameliorate cerebral ischemic injury and attenuate changes in multiple links of molecular reaction included in the paths to apoptosis. The experiment was aimed to evaluate whether propofol neuroprotection was mediated through the ability to regulate pathologic time-course of apoptosis.
Methods: The effect of propofol given at a series of time points during ischemia–reperfusion period was determined using an intraluminal middle cerebral artery occlusion model in rats. The morphological changes of apoptosis under different duration of ischemia were detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin in situ nick labeling staining, and the effect of propofol on apoptosis was observed. The expression of anti-apoptotic protein bcl-2 in post-ischemia neurons and the influence of propofol was analyzed by immunochemistry staining.
Results: Propofol attenuated neurological deficit, reduced infarct volumes, when given prior the onset of ischemia, during ischemia or 3 h after reperfusion. Apoptosis obviously appeared at 6 h post-reperfusion preceded by 90 min ischemia, rose to the maximum value at 24 h post-reperfusion and gradually diminished after 3 days reperfusion. Propofol inhibited apoptotic morphological changes between 6 h and 3 days post-reperfusion. Propofol enhanced the expression of anti-apoptotic protein bcl-2 in post-reperfusion neurons.
Conclusions: The pathologic outcome of focal cerebral ischemia–reperfusion injury was displayed by co-existence of apoptosis and necrosis. A short duration of ischemia induced apoptosis. The therapeutic window for propofol initiated before the onset of ischemia and lasted until early stage of reperfusion. The neuroprotection of propofol might be attributed to the inhibition of apoptosis.     

Circulatory characteristics of normovolemia and normotension therapy after subarachnoid hemorrhage, focusing on pulmonary edema

Background and purpose

Cardiopulmonary complications are common after subarachnoid hemorrhage (SAH), and include pulmonary edema (PE). The purpose of this study was to investigate circulatory characteristics of normovolemia and normotension therapy after SAH using pulse contour analysis, and to reveal the mechanisms of PE after SAH.

Methods

Pulse contour analysis was performed from day 3 until day 12 after the onset of SAH in 49 patients.

Results

Global end-diastolic volume index (GEDI) was normal, although net water balance was estimated to be negative and central venous pressure (CVP) was low in all patients. Seven patients (14?%) suffered from pulmonary edema. Cardiac function index (CFI) and global ejection fraction (GEF) were lower in patients with pulmonary edema (PE group) than in patients without PE (non-PE group) throughout the study period (CFI, P≤0.0119; GEF, P≤0.0348). The PE group showed higher GEDI from days 7 to 10, and higher extravascular lung water index (ELWI) throughout the entire study period compared to the non-PE group (GEDI, P≤0.0094; ELWI, P≤0.0077).

Conclusions

The appropriate preload was kept despite negative net water balance and low CVP. PE after SAH was biphasic, with cardiogenic PE caused by low cardiac contractility immediately after SAH, and hydrostatic PE caused by low cardiac contractility and hypervolemia on and after day 7 of SAH. Pulse contour analysis was useful to monitor this unique circulatory change and effective for detecting cardiopulmonary complications after SAH.