GluN2B-BDNF pathway in the cerebrospinal fluid-contacting nucleus mediates nerve injury-induced neuropathic pain in rats.

The present study was aimed to investigate the role of GluN2B-BDNF pathway in the cerebrospinal fluid-contacting nucleus (CSF-CN) in neuropathic pain. Intra-lateral ventricle injection of cholera toxin subunit B conjugated with horseradish peroxidase (CBHRP) was used to label the CSF-CN. Double-labeled immunofluorescent staining and Western blot were used to observe the expression of GluN2B and BDNF in the CSF-CN. Chronic constriction injury of sciatic nerve (CCI) rat model was used to duplicate the neuropathic pain. Pain behavior was scored to determine the analgesic effects of GluN2B antagonist Ro 25-6981 and BDNF neutralizing antibody on CCI rats. GluN2B and BDNF were expressed in the CSF-CN and their expression was up-regulated in CCI rats. Intra-lateral ventricle injection of GluN2B antagonist Ro 25-6981 or BDNF neutralizing antibody notably alleviated thermal hyperalgesia and mechanical allodynia in CCI rats. Moreover, the increased expression of BDNF protein in CCI rats was reversed by intra-lateral ventricle injection of Ro 25-6981. These results suggest that GluN2B and BDNF are expressed in the CSF-CN and alteration of GluN2B-BDNF pathway in the CSF-CN is involved in the modulation of the peripheral neuropathic pain.

The effects of morphine treatment on the NCAM and its signaling in the MLDS of rats.

Prolonged exposure to opiates induces a constellation of neuroadaptations, especially in the mesolimbic dopamine system (MLDS), which leads to alteration in the function of motivational circuitry. The neural cell adhesion molecule (NCAM) mediates cell-cell interactions and plays an important role in processes associated with neural plasticity. Moreover, it has been shown that NCAM were related to risk of alcoholism in human populations. Here, coimmunoprecipitation and western blotting were used to investigate whether morphine treatment induced alteration of the expression of NCAM or its signaling level in MLDS. The rats receiving escalating dose of morphine treatment were divided into three groups: morphine 1d, 3d and 5d group, which were injected subcutaneously with morphine hydrochloride for 1 day, 3 days and 5 days, respectively. Twelve hours after the last injection, animals were sacrificed and the tissues of ventral tegmental area (VTA), prefrontal cortex (PFC) and nucleus accumbens (NAc) were punched out to examine the expression of NCAM or its signaling level. The results showed that morphine treatment had no significant effect on the expression of NCAM, but downregulated the phosphorylation of NCAM-associated focal adhesion kinase (FAK) in the VTA and PFC of rats. In the NAc of rats, however, the expression of NCAM and its signaling were not altered significantly by morphine treatment. These results indicated that the downregulation of NCAM signaling in the VTA and PFC might be involved in the formation of morphine addiction.

Transient folate deprivation in combination with small-molecule compounds facilitates the generation of somatic cell-derived pluripotent stem cells in mice.

Induced pluripotent stem cells (iPSCs) can be propagated indefinitely, while maintaining the capacity to differentiate into all cell types in the body except for the extra-embryonic tissues. This iPSC technology not only represents a new way to use individual-specific stem cells for regenerative medicine but also constitutes a novel method to obtain large numbers of disease-specific cells for biomedical research. However, the low efficiency of reprogramming and genomic integration of oncogenes and viral vectors limit the potential application of iPSCs. Chemical-induced reprogramming offers a novel approach to generating iPSCs. In this study, a new combination of small-molecule compounds (SMs) (sodium butyrate, A-83-01, CHIR99021, Y-27632) under conditions of transient folate deprivation was used to generate iPSC. It was found that transient folate deprivation combined with SMs was sufficient to permit reprogramming from mouse embryonic fibroblasts (MEFs) in the presence of transcription factors, Oct4 and Klf4, within 25 days, replacing Sox2 and c-Myc, and accelerated the generation of mouse iPSCs. The resulting cell lines resembled mouse embryonic stem (ES) cells with respect to proliferation rate, morphology, pluripotency-associated markers and gene expressions. Deprivation of folic acid, combined with treating MEFs with SMs, can improve the inducing efficiency of iPSCs and reduce their carcinogenicity and the use of exogenous reprogramming factors.

Proliferation and differentiation of neural stem cells co-cultured with cerebral microvascular endothelial cells after oxygen-glucose deprivation.

Various stem cells, including neural stem cells (NSCs), have been extensively studied in stroke models, but how to increase neuronal differentiation rate of NSCs remains unresolved, particularly in a damaged environment. The purpose of this study was to investigate the effects of cerebral microvascular endothelial cells (CMECs) on the neurogenesis of NSCs with or without oxygen-glucose deprivation (OGD). The NSCs acquired from primary culture were immunostained to prove cell purity. Survival and proliferation of NSCs were determined after the co-culture with CMECs for 7 days. After removing the CMECs, NSCs were randomly divided into two groups as follows: OGD and non-OGD groups. Both groups were maintained in differentiation culture for 4 days to evaluate the differentiation rate. Mouse embryo fibroblast (MEF) cells co-cultured with NSCs served as control group. NSCs co-cultured with CMECs had an increase in size (on the 7th day: 89.80±26.12 µm vs. 73.08±15.01 µm, P<0.001) (n=12) and number [on the 7th day: 6.33±5.61/high power objective (HP) vs. 2.23±1.61/HP, P<0.001] (n=12) as compared with those co-cultured with MEF cells. After further differentiation culture for 4 days, NSCs co-cultured with CMECs had an increase in neuronal differentiation rate in OGD and non-OGD groups, but not in the control group (15.16% and 16.07% vs. 8.81%; both P<0.001) (n=6). This study provided evidence that OGD could not alter the effects of CMECs in promoting the neuronal differentiation potential of NSCs. These findings may have important implications for the development of new cell therapies for cerebral vascular diseases.

Dramatic decrease of aortic longitudinal elastic strength in a rat model of aortic dissection.

BACKGROUND: This study aimed to evaluate thoracic aortic longitudinal elastic strength in a rat model of aortic dissection (AD). METHODS: Young Sprague Dawley rats were fed 0.25% ß-aminopropionitrile (BAPN). Biomechanical and biochemistry properties of the aorta were analyzed. Elasticity modulus, maximum stretching length, draw ratio, maximum load, maximum strength, and maximum extensibility were measured. RESULTS: More than one-half of BAPN-treated rats (52.9%) died of aortic rupture secondary to AD during the experiment. The diameter of the aneurysms was 6.33 ± 1.17 mm and the length was 9.33 ± 4.95 mm. The maximum diameter was significantly increased in BAPN-treated rats with AD (group B2) compared with rats without AD (group B1) and control group (group A) (P = 0.001 and P < 0.001, respectively), but was not different between group B1 and group A (P = 0.108). Thickness of media and initial area in aorta of BAPN-treated rats were significantly increased compared with control group (P = 0.001 and P < 0.001, respectively), but no difference in initial area was observed between group B1 and group B2 (P = 0.54). Maximum stretching length, draw ratio, maximum load, maximum strength, maximum extensibility, and elasticity modulus were dramatically decreased in group B2 compared with group B1 and group A (group B2 vs. group B1: P < 0.001; group B1 vs. group A: P < 0.001). CONCLUSIONS: We successfully established a rat model of AD with a high incidence of rupture and mortality. Examinations of strain and stress parameters as well as elasticity modulus of the dissected and the nondissected aorta help understand pathogenesis of AD.

Effectiveness, Safety and Risk Factors of Woven EndoBridge Device in the Treatment of Wide-Neck Intracranial Aneurysms: Systematic Review and Meta-Analysis.

OBJECTIVE: To assess the current efficacy, safety, and risk factors of the Woven EndoBridge (WEB) in treating wide-neck intracranial aneurysms. METHODS: We searched the PubMed, Ovid MEDLINE, and Embase databases between December 1, 2012 and June 30, 2018. Studies were included if they featured ≥5 patients undergoing WEB for wide-neck intracranial aneurysms, reported an angiographic or clinical outcome and risk factors, and were published after December 1, 2012. Major outcomes included initial or short-term complete and adequate occlusion. Secondary outcomes included treatment failure, recanalization, mortality, morbidity, and complication rates. A random-effect model was used to pool the data. To assess risk factors for short-term angiographic outcomes and the most common complications, we conducted subgroup analyses. RESULTS: We included 36 studies (1759 patients with 1749 aneurysms). The initial complete and adequate occlusion rates were 35% and 77%, respectively. The short-term (mean follow-up, 9.34 months) complete and adequate occlusion rates were 53% and 80%, respectively. Thromboembolism and recanalization had the highest occurrence (both 9%), followed by mortality (7%), morbidity (6%), failure (5%) and intraoperative rupture (3%). The following factors were related to higher short-term obliteration rates: unruptured status, in the anterior circulation, a medium neck (4-9.9 mm), newer-generation WEB, and treatment without additional devices. Ruptured status, anterior circulation, preoperative antiplatelet therapy, and newer-generation WEB were not significantly related to thromboembolism. CONCLUSIONS: WEB is safe and shows promising efficacy in treating wide-neck intracranial aneurysms. We preliminarily identified several risk factors for short-term angiographic outcomes.

Dynamic alterations of cerebral pial microcirculation during experimental subarachnoid hemorrhage.

The study aimed to investigate the involvement of cerebral microcirculation turbulence after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH and SAH groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. Changes of pial microcirculation within 2 h were observed. It was found that there were no obvious changes of the diameters, flow velocity, and fluid state of microvessels in non-SAH group. With the exception of rare linear-granular flow in A4 arteriole, linear flow was observed in most of the arterioles. There was no blood agglutination in any of the arterioles. After SAH, abnormal cerebral pial microcirculation was found. Spasm of microvessels, decreased blood flow, and agglutination of red blood cells occurred. Five minutes following the induction of SAH, the diameters of the arterioles and venules significantly decreased. The decreased diameters persisted for 2 h after cisternal injection. Decreased flow velocity of venules was found from 5 to 90 min after induction of SAH. Spasm of the basilar artery and increased brain malondialdehyde were also found after SAH. We concluded that cerebral microcirculation turbulence plays an important role in the development of secondary cerebral ischemia following SAH.

Extract of Ginkgo biloba promotes the expression of VEGF following subarachnoid hemorrhage in rats.

The study aimed to investigate the effect of extract of Ginkgo biloba (EGb) on the expression of vascular endothelial growth factor (VEGF) after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, vehicle, EGb1 (low-dose), and EGb2 (high-dose) groups. VEGF mRNA and VEGF protein were measured from brain tissues. The expressions of VEGF mRNA in SAH and vehicle groups were enhanced 24 and 72 hr after the establishment of SAH. Increased VEGF positive cells were found in the brain tissues in SAH and vehicle groups. The expressions of VEGF mRNA and VEGF protein were further increased by the pretreatment of EGb. We concluded that EGb exerts protective effects on secondary cerebral ischemic injury after SAH via the promotion of the expression of VEGF.

[Experimental study of implantation of neurotropin-3 modified olfactory ensheathing cells in experimental allergic encephalomyelitis].

OBJECTIVE: To investigate the therapeutic effect of neurotrophin-3 (NT-3) modified olfactory ensheathing cell (OEC) upon experimental allergic encephalomyelitis (EAE). METHODS: OEC-NT-3 gene engineering cell, constructed by neurotrophin-3 transinfecting GEC inducted by retrovirus, was transplanted into lateral ventricle. The migration and distribution were observed and compared with control group and OEC transplantation group. Then myelin repairing and axon regeneration were evaluated from conical somatosensory evoked potential (CSEP), function score and ultrastructural morphology. RESULTS: (1) OEC-NT-3 could survive, migrate within axons and spread diffusely away from the focus at Day 28 post-transplantation; (2) as compared with other two groups, more nerve fibers, better myelin repair and more distinct myelin structure were observed in the transgene group; (3) as compared with other two groups, the latent time was obviously shortened and the amplitude higher in the transplantation group (P < 0.05); (4) the transcription level of NT-3mRNA in the transgene group was significantly higher than the GEC group and the contrast group (212.32 +/- 16.14) x 10(-2) vs. (1.98 +/- 0.19) x 10(-2), (1.23 +/- 0.13) x 10(-2) (P < 0.01). CONCLUSION: OEC-NT-3 cell expresses NT-3 stably and effectively in EAE. It may contribute to the repairing of myelin and the regeneration of axon.

Regionspecific survival and differentiation of mouse embryonic stem cell-derived implants in the adult rat brain.

Totipotent and regionally non-specified embryonic stem (ES) cells provide a powerful tool to understand mechanisms controlling stem cell differentiation in different regions of the adult brain. As the development capacity of ES cells in the adult brain is still largely unknown, we grafted small amounts of mouse ES (mES) cells into adult rat brains to explore the survival and differentiation of implanted mES cells in different rat brain regions. We transplanted the green fluorescent protein (GFP)-positive mES cells into the hippocampus, septal area, cortex and caudate nucleus in rat brains. Then the rats were sacrificed 5, 14 and 28 d later. Of all the brain regions, the survival rate of the transplanted cells and their progeny were the highest in the hippocampus and the lowest in the septal area (P<0.01). The grafted ES cells could differentiate into nestin-positive neural stem cells. Nestin-positive/GFP-positive cells were observed in all brain regions with the highest frequency of nestin-positive cells in the hippocampus and the lowest in the medial septal area (P<0.01). mES cells differentiated into end cells such as neurons and glial cells in all transplantation sites in recipient brains. In the hippocampus, the ES cells differentiated into neurons in large amounts. These results demonstrate that only some brain regions permit survival of mES cells and their progeny, and form instructive environments for neuronal differentiation of mES cells. Thus, because of region specific presence of microenvironmental cues and their environmental fields, the characteristics of the recipient tissue were considerably important in formulating cell replacement strategies for neural disorders.

[Study on distribution of neural stem cells in the brain of Alzheimer disease transgenic mice through caudal vein transplantation].

OBJECTIVE: To observe whether neural stem cells (NSCs) can successfully permeate into the brain through the blood-brain barrier (BBB) of Alzheimer disease (AD) transgenic mice and explore the methods of distribution and migration. METHODS: NSCs were isolated from 12-day-old fetal mice, cultured, labeled with enhanced green fluorescent protein (eGFP) and then transplanted into 10 AD transgenic mice and normal mice as controls through caudal vein. The mice were killed 48 h, 1 w, 2 w, and 4 w after transplantation respectively. The brains of the mice were made into continual frozen sections, the distribution and migration of the eGFP-labeled NSCs were studied under fluorescence microscope. RESULTS: At different time points after transplantation the eGFP-labeled NSCs were diffusely distributed in the brain: distributed around the blood vessels in the first 48 h, and then migrated gradually towards the hippocampus and cortex until 4 weeks later. There were no obvious abnormal complications occurring after transplantation. CONCLUSION: NSCs can successfully permeate into the brain through the BBB of AD transgenic mice, and migrate into the brain parenchyma gradually.

[Establishment of two human embryonic stem cell lines from cleavage arrested embryos].

OBJECTIVE: To determine whether cleavage developmentally retarded embryos have not cleaved during a 24 hour period could develop into blastocysts and produce hESC cell lines. METHODS: A total of 120 such embryos were cultured to blastocyst stage by sequential culture. Blastocysts formation rate and quality of blastocyst were detected under microscope. The relation between blastocyst formation rate and blastomere number, the fragment of blastomere and blastomere symmetry were analyzed by stepwise Logistical regression analysis. Inner cell masses (ICMs) were isolated by immunosurgery. Colonies derived from the ICMs were passed every 4 - 7 days and the derivatives were passaged and identified. RESULTS: A total of 22 blastocysts were obtained from 120 embryos. The blastulation rate was 18.7%. Early blatocyst, blastocyst, full blastocyst, expanded blastocyst, hatching blastocyst and hatched blastocyst accounted for 5.9%, 23.5%, 35.3%, 23.5%, 5.9%, and 5.9% respectively. The grade of ICM and trophoblast was mostly scored C or B. Blastocyst formation rate was related to cell number and blastomere symmetry but not fragment. Immunosurgery resulted in the formation of 7 ICMs and 3 primary colonies, which produced 2 cell lines. The cell lines satisfied the criteria that characterize pluripotent hESC cells. Undifferentiated cells were positive for AKP, SSEA-4, TRA-1-60, and TRA-1-81. It could continue to proliferate in vitro and form embryoid bodies when cultured in suspension. It had capability to form teratoma in SCID mice. Both cell lines had normal karyotypes after 45 and 34 passages respectively. CONCLUSIONS: Our results suggest that a subset of developmentally retarded embryos can form blastocysts and give rise to hESC cell lines.

Expression of the receptors of VEGF and the influence of extract of Ginkgo biloba after cisternal injection of autologus arterial hemolysate in rats.

The study was aimed to investigate the alterations of vascular endothelial growth factor (VEGF) receptors and the influence of extract of Ginkgo biloba (EGb) after subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, vehicle, EGb1 (lower dose), and EGb2 (higher dose) groups. Autologus arterial hemolysate was injected into cisterna magna to induce SAH. The non-SAH rats received cisternal injection of saline instead. Rats underwent RT-PCR determination of one of the VEGF receptors flt-1mRNA, and immunohistochemistry for VEGF receptors Flt-1 and Flk-1. The results revealed that there was only slight expression of flt-1mRNA in the brain tissue in non-SAH rats. The expression in SAH group was enhanced 24 hours and 72 hours after cisternal injection. No Flt-1 and Flk-1 positive cell was observed in the brain in non-SAH group. A good few Flt-1 and Flk-1 positive cells were found in cortex and other regions of the brain in SAH group. The expression of flt-1mRNA, Flt-1 and Flk-1 proteins were increased by the use of two doses of EGb. It was concluded that the up-regulated expression of the two kinds of VEGF receptors may be an intrinsic protective mechanism in the process of SAH, which can be enhanced by EGb.

Effects of blockade of cerebral lymphatic drainage on regional cerebral blood flow and brain edema after subarachnoid hemorrhage.

The study was designed to observe the influence of blockade of cerebral lymphatic drainage on the regional cerebral blood flow (rCBF) and brain edema after experimental subarachnoid hemorrhage (SAH). Wistar rats were divided into non-SAH, SAH, and SAH plus cervical lymphatic blockade (SAH + CLB) groups. Autologous arterial hemolysate was injected into rat's cisterna magna to induce SAH. The rCBF was recorded continuously by a laser Doppler flowmeter. Intracranial pressure (ICP) was also monitored. After 24 hours and 72 hours of SAH, the rats were sacrificed and the brain was harvested for water content detection. It was found that there was no obvious change of rCBF and brain water content during the experiment in non-SAH group. An immediate and persistent drop in rCBF was found in SAH group. The drop in rCBF was more obvious in SAH + CLB group. CLB also worsened the SAH-induced increase in ICP. The brain water content 24 hours and 72 hours after induction of SAH in SAH group increased significantly. CLB led to a further increase of brain water content. In conclusion, blockade of cerebral lymphatic drainage pathway deteriorates the secondary cerebral ischemia and brain edema after SAH.

Effects of continuous positive airway pressure therapy on plasma aldosterone levels in patients with obstructive sleep apnea: A meta-analysis.

Obstructive sleep apnea (OSA) is an independent risk factor for cardiovascular diseases. Aldosterone was reported to be increased in patients with OSA and correlated with OSA severity. Many studies investigated the effect of continuous positive airway pressure (CPAP) therapy on plasma aldosterone concentrations (PAC) in OSA patients. The results, however, were inconsistent. In the present study, we aimed to evaluate the effects of CPAP therapy on PAC by performing a meta-analysis. Literature search was carried out in electronic databases including PubMed/Medline, Cochrane Library, Embase and Web of Science. Eligible full-text articles were identified, and important data were extracted. Pooled analysis was performed using the STATA12.0 and RevMan 5.2. Standardized mean difference (SMD) was calculated to estimate the treatment effects. A total of eight studies involving 219 patients were included for our final analysis. PAC was found unchanged after CPAP treatment in OSA patients (SMD=-0.36, 95% CI:-0.91 to 0.18, Z=1.32, P=0.19). Meanwhile, CPAP therapy showed no impact on PAC (SMD=-0.21, 95% CI:-0.85 to 0.42, Z=0.66, P=0.51) in a separate meta-analysis including 3 randomized controlled trials. In conclusion, the evidence for the use of CPAP therapy to decrease PAC in OSA patients is low, and further studies are still warranted.

A new method for evaluating regional cerebral blood flow changes: Laser speckle contrast imaging in a C57BL/6J mouse model of photothrombotic ischemia.

The present study aimed to improve the processing of data acquired from laser speckle contrast imaging (LSCI) to provide a standardization method to explore changes in regional cerebral blood flow (rCBF) and to determine the correlations among rCBF, cerebral ischemic lesion volume and microvascular density over time in a focal ischemic region. C57BL/6J mice were subjected to focal photothrombotic (PT) ischemia. rCBF was measured using LSCI at different time points before and after PT ischemia through an intact skull. Standardized rCBF (SrCBF), defined as the ratio of rCBF measured in the ipsilateral region of interest (ROI) to that in the corresponding contralateral region, was calculated to evaluate potential changes. In addition, the volume of the ischemic lesion and the microvascular density were determined using Nissl staining and immunofluorescence, respectively. The relationships among the ischemic lesion volume, microvascular density and SrCBF were analyzed over time. The results showed that the cortical rCBF measured using LSCI following PT ischemia in the C57BL/6J mice gradually increased. Changes in the cerebral ischemic lesion volume were negatively correlated with SrCBF in the ischemic region. Changes in the microvascular density were similar to those observed in SrCBF. Our findings indicate that LSCI is a practical technique for observing changes in murine cortical rCBF without skull opening and for analyzing the relationships among the ischemic lesion volume, microvascular density and SrCBF following focal cerebral ischemia. Preliminary results also suggest that the use of LSCI to observe the formation of collateral circulation is feasible.

[Effects of injecting heparin into the center of hematoma on peri-hematoma edema and hematoma volume in pigs with intracerebral hemorrhage].

OBJECTIVE: To investigate the safety and effect of injecting heparin into hematoma on peri-hematoma edema and hematoma volume in pigs with intracerebral hemorrhage (ICH). METHODS: Thirteen sucking pigs were divided randomly into two groups: hemorrhage group, in which 2.5 ml arterial blood was injected into the right frontal lobe and heparin group, in which 0.2 ml of heparin was injected into the hematoma produced by the injection of 2.3 ml of blood into the similar site. The hematoma volume and peri-hematoma edema were determined by the sequences of T2* weighted image (T2*WI), fluid-attenuated inversion- recovery (FLAIR) image and diffusion weighted image (DWI) by 1.5 T magnetic resonance image (MRI) from 30-60 minutes afterwards to 24 hours. The peri-hematoma apparent diffusion coefficient (ADC) was compared with that of contralateral hemisphere, and the corresponding histologic changes were studied. RESULTS: The average volume, shown by T2*WI at 24 hours, was significantly larger than that at 30-60 minutes after hematoma formation in hemorrhagic group [(5.29+/-0.98) cm3 vs. (3.09+/-0.38) cm3, P<0.01]. But there was no significant change in hematoma volume in hemorrhagic group from 30-60 minutes on to 24 hours [(2.21+/-0.28) cm3 vs. (2.33+/-0.30) cm3, P>0.05]. Both increased and decreased ADC were found around the hematoma in some animals of the heparin group compared with that of the contralateral hemisphere. On the other hand, in hemorrhagic group, only increased ADC could be found around the lesion, and there was no decreased ADC. CONCLUSION: Injection of heparin into an intracerebral hematoma leads to enlargement of the hematoma and more marked peri-lesion edema. On ADC maps, enlargement of hematoma is attributed to the edema around the lesion leading to injury to the brain tissue.

Relationship between encephalopathy and portal vein-vena cava shunt: value of computed tomography during arterial portography.

AIM: To assess the value of computed tomography during arterial portography (CTAP) in portal vein-vena cava shunt, and analysis of the episode risk in encephalopathy. METHODS: Twenty-nine patients with portal-systemic encephalopathy due to portal hypertension were classified by West Haven method into grade I(29 cases), grade II(16 cases), grade III(10 cases), grade IV( 4 cases). All the patients were scanned by spiral-CT. Plane scans, artery phase and portal vein phase enhancement scans were performed, and the source images were thinly reconstructed to 1.25 mm. We reconstructed the celiac trunk, portal vein, inferior vena cava and their branches and subjected them to three-dimensional vessel analysis by volume rendering (VR) technique and multiplanar volume reconstruction (MPVR) technique. The blood vessel reconstruction technique was used to evaluate the scope and extent of portal vein-vena cava shunt, portal vein emboli and the fistula of hepatic artery-portal vein. The relationship between the episode risk of portal-systemic encephalopathy and the scope and extent of portal vein-vena cava shunt, portal vein emboli and fistula of hepatic artery- portal vein was studied. RESULTS: The three-dimensional vessel reconstruction technique of spiral-CT could display celiac trunk, portal vein, inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cava shunt, portal vein emboli and the fistula of hepatic artery- portal vein. In twenty-nine patients with portal-systemic encephalopathy, grade I accounted for 89.7% esophageal varices, 86.2% paragastric varices; grade II accounted for 68.75% cirsomphalos, 56.25% paraesophageal varices, 62.5% retroperitoneal varices and 81.25% dilated azygos vein; grade III accounted for 80% cirsomphalos, 60% paraesophageal varices, 70% retroperitoneal varices, 90% dilated azygos vein, and part of the patients in grades II and III had portal vein emboli and fistula of hepatic artery-portal vein; grade IV accounted for 75% dilated left renal vein, 50% paragallbladder varices, all the patients had fistula of hepatic artery- portal vein. CONCLUSION: The three-dimensional vessel reconstruction technique of spiral-CT can clearly display celiac trunk, portal vein, inferior vena cava and their branches at any planes and angles and the scope and extent of portal vein-vena cava shunt. The technique is valuable for evaluating the episode risk in portal-systemic encephalopathy.

Effects of extract of Ginkgo biloba on spasms of the basilar artery and cerebral microcirculatory perfusion in rats with subarachnoid hemorrhage.

This study was aimed at investigating the effects of extract of Ginkgo biloba (EGb) on cerebral vasospasm and microcirculatory perfusion after subarachnoid hemorrhage (SAH). An endovascular piercing method was used to induce Wistar rat SAH models, and animals were divided into sham-operated, vehicle controls, and EGb-treated groups. EGb was injected intraperitoneally 30 minutes before operation and was repeated every 6 hours, with a single dose of 15 mg/kg bw. Diameters of basilar arteries before and after operation were measured. Microcirculatory blood perfusion of parietal lobe cortex was detected using a laser Doppler flow-meter probe within 24 hours. Endothelin-1 levels in both plasma and brain tissue were detected at different time points. The results showed that SAH caused an immediate drop in microcirculatory blood flow in vehicle controls, which persisted for 24 hours. Endothelin-1 levels in both plasma and brain tissue increased after SAH. EGb partly reversed spasms of the basilar artery and antagonized a drop in microcirculatory blood flow. EGb also prevented an increase in endothelin-1 both in plasma and in brain tissue. In conclusion, EGb, by antagonizing the overproduction of endo- thelin-1, partly reverses cerebral vasospasm and improves microcirculation, and thus relieves secondary ischemic brain injury after experimental SAH.