Applied anatomical study of the vascularized ulnar nerve and its blood supply for cubital tunnel syndrome at the elbow region

Cubital tunnel syndrome is often accompanied by paresthesia in ulnar nerve sites and hand muscle atrophy. When muscle weakness occurs, or after failure of more conservative treatments, anterior transposition is used. In the present study, the ulnar nerve and its blood vessels were examined in the elbows of 18 adult cadavers, and the external diameter of the nutrient vessels of the ulnar nerve at the point of origin, the distances between the origin of the vessels and the medial epicondyle of the humerus, and the length of the vessels accompanying the ulnar nerve in the superior ulnar collateral artery, the inferior ulnar collateral artery, and the posterior ulnar recurrent artery were measured. Anterior transposition of the vascularized ulnar nerve was per- formed to treat cubital tunnel syndrome. The most appropriate distance that the vascularized ulnar nerve can be moved to the subcutaneous tissue under tension-free conditions was 1.8 ± 0.6 cm （1.1-2.5 cm）, which can be used as a reference value during the treatment of cubital tunnel syndrome with anterior transposition of the vascularized ulnar nerve.

Transplantation of autologous peripheral blood mononuclear cells in the subarachnoid space for amyotrophic lateral sclerosis:a safety analysis of 14 patients

There is a small amount of clinical data regarding the safety and feasibility of autologous peripheral blood mononuclear cell transplantation into the subarachnoid space for the treatment of amyotrophic lateral sclerosis.The objectives of this retrospective study were to assess the safety and efficacy of peripheral blood mononuclear cell transplantation in 14 amyotrophic lateral sclerosis patients to provide more objective data for future clinical trials.After stem cell mobilization and collection,autologous peripheral blood mononuclear cells（1 × 109） were isolated and directly transplanted into the subarachnoid space of amyotrophic lateral sclerosis patients.The primary outcome measure was incidence of adverse events.Secondary outcome measures were electromyography 1 week before operation and 4 weeks after operation,Functional Independence Measurement,Berg Balance Scale,and Dysarthria Assessment Scale 1 week preoperatively and 1,2,4 and 12 weeks postoperatively.There was no immediate or delayed transplant-related cytotoxicity.The number of leukocytes,serum alanine aminotransferase and creatinine levels,and body temperature were within the normal ranges.Radiographic evaluation showed no serious transplant-related adverse events.Muscle strength grade,results of Functional Independence Measurement,Berg Balance Scale,and Dysarthria Assessment Scale were not significantly different before and after treatment.These findings suggest that peripheral blood mononuclear cell transplantation into the subarachnoid space for the treatment of amyotrophic lateral sclerosis is safe,but its therapeutic effect is not remarkable.Thus,a large-sample investigation is needed to assess its efficacy further.

Intranasal nerve growth factor bypasses the blood-brain barrier and affects spinal cord neurons in spinal cord injury

The purpose of this work was to investigate whether, by intranasal administration, the nerve growth factor bypasses the blood-brain barrier and turns over the spinal cord neurons and if such therapeutic approach could be of value in the treatment of spinal cord injury. Adult Sprague-Dawley rats with intact and injured spinal cord received daily intranasal nerve growth factor administration in both nostrils for 1 day or for 3 consecutive weeks. We found an in-creased content of nerve growth factor and enhanced expression of nerve growth factor receptor in the spinal cord 24 hours after a single intranasal administration of nerve growth factor in healthy rats, while daily treatment for 3 weeks in a model of spinal cord injury improved the deifcits in locomotor behaviour and increased spinal content of both nerve growth factor and nerve growth factor receptors. These outcomes suggest that the intranasal nerve growth factor bypasses blood-brain barrier and affects spinal cord neurons in spinal cord injury. They also suggest exploiting the possible therapeutic role of intranasally delivered nerve growth factor for the neuroprotection of damaged spinal nerve cells.

Silk-based nerve guidance conduits with macroscopic holes modulate the vascularization of regenerating rat sciatic nerve

Peripheral nerve injuries induce a severe motor and sensory deficit. Since the availability of autologous nerve transplants for nerve repair is very limited, alternative treatment strategies are sought, including the use of tubular nerve guidance conduits(tNGCs). However, the use of tNGCs results in poor functional recovery and central necrosis of the regenerating tissue, which limits their application to short nerve lesion defects(typically shorter than 3 cm). Given the importance of vascularization in nerve regeneration, we hypothesized that enabling the growth of blood vessels from the surrounding tissue into the regenerating nerve within the tNGC would help eliminate necrotic processes and lead to improved regeneration. In this study, we reported the application of macroscopic holes into the tubular walls of silk-based tNGCs and compared the various features of these improved silk^(+) tNGCs with the tubes without holes(silk^(–) tNGCs) and autologous nerve transplants in an 8-mm sciatic nerve defect in rats. Using a combination of micro-computed tomography and histological analyses, we were able to prove that the use of silk^(+) tNGCs induced the growth of blood vessels from the adjacent tissue to the intraluminal neovascular formation. A significantly higher number of blood vessels in the silk^(+) group was found compared with autologous nerve transplants and silk^(–), accompanied by improved axon regeneration at the distal coaptation point compared with the silk^(–) tNGCs at 7 weeks postoperatively. In the 15-mm(critical size) sciatic nerve defect model, we again observed a distinct ingrowth of blood vessels through the tubular walls of silk^(+) tNGCs, but without improved functional recovery at 12 weeks postoperatively. Our data proves that macroporous tNGCs increase the vascular supply of regenerating nerves and facilitate improved axonal regeneration in a short-defect model but not in a critical-size defect model. This study suggests that further optimization of the macroscopic holes silk^(+) tNGC approach containing macroscopic holes might result in improved grafting technology suitable for future clinical use.

Extracorporeal membrane oxygenation states basilar artery thrombectomy and left posterior cerebral artery stent thrombectomy:A case report

BACKGROUND Extracorporeal membrane oxygenation(ECMO)is a new type of extracorporeal respiratory and circulatory assistance device.It can drain venous blood out of the body and inject it into veins or arteries after being oxygenated by an oxygenator(membrane lung)to replace lung and heart functions in a short time.ECMO can provide tissue blood perfusion and gas exchange almost equivalent to cardiac output and extend the effective treatment time window for patients with acute circulatory failure to restore cardiopulmonary function.CASE SUMMARY We report a case of an 81-year-old woman who underwent whole cerebral angiography,basilar artery thrombectomy and stent thrombectomy in the posterior artery of the left brain after implantation of ECMO.The patient was admitted to the hospital due to myocardial infarction.Considering that the cause of the patient’s disturbance of consciousness was unknown and cerebrovascular accident could not be ruled out after the implantation of ECMO,the department of Radioactive Intervention performed cerebral angiography.And the result of the angiography indicated vascular occlusion.After the basilar artery thrombectomy and stent thrombectomy in the posterior artery of the left brain,the patency of the occlusive vessel was achieved.CONCLUSION Although the patient eventually died of circulatory failure,the result of this case verifies the feasibility of cerebral angiography and thrombectomy in patients with implanted ECMO in the intubated state.

Hyperoside protects the blood-brain barrier from neurotoxicity of amyloid beta 1–42

Mounting evidence indicates that amyloid β protein（Aβ） exerts neurotoxicity by disrupting the blood-brain barrier（BBB） in Alzheimer＇s disease. Hyperoside has neuroprotective effects both in vitro and in vivo against Aβ. Our previous study found that hyperoside suppressed Aβ1-42-induced leakage of the BBB, however, the mechanism remains unclear. In this study, bEnd.3 cells were pretreated with 50, 200, or 500 μM hyperoside for 2 hours, and then exposed to Aβ1-42 for 24 hours. Cell viability was determined using 3-（4,5-dimethyl-2-thiazolyl）-2,5-diphenyl-2-H-tetrazolium bromide assay. Flow cytometry and terminal deoxynucleotidyl transferase-mediated d UTP nick-end labeling assay were used to analyze cell apoptosis. Western blot assay was carried out to analyze expression levels of Bax, Bcl-2, cytochrome c, caspase-3, caspse-8, caspase-9, caspase-12, occludin, claudin-5, zonula occludens-1, matrix metalloproteinase-2（MMP-2）, and MMP-9. Exposure to Aβ1-42 alone remarkably induced bEnd.3 cell apoptosis; increased ratios of cleaved caspase-9/caspase-9, Bax/Bcl-2, cleav ed caspase-8/caspase-8, and cleaved caspase-12/caspase-12; increased expression of cytochrome c and activity of caspase-3; diminished levels of zonula occludens-1, claudin-5, and occludin; and increased levels of MMP-2 and MMP-9. However, hyperoside pretreatment reversed these changes in a dose-dependent manner. Our findings confirm that hyperoside alleviates fibrillar Aβ1-42-induced BBB disruption, thus offering a feasible therapeutic application in Alzheimer＇s disease.

Non-viral liposome-mediated transfer of brain-derived neurotrophic factor across the blood-brain barrier

Brain-derived neurotrophic factor（BDNF） plays an important role in the repair of central nervous system injury,but cannot directly traverse the blood-brain barrier.Liposomes are a new type of non-viral vector,able to carry macromolecules across the blood-brain barrier and into the brain.Here,we investigate whether BDNF could be transported across the blood-brain barrier by tail-vein injection of liposomes conjugated to transferrin（Tf） and polyethylene glycol（PEG）,and carrying BDNF modified with cytomegalovirus promoter（pC MV） or glial fibrillary acidic protein promoter（p GFAP）（Tf-p CMV-BDNF-PEG and Tf-p GFAP-BDNF-PEG,respectively）.Both liposomes were able to traverse the blood-brain barrier,and BDNF was mainly expressed in the cerebral cortex.BDNF expression in the cerebral cortex was higher in the Tf-p GFAP-BDNF-PEG group than in the Tf-p CMV-BDNF-PEG group.This study demonstrates the successful construction of a non-virus targeted liposome,Tf-p GFAP-BDNF-PEG,which crosses the blood-brain barrier and is distributed in the cerebral cortex.Our work provides an experimental basis for BDNF-related targeted drug delivery in the brain.

The development of blood-retinal barrier during the interaction of astrocytes with vascular wall cells

Astrocytes are intimately involved in the formation and development of retinal vessels. Astrocyte dysfunction is a major cause of blood-retinal barrier injury and other retinal vascular diseases. In this study, the development of the retinal vascular system and the formation of the blood-ret-inal barrier in mice were investigated using immunolfuorescence staining, gelatin-ink perfusion, and transmission electron microscopy. The results showed that the retinal vascular system of mice develops from the optic disc after birth, and radiates out gradually to cover the entire retina, taking the papilla optica as the center. First, the superifcial vasculature is formed on the inner retinal layer;then, the vasculature extends into the inner and outer edges of the retinal inner nuclear layer, forming the deep vasculature that is parallel to the superifcial vasculature. The blood-retinal barrier is mainly composed of endothelium, basal lamina and the end-feet of astrocytes, which become mature during mouse development. Initially, the naive endothelial cells were immature with few organelles and many microvilli. The basal lamina was uniform in thickness, and the glial end-feet surrounded the outer basal lamina incompletely. In the end, the blood-retinal barrier matures with smooth endothelia connected through tight junctions, rela-tively thin and even basal lamina, and relatively thin glial cell end-feet. These ifndings indicate that the development of the vasculature in the retina follows the rules of“center to periphery”and“superifcial layer to deep layers”. Its development and maturation are spatially and tempo-rally consistent with the functional performance of retinal neurons and photosensitivity. The blood-retinal barrier gradually becomes mature via the process of interactions between astro-cytes and blood vessel cells.

Decreased numbers of circulating endothelial progenitor cells are associated with hyperglycemia in patients with traumatic brain injury

Hyperglycemia reduces the number of circulating endothelial progenitor cells, accelerates their senescence and impairs their function.However, the relationship between blood glucose levels and endothelial progenitor cells in peripheral blood of patients with traumatic brain injury is unclear. In this study, 101 traumatic brain injury patients admitted to the Department of Neurosurgery, Tianjin Medical University General Hospital or the Department of Neurosurgery, Tianjin Huanhu Hospital, China, were enrolled from April 2005 to March 2007. The number of circulating endothelial progenitor cells and blood glucose levels were measured at 1, 4, 7, 14 and 21 days after traumatic brain injury by flow cytometry and automatic biochemical analysis, respectively. The number of circulating endothelial progenitor cells and blood sugar levels in 37 healthy control subjects were also examined. Compared with controls, the number of circulating endothelial progenitor cells in traumatic brain injury patients was decreased at 1 day after injury, and then increased at 4 days after injury,and reached a peak at 7 days after injury. Compared with controls, blood glucose levels in traumatic brain injury patients peaked at 1 day and then decreased until 7 days and then remained stable. At 1, 4, and 7 days after injury, the number of circulating endothelial progenitor cells was negatively correlated with blood sugar levels(r =-0.147, P < 0.05). Our results verify that hyperglycemia in patients with traumatic brain injury is associated with decreased numbers of circulating endothelial progenitor cells. This study was approved by the Ethical Committee of Tianjin Medical University General Hospital, China(approval No. 200501) in January 2015.

Transplantation of human umbilical cord blood mesenchymal stem cells to treat a rat model of traumatic brain injury

In the present study, human umbilical cord blood mesenchymal stem cells were injected into a rat model of traumatic brain injury via the tail vein. Results showed that 5-bromodeoxyuridine-labeled cells aggregated around the injury site, surviving up to 4 weeks post-transplantation. In addition, transplantation-related death did not occur, and neurological functions significantly improved. Histological detection revealed attenuated pathological injury in rat brain tissues following human umbilical cord blood mesenchymal stem cell transplantation. In addition, the number of apoptotic cells decreased. Immunohistochemistry and in situ hybridization showed increased expression of brain-derived neurotrophic factor, nerve growth factor, basic fibroblast growth factor, and vascular endothelial growth factor, along with increased microvessel density in surrounding areas of brain injury. Results demonstrated migration of transplanted human umbilical cord blood mesenchymal stem cells into the lesioned boundary zone of rats, as well as increased angiogenesis and expression of related neurotrophic factors in the lesioned boundary zone.

Human umbilical cord blood stem cells and brainderived neurotrophic factor for optic nerve injury: a biomechanical evaluation

Treatment for optic nerve injury by brain-derived neurotrophic factor or the transplantation of human umbilical cord blood stem cells has gained progress, but analysis by biomechanical indicators is rare. Rabbit models of optic nerve injury were established by a clamp. At 7 days after injury, the vitreous body received a one-time injection of 50 μg brain-derived neurotrophic factor or 1 × 10^6 human umbilical cord blood stem cells. After 30 days, the maximum load, maximum stress, maximum strain, elastic limit load, elastic limit stress, and elastic limit strain had clearly improved in rabbit models of optical nerve injury after treatment with brain-derived neurotrophic factor or human umbilical cord blood stem cells. The damage to the ultrastructure of the optic nerve had also been reduced. These findings suggest that human umbilical cord blood stem cells and brain-derived neurotrophic factor effectively repair the injured optical nerve, improve biomechanical properties, and contribute to the recovery after injury.

From nerve to blood vessel:a new role of Olfm2 in smooth muscle differentiation from human embryonic stem cell-derived mesenchymal cells

Vascular smooth muscle cell （SMC） differentiation is an important process in vasculogenesis and angio- genesis during embryonic development. The altera- tions in the differentiated state in SMCs contribute to a variety of major cardiovascular diseases such as atherosclerosis, hypertension, restenosis and vascular aneurysm . A better understanding of the cellular and molecular mechanisms that control SMC differen-tiation is essential to help develop new approaches to both prevent and treat these diseases. Therefore, development of reliable and reproducible in vitro cellular models in order to study the differentiation mechanisms is important although it has been challenging because of intrinsic peculiarities of SMC.

Management of an intracranial hypotension patient with diplopia as the primary symptom:A case report

BACKGROUND Intracranial hypotension(IH)is a disorder involving cerebrospinal fluid(CSF)hypovolemia due to spontaneous or traumatic spinal CSF leakage and is easily being misdiagnosed or missed,especially in these patients without the prototypical manifestation of an orthostatic headache.At present,the management of IH with both cranial nerve VI palsy and bilateral subdural hematomas(SDHs)is still unclear.CASE SUMMARY A 67-year-old male Chinese patient complained of diplopia on the left side for one and a half mo.Computed tomography revealed bilateral SDHs and a midline shift.However,neurotrophic drugs were not effective,and 3 d after admission,he developed a non-orthostatic headache and neck stiffness.Enhanced magnetic resonance imaging revealed dural enhancement as an additional feature,and IH was suspected.Magnetic resonance myelography was then adopted and showed CSF leakage at multiple sites in the spine,confirming the diagnosis of having IH.The patient fully recovered following multiple targeted epidural blood patch(EBP)procedures.CONCLUSION IH is a rare disease,and to the best of our knowledge,IH with diplopia as its initial and primary symptom has never been reported.In this study,we also elucidated that it could be safe and effective to treat IH patients with associated cranial nerve VI palsy and bilateral SDHs using repeated EBP therapy.

Changes in the blood-nerve barrier after sciatic nerve cold injury:indications supporting early treatment

Severe edema in the endoneurium can occur after non-freezing cold injury to the peripheral nerve, which suggests damage to the blood-nerve barrier. To determine the effects of cold injury on the blood-nerve barrier, the sciatic nerve on one side of Wistar rats was treated with low tem- peratures （3-5℃） for 2 hours. The contralateral sciatic nerve was used as a control. We assessed changes in the nerves using Evans blue as a fluid tracer and morphological methods. Excess fluid was found in the endoneurium 1 day after cold injury, though the tight junctions between cells remained closed. From 3 to 5 days after the cold injury, the fluid was still present, but the tight junctions were open. Less tracer leakage was found from 3 to 5 days after the cold injury compared with 1 day after injury. The cold injury resulted in a breakdown of the blood-nerve barrier func- tion, which caused endoneurial edema. However, during the early period, the breakdown of the blood-nerve barrier did not include the opening of tight junctions, but was due to other factors. Excessive fluid volume produced a large increase in the endoneurial fluid pressure, prevented liquid penetration into the endoneurium from the microvasculature. These results suggest that drug treatment to patients with cold injuries should be administered during the early period after injury because it may be more difficult for the drug to reach the injury site through the microcirculation after the tissue fluid pressure becomes elevated.

Effects of emergency hyperbaric oxygen therapy on nerve injury, angiogenesis and cerebral blood perfusion in patients with acute cerebral infarction

Objective:To explore the effects of emergency hyperbaric oxygen therapy on nerve injury, angiogenesis and cerebral blood perfusion in patients with acute cerebral infarction.Methods:A total of118 patients with acute cerebral infarction who were treated in the hospital between April 2015 and October 2017 were selected as study subjects and divided into hyperbaric oxygen group (n=59) and control group (n=59) by random number table method. Control group received conventional therapy, hyperbaric oxygen group received conventional therapy combined with hyperbaric oxygen therapy, and both groups were treated for 2 weeks. The differences in nerve injury, angiogenesis and cerebral blood perfusion were compared between the two groups before and after treatment.Results: Differences in nerve injury, angiogenesis and cerebral perfusion were not significant between the two groups immediately after diagnosis. After 2 weeks of treatment, serum nerve injury indexes IGF-1, Copeptin, PAO, AQP4 and H-FABP contents of hyperbaric oxygen group were lower than those of control group;serum angiogenesis indexes PEDF, Ang-1 and VEGF contents were higher than those of control group whereas ES content was lower than that of control group;stenotic-side cerebral blood perfusion parameters CBF and CBV levels were higher than those of control group whereas TTP level was lower than that of control group.Conclusion: Emergency hyperbaric oxygen therapy can effectively reduce nerve injury, promote cerebral angiogenesis and increase cerebral blood perfusion in patients with acute cerebral infarction.

Human umbilical cord blood-derived mesenchymal stem cells promote regeneration of crush-injured rat sciatic nerves

Several studies have demonstrated that human umbilical cord blood-derived mesenchymal stem cells can promote neural regeneration following brain injury. However, the therapeutic effects of human umbilical cord blood-derived mesenchymal stem cells in guiding peripheral nerve regeneration remain poorly understood. This study was designed to investigate the effects of human umbilical cord blood-derived mesenchymal stem cells on neural regeneration using a rat sciatic nerve crush injury model. Human umbilical cord blood-derived mesenchymal stem cells （1 ~ 106） or a PBS control were injected into the crush-injured segment of the sciatic nerve. Four weeks after cell injection, brain-derived neurotrophic factor and tyrosine kinase receptor B mRNA expression at the lesion site was increased in comparison to control. Furthermore, sciatic function index, Fluoro Gold-labeled neuron counts and axon density were also significantly increased when compared with control. Our results indicate that human umbilical cord blood-derived mesenchvmal stem cells promote the functinnal r~.RcJv^rv nf P.n I^h-inillr^4 ~r^i~tit, n^r~e

Targeting brain microvascular endothelial cells: a therapeutic approach to neuroprotection against stroke

Brain microvascular endothelial cells form the interface between nervous tissue and circulating blood, and regulate central nervous system homeostasis. Brain microvascular endothelial cells differ from peripheral endothelial cells with regards expression of specific ion transporters and receptors, and contain fewer fenestrations and pinocytotic vesicles. Brain microvascular endothelial cells also synthesize several factors that influence blood vessel function. This review describes the morphological characteristics and functions of brain microvascular endothelial cells, and summarizes current knowledge regarding changes in brain microvascular endothelial cells during stroke progression and therapies. Future studies should focus on identifying mechanisms underlying such changes and developing possible neuroprotective therapeutic interventions.

In vitro model of the blood-brain barrier established by co-culture of primary cerebral microvascular endothelial and astrocyte cells

Drugs for the treatment and prevention of nervous system diseases must permeate the bloodbrain barrier to take effect.In vitro models of the blood-brain barrier are therefore important in the investigation of drug permeation mechanisms.However,to date,no unified method has been described for establishing a blood-brain barrier model.Here,we modified an in vitro model of the blood-brain barrier by seeding brain microvascular endothelial cells and astrocytes from newborn rats on a polyester Transwell cell culture membrane with 0.4-μm pores,and conducted transepithelial electrical resistance measurements,leakage tests and assays for specific bloodbrain barrier enzymes.We show that the permeability of our model is as low as that of the bloodbrain barrier in vivo.Our model will be a valuable tool in the study of the mechanisms of action of neuroprotective drugs.

Neurovascular compression and decompression of the intracranial vagus for blood pressure

BACKGROUND： Previous researches demonstrated that neurovascular decompression could cure hypertension; however, whether it could effectively control refractory hypertension after hypertensive cerebral hemorrhage should be further studied. OBJECTIVE： To observe the effect of neruovascular compression on intracranial vagus for blood pressure of dogs and investigate the effect of neurovascular decompression on blood pressure of patients with hypertensive cerebral hemorrhage. DESIGN： Randomized controlled animal study, clinical effects and retrospective analysis. SETTING： Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA. MATERIALS： The experiment was carried out in the Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA from May to October 2006. A total of 15 healthy adult dogs of both genders were randomly divided into experimental group （n =10） and control group （n =5）. Clinical observation： A total of 41 patients with hypertensive cerebral hemorrhage were selected from the Department of Neurosurgery, General Hospital of Nanjing Military Area Command of Chinese PLA and the Department of Neurosurgery, Changzheng Hospital Affiliated to the Second Military Medical University of Chinese PLA from October 1999 to October 2006. Among them, one patient had brain stem hemorrhage. There were 27 males and 14 females aged from 41 to 66 years. Inclusion criteria： All patients were diagnosed with CT examination once or several times. Volume of hematoma ranged from 50 to 120 mL and had obviously operative indication. All patients provided consents. In addition, another 281 patients with hypertensive cerebral hemorrhage who received traditionally internal and surgical therapies in our departments of neurosurgery, neurology and emergency room were selected in the control group. METHODS： ①Animal experiments： 20 cm autochthonous great saphenous vein was taken from dogs in the experimental group and coincided with tip of facial artery to form arterial loop so as to oppress left vagus and lateral bulb abdomen. In addition, 20 cm autochthonous great saphenous vein was taken from dogs in the control group and coincided with tip of facial artery to establish arterial loop so as to oppress left cerebellum to observe changes of blood pressure before and at 1, 2, 3 and 4 weeks after operation. ②Clinical observation： Among 41 patients with hypertensive cerebral hemorrhage including one with brain stem hemorrhage, they received microvascular decompression of vagus immediately after getting rid of intracerebral hematoma and stopping bleeding to observe its effect of depressurization. ALL patients and their relatives provided consents. ③A total of 281 patients with hypertensive cerebral hemorrhage who discharged after the treatment of traditionally internal and surgical therapies were studied retrospectively to observe changes of blood pressure after routine treatment and compare the results with neurovascular decompression. MAIN OUTCOME MEASURES： ①Changes of blood pressure of experimental dogs; ②effect of vascular decompression of vagus for blood pressure of patients with hypertensive cerebral hemorrhage after cleating intracerebral hematoma; ③different effects ofneurovascular decompression and routinely internal and surgical therapies on hypertension. RESULTS： ①Results of animal experiments： Nine dogs in the experimental group survived. At 1, 2, 3 and 4 weeks after operation, blood pressure of dogs in the experimental group was （139.77 ±4.06）, （149.11 ±4.90）, （148.10±4.16）, （147.76±4.15） mm Hg （1mm Hg=0.133 kPa）, which was higher than that of dogs in the control group [（117.20±2.74）, （116.65±3.74）, （116.26±1.8）, （115.81±3.76） mm Hg, P 〈 0.01]. ②Results of clinical observation： Among 41 patients, 8 （20%） cases died during the operation. In addition,among other 33 （80%） survival patients, 11 （33%） cases had normal blood pressure; blood pressure of 14 （43%） cases was improved or closed to nonnal value; blood pressure of 8 （24%） cases was not changed obviously as compared with that before operation. ③ The restllts demonstrated that, by using traditionally internal and surgical therapies, among 281 patients with hypertensive cerebral hemorrhage, blood pressure of about 15% cases was recovered or closed to normal value. Those mentioned above did not have history of hypertension before hemorrhage. However, patients who had history of hypertension before hemorrhage received the traditionally internal or surgical therapies, and the blood pressure was not improved to the normal value after the treatment. CONCLUSION： ① Neurovascular compression in left intracranial vagus can cause obvious increase of blood pressure of dogs, and the increasing volume was 30 mm Hg. ② Vascular decompression of vagus has a great effect on refractory hypertension, and the improvement of blood pressure is superior to traditionally internal and surgical therapies in clinic.

Effects of mechanical tension on intraneural blood circulation of the median nerve in rabbits

Simple stretching was applied to the median nerve of rabbits in vivo to study the relationship of different tension with the change of intraneural blood vessels. It was found that when the tension on the nerve was 42 g, the intraneural blood backflow was blocked, while the arterioles entering the nerve trunk remained open; when the tension was increased to 93 g, the intraneural blood volume was decreased along with the increase of vascular permeability; and when the tension was further increased to 137 g, the intraneural blood supply was completely interrupted.The main injurious factors resulting in acute stretching injury of the peripheral nerves and the clinical significance of the changes of intraneural blood circulation were discussed.