Objective To investigate the neuroprotective effect of vagus nerve stimulation ( VNS) on a model rat of focal cerebral ischemia. Methods A total of 42 adult male Sprague-Dawle ( SD) rats were randomly divided into a sham operation group (n=10),a model group (n=16),and a VNS-treated group ( n = 16 ) . Each group was randomly redivided into 2 subgroups:left VNS subgroup and right VNS subgroup. A model of focal cerebral ischemia (2 h) in rats was induced by the intraluminal suture method. At 30 minutes after modeling, the VNS-treated group received cervical VNS, the stimulation intensity was 0. 5 mA,the interval was 0. 5 ms,and the frequency was 20 Hz. Stimulation was once every 5 min within 1 h and each lasted for 30 s. The model group did not give any stimulation. Neither blood vessels were embolized nor were the nerves stimulated in the sham operation group. The changes of somatosensory evoked potentials ( SEP) on the lesion sides during operation were monitored. At 24 h after modeling,the neurobehavioral scores were performed. The rats were sacrificed,and their brain infarct volume was measured. Results (1) During the stimulation of left VNS in rats,the neurobehavioral scores of the sham operation group,model group and VNS-treated group were 0. 4 ± 0. 2,9. 5 ± 0. 4,6. 4 ± 0. 3,respectively;during the stimulation of right VNS in rats,the neurobehavioral scores of the 3 groups were 0. 6 ± 0. 2,9. 3 ± 0. 4,and 6. 9 ± 0. 4,respectively. There were significant differences between the scores of the model group and those of the other 2 groups (P<0. 05). (2) Compared with the model group,the brain infarct volume of the VNS-treated group was reduced ( stimulating the left VNS of the 2 groups was 120 ± 7 and 56 ± 7 mm3 respectively;stimulating the right VNS was 115 ± 10 and 54 ± 8 mm3 respectively ) . There were significant differences ( P <0. 05). (3) Compared with the sham operation group and the VNS-treated group,the SEP N1 amplitude of the model group was decreased significantly and the P1 latency was prolonged significantly. There was significant difference (P<0. 05). (4) There were no significant differences in the stimulation of the left or right VNS in the VNS-treated group among the infarct volume, neurobehavioral scores, SEP amplitude,and latency (P>0. 05). Conclusion No matter whether to stimulate the left or right vagus nerves, they both have neuroprotective effects on ischemic brain injury, and there was no significant difference on the action effects.

Objectives To investigate the neuroprotective mechanism of vagus nerve stimulation ( VNS) by stimulating the vagus nerve in ischemic cerebral tissue in a rat model of transient focal cerebral ischemia. Methods Twenty-six adult male Sprague-Dawley ( SD ) rats were randomly divided into sham operation group (n=6),model group (n=10),and VNS-treated group (n=10) . The model of rat transient focal cerebral ischemia was induced by the intraluminal suture method. At 30 min after modeling,the right side neck VNS in the VNS-treated group was stimulated ( stimulus intensity 0. 5 mA, interval 0. 5 ms, frequency 20 Hz),once every 5 min within 1 h,and once for 30 s. The model group repeated the steps of the VNS-treated group,but did not stimulate. The sham operation group repeated the experimental steps,but it neither embolized the vessels nor stimulated nerves. The changes of cerebral blood flow were monitored with a laser Doppler flowmeter. The rats were sacrificed after 24 h. The expressions of interleukin 6(IL-6) and caspase-3 in brain tissue were determined by immunohistochemistry staining. The neuronal apoptosis was observed by the in situ end-labelling technique. Results ( 1 ) Compared with the sham operation group, the number of positive cells of IL-6,caspase-3,and the numbers of neuronal apoptosis in the model group were significantly increased (20. 7 ± 5. 0 cells/HP vs. 2. 3 ± 1. 0 cells/HP,44. 5 ± 9. 5 cells/HP vs. 0,30. 9 ± 9. 0 cells/HP vs.0).Thereweresignificantdifferences(P<0.05).(2)Comparedwiththemodelgroup,thenumber of positive cells of IL-6(10. 9 ± 3. 7 cells/HP),the caspase-3 (18. 9 ± 6. 7 cells/HP),and the numbers of neuronal apoptosis (14. 0 ± 5. 2 cells/HP) in the VNS-treated group decreased significantly. There were significant differences (P<0. 01). (3) Before and after modeling,there were no significant differences in cerebral blood flow in various periods between the model group and the VNS-treated group (P>0. 05). Conclusion The neuroprotective mechanism of VNS for cerebral ischemia may be associated with the inhibition of neuronal apoptosis and decreasing inflammatory response. It may not be associated with the changes of cortical cerebral blood flow.

Objective To retrospectively analyze the effect of two kinds of biological agents in volume -re-duced bullae .Methods 11 patients who suffered from bullae were operated under large C-arm locating ,and infused two kinds of biological agents through micro catheter of fibreoptic bronchoscopy .All of them were randomly divided into the two groups .The biological agents in group A were fibrinogen and diluent thrombin , and that of group B was Porcine Fibrin Sealant Kit .In group A,the micro catheter with diameter of micro thread less than 1.2mm was placed in bullae through fibreoptic bronchoscope ,and then the 2mL lidocaine,5 ml fibrinogen,and double of 500u diluent thrombin were inproperorder injected through micro catheter .In group B,the Porcine Fibrin Sealant Kit was injected at the same method,and then the suspension fluid was exacted .The operation time was recorded ,and then the clinical efficacy and incidence rate of complications were compared .Results The operation time of group A was 5-15 minutes, and that of group B was 6-20 minutes.For all the patients ,4 cases were totally effective ,2 cases were significantly effective,and 2 cases were totally non-effective.The total effective rate was 81.82%(9/11).The incidence rates of common complications in group A and B were 52.38%(22/42),58.33%(14/24),respectively,the difference was not significant (χ2 =0.22,P>0.05).Moreover,there were no serious complications in all cases .Conclusion The security and effect of two kinds of biological agents might be well enough ,but in view of less cases ,they were worth to further popularized and applied in clinical practice .

OBJECTIVETo discuss the surgical strategies and analyze the clinical outcomes of multiple intracranial aneurysms (MIA).

METHODSThe clinical data of 49 MIA patients surgically treated between January 2009 and December 2013 was analyzed retrospectively. Among the 49 patients, 12 patients were male and 37 were female, mean age (49 ± 11) years. Thirty-five patients had ruptured aneurysms, and 14 had unruptured aneurysms. Treatment strategies included one-stage operation (MIA were treated in one-stage with an unilateral approach), two-stage treatment (MIA were treated stage by stage) and partial treatment (only ruptured aneurysm was treated). Postoperative CT angiograms (CTA) or digital subtraction angiograms (DSA) were reviewed and the Glasgow Outcome Scale (GOS) scores were evaluated during follow-up period.

RESULTSThirty-two patients (65.3%) underwent one-stage operation, 9 patients (18.4%) underwent two-stage treatment, and 8 patients (16.3%) underwent partial treatment. Forty-seven patients were followed up 4-49 months, mean (22 ± 7) months. Postoperative CTA or DSA showed no aneurysm recurrence. According to the GOS scores, 41 patients (83.7%) with good outcomes (GOS 4, 5), 6 patients (12.2%) were disabled (GOS 2, 3) and 2 patients (4.1%) were dead (GOS 1).

CONCLUSIONSelecting the right patients for surgery and making personalized surgical strategies based on the characteristics of patients and aneurysms could improve the surgical outcomes of MIA.

Adult ; Aneurysm, Ruptured ; surgery ; Cerebral Angiography ; Female ; Humans ; Intracranial Aneurysm ; surgery ; Male ; Middle Aged ; Patient Selection ; Prospective Studies ; Recurrence ; Retrospective Studies ; Vascular Surgical Procedures ; methods