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Objective: To evaluate the effect of prophylactic nimodipine in vasospasm prevention and outcome improvement in children with subarachnoid hemorrhage (SAH). Methods: A prospective, randomized controlled clinical trial which enrolled children with SAH who were admitted to pediatric intensive care unit (PICU) of Beijing Children's Hospital from January 2015 to October 2018 was conducted. A total of 43 patients were randomly divided into nimodipine group (24 patients) and control group (19 patients) according to random number table. Transcranial Doppler (TCD) was used to dynamically monitor blood flow velocity and spectrum monography of bilateral middle cerebral artery (MCA) for vasospasm evaluation. Pediatric cerebral performance category (PCPC) scale was used to evaluate patients' brain function on 28(th) day after discharge. Data were analyzed by t test, Mann-Whitney U test, χ(2) test. Results: Except heart rate ((157±26) vs. (137±34) beats/min, t =2.079, P =0.045), no significant differences existed between the two groups in basic demographic characteristics, primary diseases, and clinical manifestations (all P >0.05). The peak velocities of bilateral MCA on the 5(th) day after admission were significantly lower in nimodipine group (left MCA (136±34) vs. (158±23) cm/s, t= -2.890, P= 0.006; right MCA (129±34) vs. (176±27) cm/s, t= -3.717, P= 0.001). Likewise, a lower peak velocity of left MCA was observed on the 7(th) day after admission in nimodipine group ((127±45) vs . (152±13) cm/s, t= -2.903, P= 0.007), but no significant difference existed in that of right MCA ((131±48) vs. (150±22) cm/s, t =-1.760, P =0.090). Eleven patients suffered from vasospasm, 25% (6/24) in nimodipine group and 26% (5/19) in control group (χ(2)=0.010, P =1.000), within whom 8 patients had complete remission after continuing nimodipine treatment, one died in hospital and the other two's vasospasm still existed at the time of discharge. No significant differences were found between the two groups in mean length of hospitalization, proportion of mechanical ventilation, Glasgow coma scale at discharge, survival rate at discharge or survival rate on 28(t)h day after discharge (all P >0.05). However, nimodipine group had a higher proportion of favorable PCPC brain function (92% (22/24) vs . 63% (12/19), χ(2)=5.208, P= 0.030). No side effects such as hypotension, rash or injection site erythema were observed. Conclusion: Prophylactic nimodipine cannot reduce vasospasm incidence in children with SAH but may improve short-term brain function, without any significant safety issues.

Objective: To review our experience in surgical management of proximal anterior cerebral artery (A1) aneurysms in 23 patients., Methods: Between January, 2004 and December, 2014, 23 patients (1.6%) with A1 aneurysms diagnosed by CTA or DSA were treated surgically. The "3H" therapy was adopted for postoperative prevention of cerebrovascular spasm. All the patients were followed up and examined with cerebrovascular CTA at 6, 12, 48 and 60 months after the operation with their Glasgow Outcome Scale score recorded., Results: The patients consisted of 15 men and 8 women with an age range of 16 to 72 years (mean 51.3 years). The average diameter of the aneurysms was 5.8 mm, ranging from 3.2 to 9.7 mm. Twenty-two saccular aneurysms were found in these patients; 21 patients presented with SAH and two had vascular malformation. All the A1 aneurysms were managed through the pterional approach, and the mean postoperative Glasgow Outcome Scale score was 4.8., Conclusion: Thorough analysis of the angiographic data is essential for the diagnosis and treatment of A1 aneurysms. Preservation of the perforators and prevention of aneurysm rupture are critical during the surgery. Full exposure of the Sylvian fissure and temporary occlusion of the parent artery ensures safe and effective dissection of A1 aneurysms.

Objective: To investigate the protective effect and potential mechanisms of hypertonic sodium chloride hydroxyethyl starch solution (HSH) against the cerebral vasospasm (CVS) following subarachnoid hemorrhage (SAH)., Methods: Twenty-four male Sprague-Dawley (SD) rats were randomly assigned to four groups according to the random number table, with 6 rats in each group. The SAH-CVS model was reproduced by injection of the blood twice through the cisterna magna. Rats in both model and HSH treatment groups received 8 mL/kg normal saline (NS) or HSH treatment everyday via caudal vein. Rats in sham group were injected with 1.5 mL/kg NS into cisterna magna followed by 8 mL/kg NS treatment. Rats in normal group received no treatment. Rats were sacrificed to harvest basilar artery after 7 days. The thickness of vessel wall and lumen area were measured using hematoxylin-eosin (HE) staining. The rate of apoptosis of vascular smooth muscle cell (VSMC) was assessed using flow cytometry. Caspase-3 activity was measured by a fluorometric assay. The expressions of Bax and Bcl-2 were determined by Western Blot. Intracellular reactive oxygen species (ROS) was detected by H2DCFDA., Results: Compared with normal group, increased thickness of vessel wall (27.72 ± 1.94 μm vs. 18.30 ± 1.10 μm, P<0.05), decreased lumen area (26 115 ± 1 991 μm² vs. 55 080 ± 2 091 μm², P<0.05), and elevation of rate of apoptosis of VSMCs [(35.05 ± 5.54) % vs. (5.93 ± 1.53) %, P<0.05] were found in model group. Compared with model group, decreased thickness of vessel wall (22.55 ± 1.50 μm vs. 27.72 ± 1.94 μm, P<0.05), increase of lumen area (48 115 ± 2 460 μm² vs. 26 115 ± 1 991 μm², P<0.05), and depressed rate of apoptosis of VSMCs [(16.54 ± 5.94) % vs. (35.05 ± 5.54) %, P<0.05] were found in HSH treatment group. Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in model group were (188.40 ± 19.35)%, (163.50 ± 17.02)%, (208.71 ± 26.04)% and (44.52 ± 9.61) % of those of normal group, and the differences of these parameters between model and normal groups were statistically significant (all P<0.05). Caspase-3 activity, intracellular ROS level, Bax and Bcl-2 expressions in HSH treatment group were (135.05 ± 19.52)%, (119.44 ± 11.50)%, (139.20 ± 18.04)% and (85.35 ± 13.12)% of those of normal group, respectively, and the differences of these parameters between HSH treatment and model groups were statistically significant (all P<0.05). The differences of all measurements between sham and normal groups were not statistically significant., Conclusions: The current results demonstrate that HSH attenuates the SAH-induced CVS, alleviates thickness of vessel wall, and increases lumen area via inhibition of VSMCs apoptosis.

Objective: To investigate the effects of nimodipine on symptomatic cerebral vasospasm in rabbits., Methods: Twenty four japanese white rabbits which ligation of bilateral common carotid arteries and no neurological deficits were randomized to sham-operation, subarachnoid hemorrhage (SAH) and nimodipine which injected of nimodipine 0.1 mg/kg, continuous vein administration 5 day. The behavior scores, neurological scores were observed everyday and cerebral angiography changes were measured twice by 3D-CTA, and basilar artery was removed for pathological examination after last CTA examination., Results: In SAH group, The basilar artery were significantly vasoconstrictive on 5 days, neurological scores were increased, and the basilar artery was found apoptosis-like changes under light microscopic and electron microscope. Nimodipine group could not dilated the basilar artery arteriospasm after SAH, but it could attenuate neurological deficit, and obviously alleviate the pathological changes of basilar artery., Conclusion: Nimodipine could not vasodilation of basilar artery in SCVS, but obviously could alleviate neurological changes and pathological changes of basilar artery in rabbits with symptomatic cerebral vasospasm.

Objective: To determine the efficacy of subarachnoid space protection in intracranial operation., Methods: Data collected from 156 consecutive cranial operations, in which subarachnoid space protective technology was prophylacticly used, were analyzed., Results: Fourteen patients had a postoperative fever for more than 1 week and 16 patients who required lumbar puncture to release blood contaminated cerebro-spinal fluid (CSF) or exclude meningitis. All except 3 patients were discharged as expected. No patients had symptomatic vasospasm and hydrocephalus., Conclusion: The subarachnoid space protective technology has good effect on preventing postoperative fever and improving the outcome of patients.

Objective: To observe the variation of endothelin (ET) and nitric oxide (NO) in plasma and cerebrospinal fluid (CSF) in rabbits, and evaluate the effects of tetramethylpyrazine (TMP) on the prevention and cure of cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH)., Methods: 24 New Zealand rabbits were randomly assigned into three groups: contrast group, experiment group and blank group. Every group contained 8 rabbits. SAH was established according to inject blood into the cisterna magna. The experiment group was administrated with TMP (20 mg/kg x d) transperitoneally. ET and NO of plasma and CSF were detected by radical immunoassay at 72 h and 168 h after SAH. Neurofunction were detected in every group at all the time scales., Results: (1) After SAH, the level of ET in CSF increased significantly in contrast group compared with that in experiment and blank groups (P<0.05). The value of ET at 168 h was higher than that at 72 h. The level of ET in plasma increased significantly in contrast group compared with blank and experiment groups (P<0.05), and no significant contrast could be found between blank and experiment group. (2) After SAH, the value of NO in CSF was lower in contrast group than in other groups (P<0.05), and the level of NO in CSF continued to decrease in all groups on some extent. As time went by, no significant contrast could be found in all groups. The value of NO in plasma was lower in contrast group than in other groups (P<0.05). There was no significant difference between experiment and blank groups. (3) The neuro-function score continued to be increased in contrast group, but decreased in experiment one. The neuro-function score was lower in experiment group than in contrast one at every time point (P<0.05)., Conclusion: After administration of TMP, the variation of ET has the continued decrease in plasma and CSF; the variation of NO shows the continued increase in plasma and CSF; neurological function gets possibly protected. TMP may prevent from and cure CVS after SAH.

Objective: To evaluate the effect of intraoperative continuous nimodipine infusion on cerebral vasospasm during intracranial aneurysm surgery., Methods: Thirty consecutive patients under-going intracranial aneurysmal surgery were prospectively randomized into two groups: Isoflurane (group A, n = 15) and nimodipine (group B, n = 15). The patients in group A were maintained with 1 minimum alveolar concentration (MAC) isoflurane anesthesia during the whole procedure. The patients in group B were given nimodipine infusion continuously (20 microg.kg(-1).h(-1)) after induction of anesthesia and anesthetized with 1 MAC isoflurane. S100B levels in cerebrospinal fluid were determined before aneurysm clipping and 0, 2, 4 h after aneurysm clipping by enzyme linked immunosorbent assay. Assessment of mean blood flow velocity of parent arterial and arterial branches were performed before and after aneurysm clipping., Results: (1) S100B in cerebrospinal fluid was increased significantly at 4 h after aneurysm was clipped in group A (F = 4.11, P < 0.05). However, S100B in cerebrospinal fluid was stable in group B in the whole procedure. (2) Mean arterial flow velocity of parent vessels in group B was lower significantly than that in group A (t = 2.08, P < 0.05). However, mean arterial flow velocity of distal vessels in both groups has no significant difference., Conclusion: Intraoperative nimodipine infusion may prevent cerebral vasospasm during intracranial aneurysm surgery.