Investigations on the Flat-Detector Computed Tomography-Based CBV Map Acquisition Using a Left Ventricle Contrast Media Injection Protocol.

OBJECTIVES: Cerebral blood volume (CBV) acquired with the use of flat-detector computed tomography with contrast media (CM) injected at the ascending aorta provides real-time brain functional information with minimized CM usage; however, unexpected asymmetric perfusion is observed for certain patients without cerebral circulatory disorders. This work tested the feasibility of left ventricle (LV) CM injection to achieve symmetric perfusion. METHODS: CBV maps were acquired for 10 patients without perfusion-related cerebral abnormities. Perfusion symmetry was predicted with the use of color-coded quantitative digital subtracted angiography with CM injected at ascending aorta. Time density curves were extracted at bilateral common carotid arteries with area under curves calculated. Planes were selected on CBV maps with regions of interest defined covering characteristic regions, where asymmetric perfusion most likely to appear. RESULTS: No adverse physiological changes were detected for any patient. Non-uniform CM distributions were detected for 4 patients with relative area under curves 0.66 ± 0.03, indicating asymmetric perfusion using ascending aorta injection. With LV injection, all the patients demonstrated good perfusion symmetry with relative CBV 1.03 ± 0.07. CONCLUSION: CBV maps acquisition with LV injection offered an approach to acquire immediate brain functional information for patients who are limited by asymmetric perfusion using ascending aorta injection and are sensitive to CM dose.

Interaction between neuronal nitric oxide synthase and inducible nitric oxide synthase after traumatic brain injury in rats / 中华创伤杂志

Objective To study the mechanism of interaction between neuronal nitric oxide syn-thase (nNOS) and inducible nitric oxide synthase (iNOS) following traumatic brain injury (TBI) in rats. Methods A total of 250 male Wistar rats were randomly divided into five groups, ie, sham oper-ation group, trauma group, 7-nitroindazole (7-NI) treatment group, aminoguanidine (AG) treatment group and combined AG and 7-NI treatment group. Severe closed TBI was made by using Marmarou meth-od. Protein expressions of nNOS and iNOS in hippocampus CAI were detected by means of immunohisto-chemical staining at 1,3, 6, 12 hours and at days 1,3, 7 and 14 after TBI. Results The expression of nNOS reached a peak at 6 hour after injury in all groups, with no statistical difference between groups (P > 0. 05), when there was no statistical difference between 7-NI treatment group and trauma group (P > 0. 05) but statistical difference in AG treatment group and combined AG and 7-NI treatment group compared with trauma group at 12 hours after TBI (P <0.05). The expression of iNOS reached maximal level at day 3 after TBI, with lower level in 7-NI group, AG treatment group and combined AG and 7-NI treatment group compared with trauma group (P < 0.05). Conclusions After TBI, nNOS interacts with iNOS by means of the feedback of nitric oxide. The enhanced expression of nNOS is initial factor for increase of iNOS expression, which can down regulate the expression of iNOS.

Effects of nNOS and iNOS on the nerve cell apoptosis of rats' HIP after traumatic brain injuries / 解放军医学杂志

Objective To explore the mechanism of neurotoxic effects of neuron nitric oxide synthase(nNOS)and inducible nitric oxide synthase(iNOS),and the therapeutic effects of 7-nitroindazole(7-NI)and aminoguanidine(AG),in traumatic brain injury(TBI)rats.Methods Two hundred and fifty adult male Wistar rats were randomly divided into 5 groups:sham operation group,traumatic group,AG group,7-NI group and AG+7-NI group.Animals in each group were divided into 8 subgroups according to the time after trauma(1,3,6,12 hours and 1,3,7,14 days).Severe diffused brain injury model was made with Marmarou method.Expressions of nNOS and iNOS in hippocampus CA1 region were determined by immunohistochemistry,nerve cells apoptosis in hippocampus CA1 region was observed by TUNEL methods,and the relationship between apoptosis and NOS was observed by double staining.Results In trauma group,the expression of nNOS in hippocampus CA1 region peaked at 6h post-trauma,the expression of iNOS and apoptosis of nerve cells in hippocampus CA1 region both peaked at 3d post-trauma,while the apoptosis was alleviated in AG group,7-NI group and AG+7-NI group.The number of both TUNEL staining and nNOS immunostaining positive cells increased at 6h post-trauma in trauma group,significantly higher than that in 7-NI group.The number of both TUNEL staining and iNOS immunostaining positive cells increased at 3d post-trauma in trauma group,significantly higher than that in AG group.Conclusions The over-expression of nNOS and iNOS has toxic effects to neural tissues of brain,serves as one of the factors inducing nerve cell apoptosis in hippocampus CA1 region.7-NI and AG can inhibit the expression of nNOS and iNOS,reduce the nerve cell apoptosis,and play an important role in neuroprotective effect.