caa a22 4500 477107214 CHVBK 20180405111557.0 cr unu---uuuuu 170330e19960701xx s 000 0 eng 10.1007/BF01411266 doi (NATIONALLICENCE)springer-10.1007/BF01411266 Nitric oxide synthase is expressed in experimental malignant glioma and influences tumour blood flow [Elektronische Daten] [I. Whittle, F. Collins, P. Kelly, I. Ritchie, J. Ironside] Summary: The distribution and function of nitric oxide synthase (NOS) was studied in the rodent C6 implantation glioma model. Using a histochemical stain for NADPH diaphorase, which colocalises with NOS, morphological studies revealed non homogenous staining of the constituent tumour cells and the neoplastic endothelium. Immunocytochemical staining for macrophages (ED1, ED2) showed dense positivity at the tumour brain interface with more patchy positivity within the tumour mass. This finding suggests that both macrophages, which are known to produce large amounts of NO, and the C6 cells contribute to the NADPH diaphorase positivity. Administration of the NOS inhibitor Ng-nitro-L-argine methyl ester (L-NAME) significantly reduced both tumour (40%) and contralateral local cerebral blood flow (20%) compared to control animals. These findings demonstrate that (i) NOS is present in experimental malignant glioma; (ii) NO mediated mechanisms contribute to tumour blood vessel dilatation and blood flow regulation; and (iii) using this model there is a significant differential sensitivity of the tumour and brain parenchymal vascular beds to a NOS inhibitor. Further investigations are required to determine the potential therapeutic and biological relevance of these findings and the relative contributions of tumour cells, neoplastic endothelium and reactive macrophages to NO mechanisms in gliomas. Springer-Verlag, 1996 Nitric oxide nationallicence glioma nationallicence cerebral blood flow nationallicence Whittle I. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut Collins F. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut Kelly P. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut Ritchie I. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut Ironside J. Department of Neuropathology Laboratory, Western General Hospital, Edinburgh, Scotland, UK aut Acta Neurochirurgica Springer-Verlag 138/7(1996-07-01), 870-876 0001-6268 138:7<870 1996 138 701 https://doi.org/10.1007/BF01411266 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01411266 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Whittle I. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut NATIONALLICENCE 700 1- Collins F. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut NATIONALLICENCE 700 1- Kelly P. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut NATIONALLICENCE 700 1- Ritchie I. Department of Clinical Neurosciences, Western General Hospital, Edinburgh, Scotland, UK aut NATIONALLICENCE 700 1- Ironside J. Department of Neuropathology Laboratory, Western General Hospital, Edinburgh, Scotland, UK aut NATIONALLICENCE 773 0- Acta Neurochirurgica Springer-Verlag 138/7(1996-07-01), 870-876 0001-6268 138:7<870 1996 138 701 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer