caa a22 4500 477107621 CHVBK 20180405111558.0 cr unu---uuuuu 170330e19960301xx s 000 0 eng 10.1007/BF01411745 doi (NATIONALLICENCE)springer-10.1007/BF01411745 Vasodilation by intrathecal lipopolysaccharide of the cerebral arteries after subarachnoid haemorrhage in dogs [Elektronische Daten] [T. Tanazawa, Y. Suzuki, M. Anzai, S. Tsugane, M. Takayasu, M. Shibuya] Summary: To investigate the influence of inducible nitric oxide synthase on cerebral arteries after subarachnoid haemorrhage (SAH) in vivo, lipopolysaccharide (LPS), a major inducer of inducible nitric oxide synthase, was injected intracisternally into control and SAH model dogs. Intracisternal injection of LPS (0.5 mg) produced a long-lasting, submaximal vasodilation of the basilar artery of control dogs on angiography. This effect became significant at 4 hours after LPS injection and plateaued after 6 hours. This vasodilation was reduced by NG-monomethyl-L-arginine. Vasopressin slightly suppressed the vasodilation, while bradykinin increased it. The concentration of L-arginine in CSF decreased after LPS injection, while that of L-citrulline increased. In cytokines, the concentration of tumour necrosis factor-α (TNF-α) in CSF increased transiently at 4 hours after LPS injection, while interleukin-1β, interleukin-6, interferon-γ did not change. These data suggest that vasodilation by LPS is mainly due to nitric oxide predominantly synthesized by an inducible nitric oxide synthase, proximally induced by TNF-α. Our data make it unlikely that SAH itself induces the inducible nitric oxide synthase in vascular tissue, since isolated endotheliumdenuded basilar artery from SAH model dogs did not respond to L-arginine. In SAH model dogs, the degree of vasodilation by LPS differed with the severity of vasospasm. Vasodilation was much greater in mild than in severe vasospasm in dogs, and was increased by superoxide dismutase. These findings suggest that the induction of inducible nitric oxide synthase or its activity may be less effective in severe vasospasm. Springer-Verlag, 1996 Angiography nationallicence dog nationallicence inducible nitric oxide synthase nationallicence lipopolysaccharide nationallicence subarachnoid haemorrhage nationallicence tumour necrosis factor-α nationallicence Tanazawa T. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Suzuki Y. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Anzai M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Tsugane S. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Takayasu M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Shibuya M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut Acta Neurochirurgica Springer-Verlag 138/3(1996-03-01), 330-337 0001-6268 138:3<330 1996 138 701 https://doi.org/10.1007/BF01411745 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/BF01411745 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Tanazawa T. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 700 1- Suzuki Y. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 700 1- Anzai M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 700 1- Tsugane S. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 700 1- Takayasu M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 700 1- Shibuya M. Department of Neurosurgery, Nagoya University School of Medicine, Nagoya, Japan aut NATIONALLICENCE 773 0- Acta Neurochirurgica Springer-Verlag 138/3(1996-03-01), 330-337 0001-6268 138:3<330 1996 138 701 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer