Targeting classical but not neurogenic inflammation reduces peritumoral oedema in secondary brain tumours.
Dexamethasone, the standard treatment for peritumoral brain oedema, inhibits classical inflammation. Neurogenic inflammation, which acts via substance P (SP), has been implicated in vasogenic oedema in animal models of CNS injury. SP is elevated within and outside CNS tumours. This study investigated the efficacy of NK1 receptor antagonists, which block SP, compared with dexamethasone treatment, in a rat model of tumorigenesis. Dexamethasone reverted normal brain water content and reduced Evans blue and albumin extravasation, while NK1 antagonists did not ameliorate oedema formation. We conclude that classical inflammation rather than neurogenic inflammation drives peritumoral oedema in this brain tumour model.
Adelaide Centre for Neuroscience Research, School of Medical Sciences, The University of Adelaide, Adelaide, South Australia 5005, Australia.
Kate M
KM
Lewis
Elizabeth
E
Harford-Wright
Robert
R
Vink
Mounir N
MN
Ghabriel
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D001812:Blood-Brain Barrier / Q000187:drug effects; D001929:Brain Edema / Q000188:drug therapy* / Q000209:etiology; D001932:Brain Neoplasms / Q000150:complications* / Q000473:pathology / Q000556:secondary; D003907:Dexamethasone / Q000494:pharmacology*; D004195:Disease Models, Animal; D007249:Inflammation / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D008297:Male; D064729:Neurokinin-1 Receptor Antagonists; D051381:Rats; D017208:Rats, Wistar; D013373:Substance P / Q000096:biosynthesis
D000893:Anti-Inflammatory Agents; D064729:Neurokinin-1 Receptor Antagonists; D013373:Substance P; D003907:Dexamethasone