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Query: UMLS:C0268318 (ICP)
 10,007 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Indomethacin has been suggested as a therapeutic tool to manage elevated intracranial pressure in patients with severe head injury and patients undergoing craniotomy for brain tumors. Indomethacin is a non-selective cyclooxygenase inhibitor. Compared to other cyclooxygenase inhibitors indomethacin has unique effects on cerebral blood flow. Administration of indomethacin causes cerebral vasoconstriction and decreases cerebral blood flow, which elicits a decrease in intracranial pressure. The mechanism of indomethacin-induced cerebral vasoconstriction is not completely understood and controversies exist whether indomethacin causes cerebral ischemia. The primary aims of this article were to review the existing knowledge of indomethacin's influence upon cerebral hemodynamics and elevated ICP in patients with brain pathology. Furthermore, indomethacin's mechanism of action and whether it causes cerebral ischemia are discussed.
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PMID:Treatment of elevated intracranial pressure with indomethacin: friend or foe? 1622 16

Treatment of malignant glioma with chemotherapy is limited mostly because of delivery impediment related to the blood-brain tumor barrier (BTB). B1 receptors (B1R), inducible prototypical G-protein coupled receptors (GPCR) can regulate permeability of vessels including possibly that of brain tumors. Here, we determine the extent of BTB permeability induced by the natural and synthetic peptide B1R agonists, LysdesArg(9)BK (LDBK) and SarLys[dPhe(8)]desArg(9)BK (NG29), in syngeneic F98 glioma-implanted Fischer rats. Ten days after tumor inoculation, we detected the presence of B1R on tumor cells and associated vasculature. NG29 infusion increased brain distribution volume and uptake profiles of paramagnetic probes (Magnevist and Gadomer) at tumoral sites (T(1)-weighted imaging). These effects were blocked by B1R antagonist and non-selective cyclooxygenase inhibitors, but not by B2R antagonist and non-selective nitric oxide synthase inhibitors. Consistent with MRI data, systemic co-administration of NG29 improved brain tumor delivery of Carboplatin chemotherapy (ICP-Mass spectrometry). We also detected elevated B1R expression in clinical samples of high-grade glioma. Our results documented a novel GPCR-signaling mechanism for promoting transient BTB disruption, involving activation of B1R and ensuing production of COX metabolites. They also underlined the potential value of synthetic biostable B1R agonists as selective BTB modulators for local delivery of different sized-therapeutics at (peri)tumoral sites.
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PMID:Induction of selective blood-tumor barrier permeability and macromolecular transport by a biostable kinin B1 receptor agonist in a glioma rat model. 2262 5