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. 2022 Apr 11;12(4):e058895. doi: 10.1136/bmjopen-2021-058895

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© Author(s) (or their employer(s)) 2022. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/.

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Concept map depicting four major pathways for the occurrence of CVS following aSAH. Inflammatory pathway is shown in yellow and explains how ibuprofen may act as a prophylactic agent in this scenario. Numbers in parentheses are representative of corresponding reference for that branch, all concept map references are available in online supplemental digital content, part 1. aSAH, aneurysmal subarachnoid haemorrhage; Ca++, Calcium ion; cGMP, cyclic guanosine monophosphate; COX, cyclooxygenase; DAG, diacylglycerol; ETA, endothelin A; ET, endothelin; Hgb, hemoglobin; ICAM-1, intercellular adhesion molecule-1; IP3, inositol trisphosphate; LFA-1, Lymphocyte function-associated antigen 1; Mac-1, macrophage-1 antigen; Met, metabolic; MLC 20, Myosin light chain 20; NO, nitric oxide; NO-LS, nitric oxide-like substance; PGF2α, prostaglandin F2 alpha; PGs, prostaglandins; PKC, protein kinase C; ROS, reactive oxygen species; SA, subarachnoid; TXAs, thromboxanes; TXA2, thromboxane A2; VCAM-1, vascular cell adhesion molecule-1.