The response of the blood-brain barrier (BBB) following a stroke, including subarachnoid hemorrhage (SAH), has been studied extensively. The main components of this reaction are endothelial cells, pericytes, and astrocytes that affect microglia, neurons, and vascular smooth muscle cells. SAH induces alterations in individual BBB cells, leading to brain homeostasis disruption. Recent experiments have uncovered many pathophysiological cascades affecting the BBB following SAH. Targeting some of these pathways is important for restoring brain function following SAH. BBB injury occurs immediately after SAH and has long-lasting consequences, but most changes in the pathophysiological cascades occur in the first few days following SAH. These changes determine the development of early brain injury as well as delayed cerebral ischemia. SAH-induced neuroprotection also plays an important role and weakens the negative impact of SAH. Supporting some of these beneficial cascades while attenuating the major pathophysiological pathways might be decisive in inhibiting the negative impact of bleeding in the subarachnoid space. In this review, we attempt a comprehensive overview of the current knowledge on the molecular and cellular changes in the BBB following SAH and their possible modulation by various drugs and substances.

• Klíčová slova
• Blood–brain barrier, Neuroinflammation, Neuronal injury, Neurovascular unit, Subarachnoid hemorrhage, Subarachnoid hemorrhage treatment,
• MeSH
• endoteliální buňky metabolismus   MeSH
• hematoencefalická bariéra metabolismus   MeSH
• ischemie mozku * metabolismus   MeSH
• mikroglie MeSH
• modely nemocí na zvířatech MeSH
• subarachnoidální krvácení * MeSH
• zvířata MeSH
• Check Tag
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• přehledy MeSH

Aneurysmal subarachnoid hemorrhage (aSAH) is a life-threatening condition associated with the development of early brain injury (EBI) and delayed cerebral ischemia (DCI). Pharmacological treatment of vasospasm following aSAH currently mainly comprises nimodipine administration. In the past few years, many drugs that can potentially benefit cases of subarachnoid hemorrhage have become available. The objective of this review is to critically assess the effects of non-steroidal anti-inflammatory drugs (NSAIDs) following aSAH. A systematic literature review was conducted following PRISMA guidelines. The search was aimed at studies addressing aSAH and NSAIDs during the 2010 to 2019 period, and it yielded 13 articles. Following the application of search criteria, they were divided into two groups, one containing 6 clinical articles and the other containing 7 experimental articles on animal models of aSAH. Inflammatory cerebral changes after aneurysm rupture contribute to the development of EBI, DCI and cerebral vasospasm. It appears that NSAIDs (especially coxibs) are even more effective in reducing vasospasm than nimodipine. Other beneficial effects of NSAIDs include reduction in mortality, improved functional outcome and increased hypoaggregability. However, despite these positive effects, there is only one randomized, double-blind, placebo-controlled trial showing a tendency towards a better outcome with lower incidence of vasospasm or mortality in patients following aSAH.

• Klíčová slova
• Aneurysmal subarachnoid hemorrhage, Cerebral ischemia, Non-steroidal anti-inflammatory drugs, Vasospasms,
• MeSH
• antiflogistika nesteroidní terapeutické užití   MeSH
• dvojitá slepá metoda MeSH
• intrakraniální vazospazmus farmakoterapie   etiologie   patofyziologie   MeSH
• ischemie mozku farmakoterapie   etiologie   patofyziologie   MeSH
• lidé MeSH
• nimodipin terapeutické užití   MeSH
• randomizované kontrolované studie jako téma metody   MeSH
• subarachnoidální krvácení komplikace   farmakoterapie   patofyziologie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• časopisecké články MeSH
• systematický přehled MeSH
• Názvy látek
• antiflogistika nesteroidní MeSH
• nimodipin MeSH