Effect of Cyclooxygenase Inhibition on Platelet-Vessel Wall Interaction

Bourgain, R.H.; Andries, R.; Maes, L.

doi:10.1159/000214711

Cited by 8 publications

(2 citation statements)

References 18 publications

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“…Like statins, aspirin has been shown to possess neuroprotective properties by inhibiting glutamatergic excitotoxicity caused by hypoxia 14 . In addition, aspirin inhibits the enzyme cyclo‐oxygenase which is involved not only in mediating inflammation but also in promoting platelet aggregation; 18,19 it may thus improve optic nerve perfusion by stabilizing microcirculatory flow 20 . One study has found a correlation between aspirin use and increased utilization of surgical management in primary OAG patients, 21 but this finding was attributed to the high incidence of comorbid systemic illnesses in patients taking aspirin.…”

Section: Discussionmentioning

confidence: 99%

Effect of statin drugs and aspirin on progression in open‐angle glaucoma suspects using confocal scanning laser ophthalmoscopy

Castro¹,

Punjabi²,

Bostrom

et al. 2007

Clinical Exper Ophthalmology

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Section: Discussionmentioning

confidence: 99%

Effect of statin drugs and aspirin on progression in open‐angle glaucoma suspects using confocal scanning laser ophthalmoscopy

Castro¹,

Punjabi²,

Bostrom

et al. 2007

Clinical Exper Ophthalmology

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“…Not long after the development and introduction of the first NSAIDs in the late seventies, the first reports on side effects in the cardiovascular and renal systems started to appear. Relationships between the inhibition of COX and platelet thrombus formation [103] and occasional decreases in glomerular filtration rate and re¬nal function [104] were reported as early as 1980s. Al-though some contradictory results have been obtained throughout the years, the evidence point out to a certain increase of the risk of cardiovascular incidences, espe-cially when high doses are administered on a long-time basis.…”

Section: Side Effects Of Cyclooxygenase-2 Inhibitorsmentioning

confidence: 99%

Cyclooxygenase-2 Inhibitors as a Therapeutic Target in Inflammatory Diseases

Ferrer

Busquets-Cortés

Capó

et al. 2019

CMC

181

106

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Inflammation plays a crucial role in the development of many complex diseases and disorders including autoimmune diseases, metabolic syndrome, neurodegenerative diseases, and cardiovascular pathologies. Prostaglandins play a regulatory role in inflammation. Cyclooxygenases are the main mediators of inflammation by catalyzing the initial step of arachidonic acid metabolism and prostaglandin synthesis. The differential expression of the constitutive isoform COX-1 and the inducible isoform COX-2, and the finding that COX-1 is the major form expressed in the gastro-intestinal tract, lead to the search for COX-2-selective inhibitors as anti-inflammatory agents that might diminish the gastrointestinal side effects of traditional non-steroidal anti-inflamatory drugs (NSAIDs). COX-2 isoform is expressed predominantly in inflammatory cells and decidedly upregulated in chronic and acute inflammations, becoming a critical target for many pharmacological inhibitors. COX-2 selective inhibitors happen to show equivalent efficacy with that of conventional NSAIDs, but they have reduced gastrointestinal side effects. This review would elucidate the most recent findings on selective COX-2 inhibition and their relevance to human pathology, concretely in inflammatory pathologies characterized by a prolonged pro-inflammatory status, including autoimmune diseases, metabolic syndrome, obesity, atherosclerosis, neurodegenerative diseases, chronic obstructive pulmonary disease, arthritis, chronic inflammatory bowel disease and cardiovascular pathologies.

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Photochemically induced cerebral infarction

et al. 1987

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Cerebral ischemia leading to infarction was produced in rats by intravascular thrombosis induced by a photochemical reaction between systemically injected rose bengal and green light (560 nm) transmitted through the intact skull for a 2-min period. At 2 or 15 min following photochemical sensitization, animals were perfusion-fixed for scanning (SEM) and transmission (TEM) electron microscopic analyses of the cerebral vasculature. At 2 minutes, ultrastructural examination of cortical regions destined to undergo infarction revealed numerous platelet aggregates within both pial and intraparenchymal vessels. Platelets close to the endothelial walls were routinely degranulated with pseudopodia. Endothelial cells were frequently swollen and contained dilated mitochondria and granular endoplasmic reticulum. The endothelial luminal membrane structure was shown by high-power TEM to be focally damaged. If brain temperature was reduced by 4 degrees C during the photochemical sensitization period, the platelet response was inhibited without interfering with other ultrastructural changes. These results are consistent with the hypothesis that photochemically induced endothelial alterations stimulate platelet activation and implicate abnormal endothelial function as a primary event in the pathogenesis of photochemically induced cerebral infarction.

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Effect of Cyclooxygenase Inhibition on Platelet-Vessel Wall Interaction

Cited by 8 publications

References 18 publications

Effect of statin drugs and aspirin on progression in open‐angle glaucoma suspects using confocal scanning laser ophthalmoscopy

Effect of statin drugs and aspirin on progression in open‐angle glaucoma suspects using confocal scanning laser ophthalmoscopy

Cyclooxygenase-2 Inhibitors as a Therapeutic Target in Inflammatory Diseases

Photochemically induced cerebral infarction

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