Abstract
Objective: To compare the venous plasma levels of endocannabinoids at different phases of acute ischemic stroke (AIS).
Background: Endocannabinoids, a family of bioactive lipids with widespread effects on vascular tone, inflammation, metabolism, and neurotransmission, are hypothesized to have anti-inflammatory and neuroprotective properties in their role as an acute phase response mechanisms during cerebral ischemia. Preclinical studies have demonstrated neuroprotective effects of endocannabinoids in acute cerebral ischemia and closed head injury. Therefore, the human endocannabinoid response to AIS warrants further investigation.
Design/Methods: We conducted an exploratory analysis of serial pooled venous endocannabinoid levels in patients with AIS or transient ischemic attack who presented to Mayo Clinic Hospital. The initial sample was collected within twelve hours of symptom onset (T1); the second sample was collected between 24 hours to 7 days after symptom onset (T2). The endocannabinoids N-arachidonoylethanolamine (AEA), 2-arachidonoylglycerol (2-AG), as well as palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) were quantified by liquid chromatography mass spectrometry. The levels of the metabolites between T1 and T2 were compared via paired t-test.
Results: Fourteen patients met study criteria. Median (Q1/Q3 range): Age - 75 years (55 – 87); body mass index - 24.6 (22 – 35); National Institutes of Health Stroke Scale score (NIHSS) - 5 (4 – 15); infarct volume - 1.8 cm3 (0.4 – 6.8); T1- 9 hours (7 – 11); T2 -51 hours (43 – 58). Levels of 2-AG were significantly elevated at T2 compared to T1 with mean difference of 122.39 nM (95% CI: 26.91 – 217.88), p=0.0159. Levels of AEA, PEA and OEA did not differ between the two time points, p>0.05.
Conclusions: Circulating 2-AG increases significantly during the early phase of AIS. Further investigation with larger sample size is warranted to understand the precise role of 2-AG in the pathophysiology of acute cerebral ischemia and to determine whether modulation of this bioactive lipid holds promise as a neuroprotective treatment for acute stroke.
Disclosure: Dr. Buciuc has nothing to disclose. Dr. Vasile has nothing to disclose. Dr. Conte has nothing to disclose. Dr. Scharf has nothing to disclose.
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