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The procoagulatory effects of delta-9-tetrahydrocannabinol in human platelets
Engelbert Deusch1, Hans Georg Kress, Birgit Kraft
1Department of General Anesthesiology and Intensive Care B, Vienna Medical University, Vienna, Austria.
Insights
Delta-9-tetrahydrocannabinol (THC) activates human platelets, increasing the risk of blood clots. Cannabinoid receptors (CB1 and CB2) on platelets may mediate these procoagulatory effects, warranting further in vivo investigation.
Area of Science:
- Pharmacology
- Hematology
- Cannabinoid Science
Background:
- Delta-9-tetrahydrocannabinol (THC) is used for chronic conditions but linked to cardiovascular risks.
- Platelets are implicated in myocardial infarction and thromboangiitis obliterans.
- The role of platelets as cannabinoid target cells remains unclear.
Purpose of the Study:
- To investigate the in vitro effects of THC on human platelets.
- To determine the expression of cannabinoid receptors on human platelets.
Main Methods:
- Human platelets were treated with varying concentrations of THC.
- Flow cytometry assessed the expression of activated platelet fibrinogen receptor (glycoprotein IIb-IIIa) and P-selectin.
- Western blotting identified cannabinoid receptor (CB1, CB2) surface expression.
Main Results:
- THC increased glycoprotein IIb-IIIa and P-selectin expression in a concentration-dependent manner.
- Both CB1 and CB2 cannabinoid receptors were detected on human platelet cell membranes.
- THC-induced platelet activation may involve a receptor-dependent pathway.
Conclusions:
- THC can activate human platelets, potentially via CB1 and CB2 receptors.
- These findings suggest a procoagulatory effect of THC.
- Further in vivo studies are needed to confirm the role of cannabinoid receptors in THC-mediated platelet activation.
Abstract:
Delta-9-tetrahydrocannabinol (THC) is increasingly used for the long-term treatment of nausea, vomiting, cachexia, and chronic pain. Recent reports, however, have indicated an increased risk of myocardial infarction and thromboangiitis obliterans after THC intake. Blood platelets have an essential role in the pathogenesis of these two diseases, but it is unclear whether platelets are potential target cells for cannabinoids. We investigated the effects of THC on human platelets and the expression of cannabinoid receptors on their cell membranes in this in vitro study. The effects of THC (final concentrations 10(-7) to 10(-5) M) on the expression of activated platelet fibrinogen receptor (glycoprotein IIb-IIIa) and P selectin were characterized by flow cytometry. Western blotting was performed with platelet membrane preparations to determine the surface expression of cannabinoid receptors on human platelets. THC increased the expression of glycoprotein IIb-IIIa and P selectin on human platelets in a concentration-dependent manner. The two known cannabinoid receptors (CB(1) and CB(2)) were both detected on the cell membrane of human platelets. Our functional results may suggest a receptor-dependent pathway of THC-induced platelet activation. However, further in vivo studies are warranted to evaluate the role of cannabinoid receptors in mediating the demonstrated procoagulatory effect of THC.
