Serotonin, atherosclerosis, and collateral vessel spasm.
Studies on animal models demonstrate that platelet products contribute to vascular spasm in ischemic syndromes and that this is reversible with administration of ketanserin and thromboxane synthesis inhibitors. Laboratory animals (dogs, rabbits, and rats) that had femoral artery ligations exhibited supersensitivity to serotonin within days in their collateral blood vessels. This supersensitivity lasted at least 6 months. The response to serotonin was reversed by ketanserin, but not by 5HT-1 antagonists. Supersensitivity does not extend to norepinephrine, and alpha blockers do not influence the response to serotonin. It appears that platelet activation by endothelial injury contributes to ischemia through blood vessel occlusion and vascular spasm. When platelet activation occurs in vivo, blood vessel occlusion and vascular spasm are reversible in part by using ketanserin or agents that block thromboxane synthesis or its action. Combining both classes of agents reverses spasm completely. These findings support existing evidence that platelet products contribute to vascular disease, and provide an approach to improved management with currently available pharmacologic agents.
D000818:Animals; D001158:Arteries / Q000502:physiology; D001161:Arteriosclerosis / Q000209:etiology*; D002309:Cardiology / Q000639:trends; D003097:Collateral Circulation; D003331:Coronary Vessels / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology; D005544:Forecasting; D006801:Humans; D012701:Serotonin / Q000502:physiology*; D012702:Serotonin Antagonists / Q000627:therapeutic use; D014661:Vasoconstriction
D012702:Serotonin Antagonists; D012701:Serotonin