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hypotension/cannabis
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Cannabinoid antagonist SR-141716 inhibits endotoxic hypotension by a cardiac mechanism not involving CB1 or CB2 receptors.
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Endocannabinoids and CB1 receptors have been implicated in endotoxin (LPS)-induced hypotension: LPS stimulates the synthesis of anandamide in macrophages, and the CB1 antagonist SR-141716 inhibits the hypotension induced by treatment of rats with LPS or LPS-treated macrophages. Recent evidence
Profound hypotension and bradycardia in the setting of synthetic cannabinoid intoxication - A case series.
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Cannabinoids are the most commonly used illegal substances in the world [1]. Synthetic Cannabinoids (SCB) are also known as "Spice", "K2", "Spike", "herbal incense", "Cloud 9", "Mojo" and many others are becoming a large public health concern due to their increasing use, unpredictable toxicity, and
A cannabinoid receptor, sensitive to O-1918, is involved in the delayed hypotension induced by anandamide in anaesthetized rats.
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OBJECTIVE
Intravenous injection of the endocannabinoid anandamide induces complex cardiovascular changes via cannabinoid CB(1), CB(2) and vanilloid TRPV1 receptors. Recently, evidence has been accumulating that in vitro, but not in vivo, anandamide relaxes blood vessels, via an as yet unidentified,
Cannabinoid-induced hypotension and bradycardia in rats mediated by CB1-like cannabinoid receptors.
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Previous studies indicate that the CB1 cannabinoid receptor antagonist, N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-met hyl-1H-pyrazole-3-carboxamide HCl (SR141716A), inhibits the anandamide- and delta9-tetrahydrocannabinol- (THC) induced hypotension and bradycardia in
Central cannabinoid 1 receptor antagonist administration prevents endotoxic hypotension affecting norepinephrine release in the preoptic anterior hypothalamic area.
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It is widely assumed that LPS lowers arterial pressure during sepsis by stimulating release of TNF-alpha and other vasoactive mediators from macrophages. However, recent data from this and other laboratories have shown that LPS hypotension can be prevented by inhibiting afferent impulse flow in the
Endogenous cannabinoids mediate hypotension after experimental myocardial infarction.
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OBJECTIVE
We sought to determine whether endocannabinoids influence hemodynamic variables in experimental models of acute myocardial infarction (MI).
BACKGROUND
Hypotension and cardiogenic shock are common complications in acute MI. Cannabinoids are strong vasodilators, and endocannabinoids are
CB(1) cannabinoid receptor antagonism promotes remodeling and cannabinoid treatment prevents endothelial dysfunction and hypotension in rats with myocardial infarction.
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1. To study the long-term effects of altered cannabinoid receptor activity on myocardial and vascular function, Wistar rats were treated with the selective CB(1) antagonist AM-251 (0.5 mg kg(-1) d(-1)), the potent synthetic cannabinoid HU-210 (50 micro g kg(-1) d(-1)) or vehicle for 12 weeks after
Platelet- and macrophage-derived endogenous cannabinoids are involved in endotoxin-induced hypotension.
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Macrophages are the primary cellular targets of bacterial lipopolysaccharide (LPS), but the role of macrophage-derived cytokines in LPS-induced septic shock is uncertain. Recent evidence indicates that activation of peripheral CB1 cannabinoid receptors contributes to hemorrhagic hypotension and that
Effect of the CB1 receptor antagonist, SR141716A, on cannabinoid-induced ocular hypotension in normotensive rabbits.
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The present study attempts to indirectly determine if a neuronal cannabinoid (CB1) receptor mediates the intraocular pressure (IOP) reduction effects of arachidonoyl ethanolamide (AEA), its R-alpha-isopropyl analog, and the non-classical cannabinoid, CP-55,940. A series of these cannabinoids were
Hypotension associated with ingestion of cannabinoids in two children with cancer.
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Prostaglandins and cannabis--XI. Inhibition of delta 1-tetrahydrocannabinol-induced hypotension by aspirin.
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Bradycardia and hypotension after synthetic cannabinoid use: a case series.
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Pharmacologic chaos: severe hypotension from interactions of anesthetics, marijuana, amphetamines, and paroxetine.
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The peripheral sympathetic nervous system is the major target of cannabinoids in eliciting cardiovascular depression.
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Our objective was to identify the sites of interaction of cannabinoids with cardiovascular sympathetic regulation in the rat. Effects on sympathetic tone were first determined in anaesthetised animals following i.v. administration of the drugs. Central effects were evaluated in anaesthetised rats
Cannabinoid-induced mesenteric vasodilation through an endothelial site distinct from CB1 or CB2 receptors.
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Cannabinoids, including the endogenous ligand arachidonyl ethanolamide (anandamide), elicit not only neurobehavioral but also cardiovascular effects. Two cannabinoid receptors, CB1 and CB2, have been cloned, and studies with the selective CB1 receptor antagonist SR141716A have implicated
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