   
    |  
				    
				   
					  
						 
						   
							  
								 
								   
									  
										 
										  
   
											 respiratory system 
											  
											  
											     
										  lung function 
										   
										  Conclusion: Our present results show that
											 the activation of prejunctional CB1 receptors inhibits cholinergic
											 contraction in human bronchi.   
										   
										  Conclusion: Cannabis has been demonstrated
											 to have bronchodilator, anti-inflammatory, and
											 antitussive activity
											 in the airways. Only Δ9-THC demonstrated effects on airway
											 hyper-responsiveness, anti-inflammatory activity, and antitussive activity in
											 the airways.  
										   
										  Conclusion: The antitussive effect of WIN
											 55212-2 is mediated by the activation of cannabinoid CB(1) receptors and mu(2)
											 (naloxonazine-insensitive)-opioid receptors, but not mu(1)
											 (naloxonazine-sensitive)- or kappa-opioid receptors.  
										   
										  Conclusion: We conclude that CBD
											 administered therapeutically, i.e. during an ongoing inflammatory process, has
											 a potent anti-inflammatory effect and also improves the lung function in
											 mice  
										   
										  Conclusion: Overall, our data indicate that
											 cannabinoids induce ICAM-1, thereby conferring TIMP-1 induction and subsequent
											 decreased cancer cell invasiveness.   
										   
										  In vivo studies in severe combined
											 immunodeficient mice, there was significant inhibition of the subcutaneous
											 tumor growth and lung metastasis of A549 cells in THC-treated animals as
											 compared to vehicle-treated controls. Tumor samples from THC-treated animals
											 revealed antiproliferative and antiangiogenic effects of THC. Our study
											 suggests that cannabinoids like THC should be explored as novel therapeutic
											 molecules in controlling the growth and metastasis of certain
											 lung cancers.  
										   
										  These findings provide proof for a novel
											 antitumorigenic mechanism of cannabinoids.   
										  
   
										   
										   
										   Marijuana-using patients were significantly
											 less likely to die (OR 0.79, p = 0.016),
											 experience shock (OR
											 0.74, p = 0.001), or require an IABP (OR 0.80, p = 0.03) post AMI than patients
											 with no reported marijuana use. These results suggest that, contrary to our
											 hypothesis, marijuana use was not associated with increased risk of adverse
											 reactions following AMI. Furthermore, marijuana use was associated with
											 decreased in-hospital mortality post-AMI.  
										   
										  Our findings suggest that
											 THC protects cardiac cells
											 against hypoxia via CB2 receptor activation by induction of NO
											 production. An NO mechanism occurs also in the classical pre-conditioning
											 process; therefore, THC probably pre-trains the
											 cardiomyocytes to hypoxic
											 conditions.   |  
									   
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