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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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