Although anecdotal reports dating back to the 19th century suggested a therapeutic role for marijuana in the relief of asthma, formal experiments first documented this effect in the 1970s. Smoke from marijuana cigarettes was found to produce short-term bronchodilation both in healthy individuals (11,12) and in patients with asthma (13). This bronchodilator effect was clearly attributable to the presence of THC, because oral administration of synthetic THC also produced a dose-dependent bronchodilatation (11). Recently, a potential mechanism for this effect on bronchomotor tone was identified. Cannabinoid type 1 (CB1) receptors were found on axon terminals of postganglionic parasympathetic nerve fibers in rat lung. These nerve terminals are in close proximity to airway smooth muscle (14). In the guinea pig airway, stimulation of these receptors by the endogenous cannabinoid anandamide resulted in dose-dependent relaxation of capsaicin-contracted airway smooth muscle, whereas anandamide caused dose-dependent bronchoconstriction in vagotomized preparations in which airway smooth muscle was maximally relaxed (14). These observations suggest that the endogenous cannabinoid system may play a regulatory role in the bidirectional control of airway smooth muscle tone.
From a clinical standpoint, however, smoking marijuana does not have a therapeutic role in obstructive airways diseases such as asthma. Despite its short-term bron-chodilator properties, the long-term pulmonary consequences of marijuana smoking include airway inflammation, edema, and mucus hypersecretion (5). On the other hand, the development of aerosolized preparations of pure THC for inhalation (15) could produce local physiological effects with a rapid and reproducible onset of action. However, inhalation of pure THC has been shown to induce bronchospasm in individuals with airways hyperreactivity because of local irritant effects (16). THC can also disrupt mitochondrial function and the generation of adenosine triphosphate (ATP) in airway epithelial cells, as well as promote necrotic cell death (8,17). These toxic effects occur rapidly, and the impact of THC on mucociliary function and noxious lung injury can be significant.
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