Cannabis has been used for recreation and medical purposes for more than a millennium across the world; however, its use's consequences remain poorly understood. Although a growing number of surgical patients are regular cannabis consumers, little is known regarding the pharmacological interactions between cannabis and general anesthetics; consequently, there is not a solid consensus among anesthesiologists on the perioperative management of these patients. The existing evidence about the molecular mechanisms underlying pharmacological interactions between cannabinoids and anesthetic agents, both in animal models and in humans, shows divergent results. While some animal studies have demonstrated that phytocannabinoids (tetrahydrocannabinol [THC], cannabidiol [CBD], and cannabinol [CBN]) potentiate the anesthetic effects of inhalation and intravenous anesthetics, while others have found effects comparable with what has been described in humans so far. Clinical studies and case reports have consistently shown increased requirements of GABAergic anesthetic drugs (isoflurane, sevoflurane, propofol, midazolam) to achieve adequate levels of clinical anesthesia. Several potential molecular mechanisms have been proposed to explain the effects of these interactions. However, it is interesting to mention that in humans, it has been observed that the ingestion of THC enhances the hypnotic effect of ketamine. Animal studies have reported that cannabinoids enhance the analgesic effect of opioids due to a synergistic interaction of the endogenous cannabinoid system (ECS) with the endogenous opioid system (EOS) at the spinal cord level and in the central nervous system. However, human data reveals that cannabis users show higher scores of postoperative pain intensity as well as increased requirements of opioid medication for analgesia. This review aims to improve understanding of the molecular mechanisms and pharmacological interactions between cannabis and anesthetic drugs and the clinical outcomes that occur when these substances are used together.

中文翻译：

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大麻素和全身麻醉剂：重新审视其药理学相互作用的分子机制。


大麻在世界范围内已被用于娱乐和医疗目的超过一千年;然而，人们对其使用的影响仍然知之甚少。尽管越来越多的手术患者是常规大麻消费者，但人们对大麻和全身麻醉剂之间的药理相互作用知之甚少;因此，麻醉师对这些患者的围手术期管理没有达成牢固的共识。关于大麻素和麻醉剂之间药理学相互作用的分子机制的现有证据，无论是在动物模型还是在人类中，都显示了不同的结果。虽然一些动物研究表明，植物大麻素（四氢大麻酚 [THC]、大麻二酚 [CBD] 和大麻酚 [CBN]）可增强吸入和静脉麻醉剂的麻醉作用，而其他动物研究则发现效果与迄今为止在人类中描述的效果相当。临床研究和病例报告一致表明，对 GABA 能麻醉药物（异氟烷、七氟烷、异丙酚、咪达唑仑）的需求增加，以达到足够的临床麻醉水平。已经提出了几种潜在的分子机制来解释这些相互作用的影响。然而，有趣的是，在人类中，已经观察到摄入 THC 会增强氯胺酮的催眠效果。动物研究报告说，由于内源性大麻素系统 （ECS） 与内源性阿片类药物系统 （EOS） 在脊髓水平和中枢神经系统中的协同相互作用，大麻素增强了阿片类药物的镇痛作用。 然而，人类数据显示，大麻使用者的术后疼痛强度得分较高，并且对阿片类药物的镇痛需求增加。本综述旨在提高对大麻和麻醉药物之间的分子机制和药理学相互作用以及这些物质一起使用时发生的临床结果的理解。