芬太尼
P2Y12
医学
类阿片
药理学
血小板
受体
刺激
麻醉
内科学
血小板聚集
作者
K Kuçzyńska,Magdalena Boncler
出处
期刊:Journal of Cardiovascular Pharmacology
[Ovid Technologies (Wolters Kluwer)]
日期:2020-06-30
卷期号:Publish Ahead of Print
被引量:6
标识
DOI:10.1097/fjc.0000000000000880
摘要
Fentanyl is a potent synthetic opioid used to alleviate severe and chronic pain, as well as an adjunct to general or local anesthesia. Although fentanyl has been used for decades, its full effects are still unknown. Its analgesic and anesthetic activity arises from the stimulation of μ-opioid receptors, resulting in the inhibition of adenyl cyclase and downregulation of cyclic adenosine 3',5'-monophosphate (cAMP), as well as decreased calcium channel activity and increased potassium channel activity. The μ-opioid receptors are abundantly distributed within the central nervous system, where they mediate analgesia, and in the nerve cells of the intestines, where they regulate gastrointestinal tract motility in the secretion or transport of fluids and electrolytes. They are also expressed in blood cells, blood vessel cells, and skin. Given the widespread distribution of μ-opioid receptors, it is likely that fentanyl may also regulate the activity of many other cells, including platelets. Recent findings indicate that it may impair the action of ticagrelor: an oral P2Y12 receptor inhibitor acting as an antiplatelet drug. It could pose a risk of insufficient platelet inhibition and result in thrombotic complications in patients with coronary artery disease. This article tackles the issue of fentanyl interactions with antiplatelet drugs. The mechanism of this phenomenon is not fully understood. Similarly, the biological effects exerted by fentanyl on platelets and the presence of opioid receptors on the platelet surface remain an open question.
科研通智能强力驱动
Strongly Powered by AbleSci AI