Abstract:

Dexmedetomidine, which is an α₂ adrenergic receptor agonist with sedative, analgesic, anxiolytic and anti-sympathetic effects, has become a widely used drug in clinical anesthesia and intensive care unit (ICU). Compared with other drugs in the department of anesthesiology, dexmedetomidine has no obvious respiratory depression and no obvious hemodynamic changes, and can significantly reduce the dosage of sedative and analgesic drugs when combined with other anesthetics. In clinical applications, dexmedetomidine has been found to induce a sedative response that is associated with rapid arousal. Dexmedetomidine is traditionally thought to act through α₂ adrenergic receptors to lower blood pressure, dilate blood vessels and lower heart rate, but it is unclear how it affects neural circuits in the brain. In recent years, there has been an increasing number of studies on the mechanism of action of dexmedetomidine, which has confirmed that the ventrolateral preoptic nucleus (VLPO), locus coeruleus (LC) and ventral tegmental area (VTA) of the hypothalamus are involved in the sedation mediated by dexmedetomidine, the dorsal root ganglion (DRG) and superior cervical ganglion (SCG) are involved in dexmedetomidine-mediated analgesia, and the hypothalamic preoptic area (PO) and hypothalamic paraventricular nucleus (PVN) are involved in the changes in body temperature and water-electrolyte balance mediated by dexmedetomidine, providing a new direction for understanding the mechanism of dexmedetomidine in the central nervous system.

Key words: dexmedetomidine, α₂ adrenergic receptor, sedation, analgesia, neural mechanism