Dexmedetomidine is a potent alpha-2-adrenergic agonist, more selective than clonidine, with widespread actions that include anxiolysis, sedation, anesthetic-sparing, analgesia and sympatholytic properties. Since its release in the US market in late 1999, it has gained remarkable attention in the adult, pediatric and geriatric populations, predominantly because of its minimal respiratory depression. A large body of recent work supports its favorable profile in many other clinical scenarios, including neuroprotection, cardioprotection and renoprotection, with promising results [1]. Even though dexmedetomidine displays various favorable pharmacological actions, it is believed that its routine use on patients undergoing surgery is not the current trend. The reason for this can be summed up in two ways. First, intraoperative hemodynamic unstability including hypotension and/or bradycardia due to sympatholysis may be problematic in some patients. Such hemodynamic effects of dexmedetomidine may be expected to be more pronounced in hypovolemic patients and in those with diabetes mellitus or chronic hypertension and in the elderly. Secondly, a delay in postanesthetic recovery is expected due to dexmedetomine’s relatively long duration of action compared to other short-acting anesthetics. This disad vantage means that dexmedetomidine is not suitable for day surgery patients. An interesting study has been carried out associated with the effects of dexmedetomidine on intraoperative hemodynamics and postoperative recovery in this issue of Korean Journal of Anesthesiology [2]. Kang et al. [2] found that the changes in mean arterial pressure (MAP) during the operation in the dexmedetomidine group were significantly less than those in the control group, which means that intraoperative administration of dexmedetomidine produced more stable hemodynamics than in the control. In addition, the authors claimed that dexmedetomidine was not associated with prolongation of extubation time or compromised recovery profile. Although their study was small-scaled, with only 10 patients involved in each group, their results are interesting in that they presented some evidence to dispel our concerns about dexmedetomidine-induced intraoperative hypotension and delay in postanesthetic recovery. These concerns have made us reluctant to the routine use of dexmedetomidine in the operating room. The hemodynamic effects of dexmedetomidine are somewhat controversial. Hypotension and/or bradycardia are not unusual, because dexmedetomidine decreases sympathetic ner vous system activity. On the other hand, transient hypertension has been observed primarily during the loading dose in association with the initial peripheral vasoconstrictive effects, although treatment of transient hypertension has generally not been necessary. Investigations in both humans and animals have revealed significant cerebral vasoconstrictive effects of dexmedetomidine [3,4]. Also, dexmedetomidine is known to be associated with higher MAP than midazolam in patients under epidural anesthesia [5]. Such controversies regarding hemodynamic effect are thought to be caused by biphasic action of dexmedetomidine, characterized by an initial short-term increase in MAP followed by a longer lasting hypotension. The biphasic action of dexmedetomidine is sometimes displayed in a dose-dependent manner, i.e., lower dosages reduce norepinephrine release, resulting in decrease