## 1 Introduction  
Dexmedetomidineomidine (DEX) is used for intraoperative anesthesia and sedation in intensive care. It is an \(\alpha\)2-adrenergic receptor agonist that also acts on imidazoline receptors. There are three \(\alpha\)2-adrenergic receptor subtypes, and DEX mainly reacts with \(\alpha\)2A-adrenergic receptors [1]. Normally, \(\alpha\)2-adrenergic receptors bind to the noradrenaline released by itself and suppress the further release of noradrenaline. Many \(\alpha\)2-adrenergic receptors are present in the locus coeeruleus of the pons, and when DEX binds to them, noradrenaline release is suppressed. The site of the central nervous system responsible for excitement and arousal is also suppressed, making it sedated. DEX causes less respiratory depression than other sedative drugs and is approved for use in children in Japan. It also has a relatively short half-life of about 2 h and is easy to use [1]. Recently, it was reported that it also has a protective effect on various organs [2]. The administration of DEX to a myocardial ischemia-reperfusion mouse model activated endothelial nitric oxide synthase in vascular endothelial cells, resulting in coronary artery dilation, decreased IL-1B/IL-6/TNF-\(\alpha\) mRNA expression in myocardial cells, and increased antioxidant enzyme levels (SOD, CAT, GPx). DEX was reported to have cardioplegic, anti-inflammatory, and antioxidant effects [3]. In addition, [PERSON] et al. reported that the administration of DEX to a hepatic ischemia-reperfusion rat model has antiapoptotic and anti-inflammatory effects that are due to an increased Bcl-2 mRNA expression and decreased IL-6 mRNA expression in hepatocytes [4]. [PERSON] et al. reported that its administration to a spinal ischemia-reperfusion rabbit model has anti-inflammatory and antiapoptotic effects that are due to suppressed TNF-\(\alpha\)/IL-1\(\beta\) and reduced number of caspase 3-positive neurons [5]. Therefore, DEX is considered to have a protective effect on various organs. However, there is a report that the organ-protective effect of DEX on the testis did not improve the pathological condition in the reperfusion model. [PERSON] et al. studied the testicular condition 6 h after a single intraperitoneal administration of DEX 60 min before torsion in rats. Compared to the torsion group, in the DEX + torsion group, the total oxidative ability (TOS) increased at 25 \(\upmu\)g/kg of administration of DEX, the total antioxidant ability (TAS) increased, and the oxidative stress index (OSI) decreased at 50 \(\upmu\)g/kg administration. It was reported that the testicular tissue was unchanged in the DEX + torsion group compared to the torsion group [6,7]. [PERSON] et al. ligated the rabbit spermatic cord for 4 h, administered 50 \(\upmu\)g/kg single intraperitoneally to DEX 1 h before reperfusion and removed the testes four weeks later. No significant differences in testis volume, spermatogenic cell count, MDA concentration, and SOD activity between the ligated group and DEX + ligated group were reported [8]. Therefore, there are no reports on the improvement in pathological conditions in testis reperfusion model animals by DEX administration, and it is possible that they do not have an organ-protective effect. In an in vitro study where DEX (0.015-1.5 \(\upmu\)M) was exposed to Leydig cells isolated from 2-week-old rats, [PERSON] et al. reported that 3B-HSD/p450 17A1/p450c11 mRNA expression and enzyme levels decreased, androgen synthesis was suppressed, and the number of reactive oxygen species (ROS)-induced apoptotic Leydig cells increased [9]. The studies in which DEX was treated alone are only in vitro studies, and there are no reports of in vivo studies. The in vivo administration of DEX alone may adversely affect the testis. In addition, since DEX reacts with cultured Leydig cells [9], Leydig cells might have a site of action for DEX. However, the localization of \(\alpha\)2A-adrenergic and imidazoline receptors in the testis is unknown.