br Conclusions According to our results

Conclusions According to our results we may suggest that FAS c.-671AG liothyronine sodium or G allele and FASLG gene c.-844T allele were not to be a risk factor, whereas FASLG gene c.-844TC genotype may be protective in the studied Turkish population. Because of the limited sample size in this study, further studies with larger groups from different ethnic backgrounds are necessary to reach the final conclusion.
Conflict of interest
Acknowledgments This work was supported by a grant from the Mustafa Kemal University Scientific Research Projects Unit, Hatay, Turkey (Project Number: 1204Y0137).
Introduction Ropivacaine is widely used in clinic as a local anesthetic; it specifically blocks sensory neurons but not motor neurons [1]. Ropivacaine, introduced as a propyl homologue of bupivacaine, is a pure S-(-)-enantiomer [2]. The lipid solubility of ropivacaine is less than bupivacaine, and its protein binding rate is up to 94% [2]. The anesthetic potency of ropivacaine is eight times that of procaine, and the anesthetic duration time of ropivacaine is four to eight times that of procaine [3,4]. Because adrenaline has no effect on the anesthetic potency and the anesthetic duration time of ropivacaine, ropivacaine not only can suppress the central nervous system but also excite the central nervous system [5]. Numerous studies have demonstrated that almost all local anesthetics have a degree of neurotoxicity, including ropivacaine [6]. High blood concentration of ropivacaine triggers both neurotoxicity and cardiovascular toxicity [7]. The adverse effects of caudal anesthesia by ropivacaine include hypotension, bradyarrhythmia, nausea, and anxiety [7]. Furthermore, several clinical trials proved that neurotoxicity and cardiovascular toxicity induced by ropivacaine were less than by bupivacaine [7,8]. Moreover, the presentation time of neurotoxicity symptoms induced by ropivacaine occurred earlier than that of cardiovascular toxicity symptoms [7]. Xing et al. reported that both ropivacaine and bupivacaine selectively impaired astrocytic mitochondrial function in primary rat hippocampal astrocyte and neuron cocultures [9]. Girsberger et al. showed that post-void residuals were significantly lower from ropivacaine than from bupivacaine for thoracic epidural analgesia, which reflected that ropivacaine triggered less impairment of detrusor function [8]. However, the mechanism of ropivacaine in triggering neurotoxicity remains unclear. To date, several studies have proven that the neurotoxicity of local anesthetics was related to cell death [10]. Moreover, Fas/FasL-mediated apoptosis is a key feature of acute human spinal cord injury [11].
Methods
Results
Discussion Ropivacaine is a local anesthetic drug belonging to the amino amide group, especially blocking the sensory neurons [1]. It was developed later than bupivacaine, which was found to be associated with cardiac arrest, especially in pregnant women [7]. Ropivacaine was reported to have less cardiotoxicity and neurotoxicity than bupivacaine in animal models [7]. Girsberger et al. compared the effect of thoracic epidural ropivacaine and bupivacaine on lower urinary tract function, and their results showed that ropivacaine had less detrimental influence on detrusor function [8]. However, ropivacaine was also reported to be linked to toxicities, including the potential for seizures, changes in behavior, and even cardiovascular collapse [16]. Ropivacaine neurotoxicity was reported in some kinds of cell models [10,17]. Lucchinetti et al. reported that local anesthetics reduced mesenchymal stem cell (MSC) proliferation, arrested the MSs at the G0/1 phase, and increased MSC apoptosis. The differentiation into osteoblasts was impaired, and in vitro wound healing was delayed after ropivacaine treatment [10]. Wen et al. reported that ropivacaine remarkably decreased cell viability and significantly increased the apoptosis rate of dorsal root ganglia (DRG) [17]. Consistent with the previous studies, our study demonstrated that ropivacaine suppressed cell viability and promoted neurogliocyte apoptosis.