鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

目的 观察鞘内注射c-Jun氨基末端蛋白激酶(c-Jun N-terminal protein kinase,JNK)特异性抑制剂SP600125对慢性压榨性损伤(chronic constriction injury,CCI)大鼠痛行为的影响.方法 雄性sD大鼠40只,随机分为5组(n=8). SP5组:CCI模型,鞘内注射SP600125 5μg;SP25组:CCI模型,鞘内注射SP600125 25 μg;SP50组:CCI模型,鞘内注射SP600125 50μg;DMSO组:CCI模型,鞘内注射2%二甲亚砜溶剂10 μl;Naive组:正常大鼠,鞘内注射SP600125 50μg.SP600125均溶于2%二甲亚砜10μl.CCI模型制作7 d后行鞘内注射,并测定大鼠机械缩足反射阈值(mechanical withdrawal threshold,MWT)及热缩足反射潜伏期(thermal withdrawal latency,TWL).结果 鞘内注射SP600125对正常大鼠的痛行为无影响.鞘内注射一定剂量SP600125能减轻CCI大鼠的机械痛敏及热痛敏.结论 鞘内注射一定剂量的SP600125能够减轻CCI大鼠的机械痛敏及热痛敏.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内预先注射氯诺昔康对福尔马林致痛大鼠的抗伤害作用

氯诺昔康是非甾体类抗炎药。本研究拟观察鞘内预先注射氯诺昔康对福尔马林致痛大鼠的抗伤害作用，为鞘内应用提供实验依据。     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

鞘内注射JNK特异性抑制剂SP600125对CCI大鼠痛行为的影响

Objective To observe the effect of intrathecal administration of SP600125 on both MWT and TWL of rats after chronic constriction injury (CCI) of the sciatic nerve. Methods 40 male SD rats were randomized to deride into 5 groups (n=8). Rats in group SP5 received SP600125 5 μg after CCI; rats in group SP25 received SP600125 25 μg after CCI; rats in group SP50 received SP600125 50 μg after CCI; rats in group DMSO received 2% DMSO 10 μl after CCI; rats in group Naive received SP600125 50 μg without sciatic nerve injury. SP600125 was dissolved in 10 μl 2%DMSO solvent. On the 7th day after CCI, MWT and TWL were determined with yon Frey filaments and thermal radiation apparatus repectively after intrathecal administration of SP600125. Results Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI rather than normal rats. Conclusion Intrathecal administration certain dosage of SP600125 could attenuate the established mechanical allodynia and thermal hyperalgesia induced by CCI.     

异丙酚对大鼠急性心肌缺血性内脏痛的镇痛作用

目的探讨异丙酚对大鼠心肌缺血性内脏痛的镇痛作用。方法健康成年雄性SD大鼠,实验分两部分。第一部分：将找到丘脑束旁核伤害性刺激反应神经元(NSRN)且对冠状动脉结扎(CAO)敏感的大鼠24只随机分为4组(n=6)：CAO+生理盐水组(CAO组)；P_(0．02)组：CAO+0．02 mg·kg~(-1)异丙酚；P_(0．2)组：CAO+0．2 mg·kg~(-1)异丙酚；P_2组：CAO+2 mg·kg~(-1)异丙酚,每只大鼠记录1个NSRN。异丙酚用生理盐水稀释到0．1 ml,在CAO后15 min尾静脉注射。整个实验从CAO开始连续记录NSRN放电频率60min；第二部分,6只大鼠尾静脉注射异丙酚2mg·kg~(-1)后观察对大鼠的麻醉效果。结果异丙酚(0．2、2mg·kg~(-1))能明显抑制CAO引起的NSRN放电频率的增加(P＜0．05),2 mg·kg~(-1)作用更明显,且该剂量的异丙酚对大鼠无麻醉作用。结论亚麻醉剂量的异丙酚对大鼠急性心肌缺性内脏痛具有一定的镇痛作用,且呈剂量依赖性。     

异丙酚注射痛预测人工流产术后疼痛程度的准确性

目的 评价异丙酚注射痛预测术后疼痛程度的准确性.方法 拟行无痛人工流产手术的患者7l例,年龄20～40岁,ASA Ⅰ或Ⅱ级.以0.5 ml/s的速率静脉输注1%异丙酚2 mg/kg,当异丙酚给药量达1/3时暂停给药,采用口语等级量表评分法(VRS)评价异丙酚注射痛,VRS评分≥1分为发生注射痛,之后再给予剩余量异丙酚完成麻醉诱导.术后20 min时采用VAS评分法评价患者静卧以及下床站立时的疼痛程度,静卧时VAS评分≥30分为发生术后疼痛.计算异丙酚注射痛预测术后疼痛程度的灵敏度和特异度.结果 异丙酚注射痛发生率为66%,VRS评分与术后静卧以及活动时VAS评分呈正相关(r=0.561,P<0.01;r=0.608,P<0.01).异丙酚注射痛预测术后疼痛的灵敏度为96%,特异度为52%.结论 术前异丙酚注射痛是预测人工流产术后患者疼痛程度的可靠指标.     

异丙酚对福尔马林致痛大鼠脊髓Fos表达的影响

目的：研究脊髓结构对福尔马林痛刺激的反应及异丙酚对其的影响。方法：采用福尔马林致痛模型及c-fos基因免疫组织化学方法（ABC法）。SD大鼠30只,随机分为6组：2．5％福尔马林注射于大鼠一侧前爪掌心皮下组、福尔马林痛刺激后腹腔注射异丙酚组、福尔马林痛刺激后腹腔注射同等容量生理盐水组、腹腔注射异丙酚后再行福尔马林痛刺激组、腹腔注射同等剂量异丙酚组、腹腔注射等容量生理盐水6组,取脊髓切片。结果：（1）予福尔马林痛刺激后,刺激侧脊髓背角出现大量Fos免疫样阳性神经元,I层及Ⅱ层外带的内侧部最为密集;（2）痛刺激之前或之后给予异丙酚,脊髓背角各层Fos免疫样阳性神经元的数量均减少（P＜0．01）,痛刺激之前给药效果优于痛后给药（P＜0．05）;（3）单纯腹腔注射异丙酚或生理盐水,脊髓未见或偶见Fos免疫样阳性神经元。结论：同侧相应脊髓节段的某些神经元参与了化学性致痛信息的传导和调控,异丙酚可抑制这些神经元的活动,从而产生一定的抗伤害作用。     

脊髓GABAA受体在异丙酚对内脏痛大鼠镇痛效应中的作用

目的 评价脊髓γ-氨基丁酸A(GABAA)受体在异丙酚对内脏痛大鼠镇痛效应中的作用.方法成年健康雌性SD大鼠,体重190～240 g,进行鞘内置管,并于直肠粘膜下注射10%福尔马林100 μl.取鞘内置管成功的大鼠32只,采用随机数字表法,将其随机分为4组(n=8):二甲基亚砜组(D组)、异丙酚组(P组)、荷包牡丹碱组(B组)和荷包牡丹碱+异丙酚组(BP组).D组、P组和B组分别鞘内注射二甲基亚砜5 μl、异丙酚10 μg、荷包牡丹碱2 μg;BP组先鞘内注射荷包牡丹碱2 μg,10min后鞘内注射异丙酚10 μg.注射福尔马林2 h时,取脊髓L5～S1节段,采用免疫组化法测定FOS蛋白表达水平.结果 与D组和B组比较,P组脊髓FOS蛋白表达下调(P＜0.05);D组和B组脊髓FOS蛋白表达差异无统计学意义(P＞0.05);与P组比较,BP组脊髓FOS蛋白表达上调(P＜0.05).结论 异丙酚可通过脊髓GABAA受体介导,对内脏痛大鼠产生镇痛效应.

Abstract：

Objective To evaluate the role of spinal cord CABAA receptors in the analgesic effect of propofol on visceral pain in rats. Methods Adult female SD rats, weighing 190-240 g, were used in this study.The animals were anesthetized with intraperitoneal ketamine 50-100 mg/kg. Intrathecal (IT) catheters were placed at L5-6 interspace according to the technique described by Storkson et al. Thirty-two animals in which IT catheters were successfully placed were randomly divided into 4 groups ( n = 8 each) : dimethyl sulphoxide (DMSO) group (group D), propofol group (group P), bicuculline group (group B) and bicuculline + propofol group (group B +P). Visceral pain was induced by injecting 10% formalin 100 μl underneath the mucous membrane of rectum.Groups D, P and B received IT DMSO 5 μl, propofol 10 μg and bicuculline 2 μg respectively. Group BP received IT bicuculline 2 μg and then IT propofol 10 μg 10 min later. The L5-S1 segment of the spinal cord was removed 2 h after formalin injection to determine FOS protein expression by hnmuno-histochemistry. Results Compared with groups D and B, FOS protein expression was significantly down-regulated in group P ( P ＜ 0.05 ) . There was no significant difference in FOS protein expression between groups D and B ( P ＞ 0.05) . FOS protein expression was significantly up-regulated in group BP compared with group P ( P ＜ 0.05) . Conclusion Propofol has analgesic effect on visceral pain in rats through spinal cord GABAA receptor action.     

大鼠肝缺血/再灌注后肝细胞凋亡的评价及异丙酚对细胞凋亡的影响

目的 观察大鼠肝脏缺血再灌注后肝窦内皮细胞凋亡及异丙酚对肝脏细胞凋亡的影响。方法 选用健康SD雄性大鼠24只,随机分为三组(n=8):A组,肝脏缺血30 min再灌注6 h,再灌注即刻从股静脉输入生理盐水10ml·kg-1·h-1 60 min;B组,再灌注即刻静脉注射异丙酚20 mg/kg,继之输入5％异丙酚50 mg·kg-1·h-1 h;C组,给予假手术处理,未予缺血,余处理同A组。再灌注6 h后取肝组织标本行病理组织学观察,同时测定血浆ALT活性和肝组织MDA含量的变化。采用DNA琼脂糖凝胶电泳、TUNEL染色观察细胞凋亡的情况。结果与C组相比,A组凋亡的肝细胞和肝窦内皮细胞明显增加,且凋亡的细胞主要是肝窦内皮细胞,肝细胞凋亡和坏死则较少。与A组相比,再灌注6 h B组TUNEL阳性肝细胞和肝窦内皮细胞数明显减少(p<0.01),肝组织DNA片段形成也明显减少。同时,B组肝组织坏死程度、血浆ALT活性和肝组织MDA含量均明显低于A组(JD<0.01)。电镜显示B组肝细胞和肝窦内皮细胞损伤也明显轻于A组。结论 细胞凋亡是再灌注早期肝脏细胞死亡的重要机制,肝窦内皮细胞凋亡是再灌注早期肝脏细胞死亡的主要特征。异丙酚可以减少再灌注后的肝脏细胞凋亡和坏死,其抗氧化作用是其减少再灌注后的肝脏细胞凋亡的机制。     

老年患者匀速注射丙泊酚的量效关系及其对痛阈的影响

目的 观察在不同剂量丙泊酚镇静下老年患者BIS、MAP及HR的变化趋势及其对痛阈的影响.方法 选择年龄65～89岁,ASA Ⅰ或Ⅱ级.行择期手术的患者40例,随机均分为四组,分别接受4个不同剂量的丙泊酚匀速静脉注射.即Ⅰ组0.75 mg/kg、Ⅱ组1 mg/kg、Ⅲ组1.25mg/kg、Ⅳ组1.5 mg/kg,注射时间均为1 min.改良警觉/镇静(OAA/S)评分法测各组丙泊酚镇静催眠深度.微电流致痛法测各组痛阈.分别于注药前、注药后1 min测四组BIS、HR、MAP及痛阈低值和高值.结果 注药后1 min,Ⅰ、Ⅱ组OAA/S评分均达到2或1分,Ⅲ、Ⅳ组0分.Ⅰ、Ⅱ组BIS值分别是70.4±12.3、68.7±6.4,Ⅲ、Ⅳ组的BIS是56.3±13.3及48.3±9.8,其中注药后1 minⅢ、Ⅳ组的BIS值分别显著低于Ⅰ、Ⅱ组(P<0.05或P<0.01).丙泊酚用药剂量与BIS之间呈显著负相关(r=-0.648,P<0.01),回归方程:BIS=96.626-31.719×丙泊酚剂量(r2=0.419,P<0.01).注药后1min,四组的MAP均显著低于注药前(P<0.01);组间比较,Ⅳ组显著低于同时点的Ⅰ、Ⅱ组(P<0.05),而注药前后各组HR值组内、组间比较差异均无统计学意义.注药后1 min的Ⅲ、Ⅳ组的痛阈低值高于注药前,也高于同时点的Ⅰ、Ⅱ组(P<0.05或P<0.01);两组的痛阈高值也显著高于注药前(P<0.05或P<0.01).结论 随着丙泊酚用药剂量的增加,BIS值相应降低,两者呈线性负相关.1.25、1.5 mg/kg的丙泊酚单次匀速静注后可满足老人全麻术中镇静催眠的需求,并使痛阈水平上升,疼痛敏感性降低.     

丙泊酚诱导Fos蛋白与脑啡肽在大鼠脊髓共同表达

目的;研究丙泊酚在脊髓的镇痛机制。方法：SD大鼠12只,随机分为对照组,丙泊酚I组（20mg/kg),丙泊酚II组（100mg/kg),药物经腹腔注射,运用免疫组织化学双标法观察丙泊酚诱导大鼠脊髓内Fos蛋白与脑啡肽（ENK）的表达。结果：对照组脊髓中可见较多ENK染色阳性神经元（ELIN）,偶见Fos染色阳性神经元（FLIN）散在分布,无Fos,ENK双标记神经元（ELI／ELIN）;丙泊酚组可见较多ELIN,FLIN分布,而且可见FLI／ELIN,主要分布于脊髓后角,三种染色阳性神经元数量明显大于对照组（P＜0．05）,而且丙泊酚两组音差异显著（P＜0．05）,结论：丙泊酚可增加脊髓内ENK含量,诱导Fos蛋白与脑啡肽共同表达,诱导c-fos基因表达调节前脑啡肽基因,增加ENK含量可能是丙泊酚在脊髓重要的镇痛机制。     

An effective dose of ketamine for eliminating pain during injection of propofol: A dose response study

Background and purpose

Ketamine can completely eliminate pain associated with propofol injection. However, the effective dose of ketamine to eliminate propofol injection pain has not been determined. The purpose of this study was to determine the effective dose of ketamine needed to eliminate pain in 50% and 95% of patients (ED50 and ED95, respectively) during propofol injections.

Methods

This study was conducted in a double-blinded fashion and included 50 patients scheduled for elective gynecological laparoscopy under general anesthesia. The initial dose of ketamine used in the first patient was 0.25 mg/kg. The dosing modifications were in increments or decrements of 0.025 mg/kg. Ketamine was administered 15 seconds before injecting propofol (2.5 mg/kg), which was injected at a rate of 1 mL/s. Patients were asked to rate their pain during propofol injection every 5 seconds using a 0–3 pain scale. The highest pain score was recorded. The ED50, ED95 and 95% confidence intervals (CI) were determined by probit analyses.

Results

The dose of ketamine ranged from 0.175 to 0.275 mg/kg. The ED50 and ED95 of ketamine for eliminating pain during propofol injection were 0.227 mg/kg and 0.283 mg/kg, respectively (95%CI: 0.211–0.243 mg/kg and 0.26–0.364 mg/kg, respectively).

Conclusion

Ketamine at an approximate dose of 0.3 mg/kg was effective in eliminating pain during propofol injection.     

脊髓阿片受体在异丙酚对大鼠抗伤害性效应中的作用

目的 探讨脊髓阿片受体在异丙酚对大鼠抗伤害性效应中的作用.方法 雄性SD大鼠,体重220～280 g,选取鞘内置管成功的大鼠90只,随机分为9组(n=10):P组、D组和A组分别鞘内注射异丙酚10μg、二甲基亚砜(DMSO)5μl,人工脑脊液5μl;PN组和DN组分别鞘内注射异丙酚10μg、DMSO 5μl,5 min后均鞘内注射纳洛酮15 μg;PC组和DC组分别鞘内注射异丙酚10 μg、DMSO 5 μl,5 min后均鞘内注射高选择性μ受体拮抗剂CTOP 1 μg,PI组和DI组分别鞘内注射异丙酚10μg和DMSO 5 μl,5 min后均鞘内注射高选择性δ受体拈抗剂ICI 174,864 1μg.于首次给药前(T0)、首次给药后10 min(T1)、20 min(T2)、40 min(T3)时采用热水缩尾法测定痛阈,并计算痛阈提高百分率.结果 与T0时比较,T1,2时P组、PN组、PI组和PC组痛阈升高(P<0.05);P组痛阈高于D组,PN组痛阈高于DN组,PI组痛阈高于DI组,PC组痛阈高于DC组(P<0.05);与T1和T2时比较,T3时P组、PN组、PC组和PI组痛阈提高百分率降低(P<0.05);与P组和PC组比较,PN组和PI组首次给药后痛阈提高百分率降低(P<0.05).结论 异丙酚通过大鼠脊髓δ受体介导产生抗伤害性效应.