Does lidocaine provoke clinically significant vasospasm?

Two cases with peripheral vasoconstriction possibly caused by topical application of lidocaine were reported. A potential risk of vasospasm provoked by lidocaine may be a pitfall for anesthesiologists because lidocaine is commonly considered a vasodilator.     

Lidocaine versus ropivacaine for continuous interscalene brachial plexus block after open shoulder surgery

BACKGROUND: This study compared the postoperative infusion of 1% lidocaine and 0.2% ropivacaine for continuous interscalene analgesia in patients undergoing open shoulder surgery. METHODS: Forty patients undergoing open shoulder surgery received an interscalene brachial plexus block with 30 ml of either 1.5% lidocaine (n = 20) or 0.5% ropivacaine (n = 20), followed by a continuous patient-controlled interscalene analgesia with 1% lidocaine or 0.2% ropivacaine, respectively. A blinded observer recorded the quality of analgesia and recovery of motor function during the first 24 h of infusion. RESULTS: Onset of the block occurred after 7.5 (5-40) min with lidocaine and 30 (10-60) min with ropivacaine (P = 0.0005). Postoperative pain intensity was higher with lidocaine than ropivacaine for the first 8 h of infusion. The ratio between boluses given and demanded from the pump was 0.5 (0.13-0.7) with lidocaine and 0.7 (0.4-1.0) with ropivacaine (P = 0.005). Rescue IV tramadol was required during the first 24 h of infusion by 16 patients of the lidocaine group (84%) and eight patients of the ropivacaine group (46%) (P = 0.05). At the 16 h and 24 h observation times a larger proportion of patients receiving ropivacaine had complete regression of motor block (70% and 95%) than patients receiving lidocaine (50% and 55%) (P = 0.05 and P = 0.013, respectively). CONCLUSIONS: Although 1% lidocaine can be effectively used for postoperative patient-controlled interscalene analgesia, 0.2% ropivacaine provides better pain relief and motor function.     

The anesthetic onset and duration of a new lidocaine/prilocaine gel intra-pocket anesthetic (Oraqix) for periodontal scaling/root planing

BACKGROUND: A new non-injection anesthetic, lidocaine/prilocaine gel (Oraqix, AstraZeneca) in a reversible thermosetting system, has been developed to provide local anesthesia for scaling/root planing (SRP). The aim of this study was to determine the anesthetic onset and duration of the gel for SRP in patients with periodontitis. METHODS: 30 patients were randomized to either 30 s, 2 min, or 5 min of treatment with the gel prior to SRP of a tooth. The gel was applied to periodontal pockets with a blunt applicator. On completion of the SRP of each tooth (2-3 teeth treated/patient), the patients rated their pain on a 100-mm visual analogue scale (VAS). RESULTS: The median VAS pain score was 7.5 mm in the 30-s group, 28.5 mm in the 2-min group, and 15.5 mm in the 5-min group, with a significant difference between the 30-s and 2-min groups (p=0.03). In 2 patients in the 5-min group, but none in the other groups, the SRP was interrupted due to pain. The mean duration of anesthesia measured as pain on probing were 18.1, 17.3, and 19.9 min in the 30-s, 2-min, and 5-min groups, respectively. There were no reports of numbness of the tongue, lip, or cheek, neither were there any adverse local reactions in the oral mucosa. The gel was easy to apply and did not interfere with the SRP procedure. CONCLUSION: Oraqix provides anesthesia after an application time of 30 s, with a mean duration of action of about 17 to 20 min.     

Pre-emptive lidocaine inhibits arterial vasoconstriction but not vasopressin release induced by a carbon dioxide pneumoperitoneum in pigs

Background. We assessed the preventive effects of i.v. or i.p.lidocaine administration on increases in vascular resistanceproduced by carbon dioxide pneumoperitoneum and related thisto vasopressin release. Methods. Carbon dioxide pneumoperitoneum (14 mm Hg intra-abdominalpressure) was performed in 32 anaesthetized young pigs and monitoredusing a pulmonary artery catheter. Animals received lidocaine0.5% (0.5 mg kg^–1) i.v. (n=9) or 2 ml kg^–1 i.p.(n=9) or saline (n=5) 15 min before the pneumoperitoneum andwere compared with a control group (n=9). Results. I.V. and i.p. lidocaine inhibited increases in meansystemic vascular resistance induced by the pneumoperitoneum[2109 (SD 935) and 2282 (895), respectively, vs 3013 (1067)dyne s^–1 cm^–5 in the control group]. Cardiac outputwas increased. Plasma lidocaine concentrations were threefoldhigher after i.p. administration than after i.v. administration.After pneumoperitoneum insufflation, plasma lysine-vasopressinconcentrations increased in all groups (control 74%, saline65%, i.p. lidocaine 57%, i.v. lidocaine 74%). Conclusions. I.V. and i.p. lidocaine blunted systemic vascularresponses to carbon dioxide pneumoperitoneum in pigs, but withoutinfluencing vasopressin release. Br J Anaesth 2003; 90: 343–8     

Evaluation of the Greenbaum sub-Tenon's block

A prospective, randomized blind study was conducted in 40 patientsundergoing phacoemulsification and posterior chamber intraocularlens implantation. They received anaesthetic infiltration of2% lidocaine with 1:200 000 epinephrine and hyaluronidase150 U ml^–1 in a volume of 2, 3, 4 or 5 mlinto the sub-Tenon’s fascial space through a Greenbaumcannula after a conjunctival incision. Reduction of ocular movements,anaesthesia, pain on injection and any incidental complicationswere recorded. Akinesia and anaesthesia occurred within 5 minwith 4 and 5 ml of local anaesthetic, and no supplementaryinjections were required. There were marked reductions in thefrequency of forced eyelid movements with these volumes. Chemosisand conjunctival haemorrhage were noted in the majority of patientsbut caused no intraoperative problems. Approximately 10–15%of patients reported slight discomfort at the time of injection.Four to 5 ml of 2% lidocaine with 1:200 000 epinephrineand 150 U ml^–1 of hyaluronidase is the optimumvolume to achieve adequate akinesia, anaesthesia and reductionof lid movements during the Greenbaum sub-Tenon’s block. Br J Anaesth 2001; 87: 631–3     

利多卡因、异丙酚对缺血再灌注心肌细胞膜Na^＋—K^＋—ATP酶、肌浆网Ca^2＋—ATP酶活性的影响

目的观察利多卡因、异丙酚对缺血再灌注心肌细胞膜Na _K _ATP酶、肌浆网Ca2 _ATP酶活性的影响。方法SD大鼠48只 ,随机均分为6组。假手术组 ;生理盐水组 ;利多卡因5mg·kg-1 组 ;利多卡因10mg·kg-1 组 ;异丙酚300μg·kg-1·min-1 组 ;异丙酚1000μg·kg-1·min-1 组。于缺血前5min ,生理盐水及利多卡因经股静脉注射给药(30s内注射完) ;异丙酚持续输注至缺血开始时为止。结扎冠脉左前降支 ,造成左室前壁相应心肌组织缺血15min ,然后松开结扎线再灌注10min ,应用分光光度法测定心肌细胞膜Na _K _ATP酶、肌浆网Ca2 _ATP酶活性。结果利多卡因可明显地促进肌浆网Ca2 _ATP酶活性的恢复(P<0.05) ,大剂量时还促进心肌细胞膜Na _K _ATP酶活性的恢复(P<0.05)。异丙酚可显著地促进心肌细胞膜Na _K _ATP酶活性的恢复(P<0.05 ,P<0.001),大剂量时促进肌浆网Ca2 _ATP酶活性的恢复(P<0.05)。结论利多卡因、异丙酚可促进再灌注期间心肌细胞膜Na _K _ATP和肌浆网Ca2 _ATP酶活性的恢复 ,从而抑制钙超载而减轻心肌缺血再灌注损伤。     

高效毛细管电泳法测定利多卡因代谢产物单乙基甘氨酰二甲苯胺

目的 :建立一种测定利多卡因代谢产物单乙基甘氨酰二甲苯胺 (MEGX)含量的高效毛细管电泳法。方法 :用50mmol/L硼酸缓冲液 (pH =8.8)为电泳电解液 ,电压 1 2kV ,运行电流 1 8.8～ 2 3 .2 μA ,检测波长 2 1 4nm ,有效毛细管长度 50cm ,管径 50 μm ,氨茶碱为内标 ,展开 1 2min。 8只昆明种小白鼠腹腔注射 0 .2 %利多卡因 4 0mg/kg ,用本法测定其 5h尿液中MEGX累积排泄量。结果 :MEGX迁移时间 7.8min ,氨茶碱迁移时间 1 0 .7min。MEGX含量为 0 .0 62～1 .0mg/ml时 ,其浓度与色谱峰面积线性关系良好 ,r =0 .9991 ,日内、日间变异系数均小于 7.8% ,回收率为98.4 %～ 1 0 1 .6% ,常用 3 0种药物对其无干扰。 8只小鼠MEGX累积排泄量为 ( 2 95.2± 55.2 ) μg ,其中游离型MEGX为 4 4.7% ,结合型为 55.3 %。结论 :该方法简单、快速、灵敏 ,特异性和重现性良好 ,具有较强实用价值。     

碳酸利多卡因在硬膜外麻醉中的药物动力学及药效学

 目的:对碳酸利多卡因在硬膜外麻醉中的临床药物动力学及药效学特性进行探讨。方法:研究对象为15例实施硬膜外麻醉患者。采用荧光偏振免疫分析方法(FPIA)测定利多卡因血药浓度;放射免疫方法测定血浆肾素浓度。通过临床观察及测定血浆肾素水平评价药效学;将药代动力学及药效学研究结果与其盐酸盐进行比较。结果:药物动力学参数:达峰时间,达峰浓度,吸收速率常数及末端相半衰期分别为(0.30±0.04)h,(3.96±1.14)mg·L^-1,(10.92±2.36)h^-1和(1.95±0.08)h;药效学参数;麻醉起效时间,阻滞完善时间及麻醉持续时间分别为(4.38±0.78)min,(8.23±1.84)min和(57.22±10.35)min。结论:碳酸利多卡因吸收速率明显高于其盐酸盐;达峰时间亦快于其盐酸盐;体内消除半衰期与其盐酸盐的消除半衰期接近。临床麻醉杭州起效时间及阻滞完善时间快于盐酸利多卡因。研究结果证明:碳酸利多卡因用于硬膜外麻醉起效较快,但体内消除过程无明显改变。     

Assessing the permeability of the rat sciatic nerve epineural sheath against compounds with local anesthetic activity: an ex vivo electrophysiological study

Abstract

Studies have shown that the sciatic nerve epineural sheath acts as a barrier and has a delaying effect on the diffusion of local anesthetics into the nerve fibers and endoneurium. The purpose of this work is to assess and to quantify the permeability of the epineural sheath. For this purpose, we isolated the rat sciatic nerve in a three-chamber recording bath that allowed us to monitor the constant in amplitude evoked nerve compound action potential (nCAP) for over 24?h. For nerves exposed to the compounds under investigation, we estimated the IT₅₀ the time required to inhibit the nCAP to 50% of its initial value. For desheathed nerves, the half-vitality time was denoted as IT₅₀(?) and for the ensheath normal nerves as IT₅₀(+). There was no significant difference between the IT₅₀ of desheathed and ensheathed nerves exposed to normal saline. The IT₅₀(?) for nerves exposed to 40?mM lidocaine was 12.1?±?0.95?s (n?=?14) and the IT₅₀(+) was 341.4?±?2.49?s (n?=?6). The permeability (P) coefficient of the epineural sheath was defined as the ratio IT₅₀(+)/IT₅₀(?). The P coefficient for 40?mM lidocaine and linalool was 28.2 and 3.48, correspondingly, and for 30?mM 2-heptanone was 4.87. This is an indication that the epineural sheath provided a stronger barrier against lidocaine, compared to natural local anesthetics, linalool and 2-heptanone. The methodology presented here is a useful tool for studying epineural sheath permeability to compounds with local anesthetic properties.     

Decreasing the toxic potential of intravenous regional anaesthesia

In an attempt to reduce the dose of local anaesthetic agent during intravenous regional anaesthesia (IVRA) of the upper limb, we have used a forearm tourniquet in 12 adult volunteers. The volume of the forearm venous system was predetermined angiographically. We performed IVRA with three solutions of lidocaine (0.25, 0.375, 0.5 per cent) administered in a volume equal to the forearm venous system. Angiographic results indicate that: a forearm tourniquet provides adequate vascular isolation; the volume of the forearm venous system can be correlated with body weight; the progression of the fluid in the venous system follows a pattern that is similar for all patients with the small veins of the distal forearm and proximal hand being filled last. With this technique, lidocaine 0.5 per cent resulted in a dose of 1.5 mg.kg-1 and provided excellent analgesia. Lower concentrations were unsatisfactory. We conclude that the use of a forearm tourniquet allows reduction of the local anaesthetic dose to a non-toxic level and thus increases the safety of IVRA.