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出 处:《中华麻醉学杂志》1998年第12期714-716,共3页Chinese Journal of Anesthesiology
摘 要:目的:通过测定脑脊液和血浆普鲁卡因浓度,探讨静脉普鲁卡因镇痛的机制。方法:ASA Ⅰ~Ⅱ级择期手术患者6例,无术前用药。静注芬太尼、维库溴铵和异丙酚行全麻诱导,气管内插管。普鲁卡因以1mg·kg^(-1)·min^(-1)速率静滴,复合异氟醚维持全麻,控制呼吸。静滴普鲁卡因10、20、30、60分和停药5、15、30、60分时,取脑脊液和动脉血测普鲁卡因浓度。结果:静滴普鲁卡因30分血浆浓度达稳态峰值14.80±2.95μg/ml;停药后血浆浓度迅速下降。静滴普鲁卡因时,脑脊液浓度增加缓慢,60分时(3.65±1.00μg/ml)达血浆浓度的25%。停药后脑脊液浓度继续上升,15分后脑脊液浓度达峰值4.47±0.94μg/ml,相当于血浆浓度(3.30±1.24μg/ml)的1.58倍。脑脊液普鲁卡因浓度下降缓慢,停药60分时仍有1.85±0.19μg/ml。结论:静脉普鲁卡因经简单扩散方式缓慢进入脑脊液,引起延迟性全蛛网膜下腔阻滞。静脉普鲁卡因不直接抑制大脑皮层,而通过减少伤害性刺激向皮层的传递,间接使皮层处于抑制状态。Objective:To investigate the mechanism of intravenous procaine analgesia. Method: Six adult patients, ASA grade Ⅰ-Ⅱ, scheduled for abdominal surgery were investigated. Anesthesia was induced with intravenous fentanyl and propofol. Endotracheal intubation was facilitated with vecuronium. Anesthesia was maintained with continuous intravenous infusion of procaine(1mg·kg^(-1)·min^(-1))and inhalation of isoflurane. All patients were artifically ventilated with 100% O_2. Cerebrospinal fluid(CSF)and plasma concentrations of procaine were measured with gascbromatography 10,20,30 and 60 min following initiation of the constant infusion of procaine,at 5th, 15th, 30th and 60th min after the discontinuation. Result: Plasma steady-state levels were achieved within 30 min after commencement of the continuous infusion of procaine, The mean plasma steady-state level was 14.8±2.95μg/ml. Fifteen min after discontinuing the procaine infusion, 78% of plasma procaine content was eliminated. CSF steady-stale level was not achieved until 15 min after discontinuing the procaine infusion. The mean CSF steady state level was 4.47±0.94μg/ml. The elimination of the procaine in CSF was quite slow,and at 60th min after discontinuing the infusion,the mean CSF procaine level was 1.85±0.19μg/ml. Conclusion: The delayed total subarachnoid blockade induced by procaine infusion may be the mechanism of intravenous procaine analgesia.
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