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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 by measuring the concentration of procaine in cerebrospinal fluid and plasma. Methods: Sixteen patients undergoing ASA Ⅰ ~ Ⅱ elective surgery without premedication. Intravenous fentanyl, vecuronium and propofol under general anesthesia induction, endotracheal intubation. Procaine infusion at a rate of 1mg · kg -1 (min -1), combined with isoflurane to maintain general anesthesia, control of breathing. Intravenous procaine 10,20,30,60 points and withdrawal 5,15,30,60 points, take CSF and arterial blood concentrations of procaine. Results: The plasma concentration of intravenous procaine at 30 minutes reached the peak value of steady state of 14.80 ± 2.95μg / ml; the plasma concentration decreased rapidly after the drug was stopped. Cerebrospinal fluid concentration increased slowly with intravenous procaine, reaching 25% of plasma concentration at 60 min (3.65 ± 1.00 μg / ml). After discontinuation of cerebrospinal fluid concentration continued to rise after 15 minutes CSF concentration of 4.47 ± 0.94μg / ml, equivalent to 1.58 times the plasma concentration (3.30 ± 1.24μg / ml). Cerebrospinal fluid procaine concentration decreased slowly, still with 1.85 ± 0.19μg / ml 60 minutes. CONCLUSION: Venous procaine slowly enters cerebrospinal fluid via simple diffusion and causes delayed total arachnoid block. Intravenous procaine did not directly inhibit the cerebral cortex, but indirectly reduced the cortex by reducing noxious stimulation to the cortex.