论文部分内容阅读
BACKGROUND: Somatosensory evoked potential (SEP) has become a method with higher sensitivity and specificity than electroencephalogram in detecting the brain function and the region, range and degree of ischemia. However, the effects of ligustrazine on SEP is still not clear. OBJECTIVE: To study the protective effects of ligustrazini injection on cerebral ischemiareperfusion injury. DESIGN: Auto-control study, random grouping. SETTING: Qilu Hospital of Shandong University. MATERIALS: The experiment was completed in the Cerebral Functional Room of Qilu Hospital Affiliated to Shandong University from March 2002 to June 2004. A totally of 24 healthy Harbin rabbits were randomly divided into blank control group (n=8), model control group (n=8) and ligustrazine treatment group (n=8). Hydrochloric ligustrazine injection, 40 mg/2 mL each ampoule, was provided by the Third Pharmaceutical Factory of Beijing (certification: 93035236273). The main component was hydrochloric ligustrazine and the chemical name was 2, 3, 5, 6-tetramethyl pyrazine hydrochloride. METHODS: ① Modeling method: The bilateral common carotid artery ligation was adopted to make the model. ② Index of cerebral functional lesion evaluated with SEP during ischemia-reperfusion: DISA 2000C neuromyoeletrometer provided by Dantec Electronics Ltd, Denmark was used to detect SEP. ③ Interventional process: Blank control group: The latencies and amplitudes of SEP were measured before injection with 1.5 mg/kg ligustrazine and at the points of 15 minutes, 20 minutes, 30 minutes, 60 minutes, 90 minutes and 120 minutes after injection. Ligustrazine treatment group: Rabbits were injected with 1.5 mg/kg ligustrazine, and those of model control group were injected the same volume of saline. Thirty minutes later, the bilateral common carotid artery of the rabbits all had been ligated for 30 minutes, and then reperfused for 120 minutes. The latencies and amplitudes of SEP were measured before injection, before ligation, at the points of 1 minute, 5 minutes, 10 minutes, 15 minutes, 20 minutes, 25 minutes and 30 minutes after ligation, and at the points of 5 minutes, 10 minutes, 15 minutes, 20 minutes, 30 minutes, 60 minutes, 90 minutes and 120 minutes after reperfusion. ④ Evaluating criteria: Normal values of P-wave latencies and amplitudes were (19.34±3.18) ms and (4.55±1.43) μV. Average value before injection in blank control group and average values before injection, after injection and before ligation in ischemia-reperfusion group were regarded as control criteria to evaluate changes of Pwave latencies and amplitudes after experiment. MAIN OUTCOME MEASURES: P-wave latencies and amplitudes of SEP in the three groups. RESULTS: A total of 24 rabbits were involved in the final analysis without any loss. ① Blank control group: The P-wave latencies delayed markedly at each time point after injection. Compared with that before injection, there was a significant difference (P < 0.05-0.01). The P-wave amplitudes did not fluctuate noticeably all the time after injection, but significantly decreased when compared with those before injection (P < 0.05-0.01). ② Ischemia-reperfusion group: The P-wave latencies delayed and amplitudes decreased in the rabbits with cerebral ischemiareperfusion at all points of time during cerebral ischemia-reperfusion, and there was significant difference when compared with the levels before ischemia (P < 0.05). When ligustrazine was injected, the latencies and amplitudes changed less, and as compared with the levels before ischemia, the difference was not significant (P > 0.05). CONCLUSION: ① Ligustrazine can inhibit P-wave latencies and amplitudes of SEP of normal rabbits. ② Ligustrazine can improve P-wave latencies and amplitudes of SEP of rabbits with cerebral ischemia-reperfusion injury.
BACKGROUND: Somatosensory evoked potential (SEP) has become a method with higher sensitivity and specificity than electroencephalogram in detecting the brain function and the region, range and degree of ischemia. However, the effects of ligustrazine on SEP is still not clear. OBJECTIVE: To : The experiment was completed in the Cerebral Functional Room of Qilu Hospital Affiliated to Shandong University from March 2002 to June 2004. A totally of 24 healthy Harbin rabbits were randomly divided into blank control group (n=8), model control group (n=8) and ligustrazine treatment group (n=8). Hydrochloric ligustrazine injection, 40 mg/ 2 mL each ampoule, was provided by the Third Pharmaceutical Factory of Beijing (certification: 93035236273). The main component was hydrochloric ligustrazine and the c Hemical name was 2, 3, 5, 6-tetramethyl pyrazine hydrochloride. METHODS: 1 Modeling method: The bilateral common carotid artery ligation was adopted to make the model. 2 Index of cerebral functional lesion evaluated with SEP during ischemia-reperfusion: DISA 2000C Neuromyoeletrometer provided by Dantec Electronics Ltd, Denmark was used to detect SEP. 3 Interventional process: Blank control group: The latencies and amplitudes of SEP were measured before injection with 1.5 mg/kg ligustrazine and at the points of 15 minutes, 20 minutes, 30 Ligustrazine treatment group: Rabbits were injected with 1.5 mg/kg ligustrazine, and those of model control group were injected the same volume of saline. Thirty minutes later, the bilateral common carotid artery Of the rabbits all had been ligated for 30 minutes, and then reperfused for 120 minutes. The latencies and amplitudes of SEP were measured before injection, before ligation, At th0 minutes, 1 minute, 5 minutes After 4 minutes and 120 minutes after reperfusion. 4 Evaluating criteria: Normal values of P-wave latencies and amplitudes were (19.34±3.18) ms and (4.55±1.43) μV. Average value before injection in blank control group and average values before injection, after p and wave latencies and amplitudes after experiment. MAIN OUTCOME MEASURES: P-wave latencies and amplitudes of SEP in the three groups. RESULTS: A total of 24 Rabbits were involved in the final analysis without any loss. 1 Blank control group: The P-wave latencies delayed markedly at each time point after injection. Compared with that before injection, there was a significant difference (P < 0.05-0.01). The P-wave The amplitudes did not fluctuate noticeably all the time after injection, but significantly decreased when compared with those before injection (P < 0.05-0.01). 2 Ischemia- reperfusion group: The P-wave latencies delayed and amplitudes decreased in the rabbits with the heart-fired ischemia impact at i points in time ischemia ischemia-reperfusion, and there was significant difference when compared with the levels before ischemia (P < 0.05). When ligustrazine was injected, the latencies and amplitudes changed less, and as compared with the levels before ischemia, the Difference was not significant (P > 0.05). CONCLUSION: 1 Ligustrazine can inhibit P-wave latencies and amplitudes of SEP of normal rabbits. 2 Ligustrazine can improve P-wave latencies and amplitudes of SEP of rabbits with cerebral ischemia-reperfusion injury.