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1.
BACKGROUND: Ketamine is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonists and plays an important role in the treatment of pain. OBJECTIVE: To analyze the preemptive analgesic effects of different doses of ketamine on growth-associated protein-43 (GAP43) expression in dorsal root ganglion in a rat model of chronic sciatic nerve constricted injury, and to study the differences between high-dose and low-dose ketamine DESIGN: Randomized controlled animal study. SETTING: Medical College of Shantou University. MATERIALS: Thirty-five adult male Sprague Dawley rats were provided by the Experimental Animal Center of Guangzhou University of Traditional Chinese Medicine. Ketamine hydrochloride injection was provided by Hengrui Pharmaceutical Co., Ltd., Jiangsu. METHODS: This study was performed at the Immunological Laboratory, Medical College of Shantou University from September to December 2006. Model of chronic sciatic nerve constricted injury: after anesthesia, the right sciatic nerve was exposed and ligated l-cm distal to the ischiadic tuberosity with a No. 3-0 cat gut suture. Grouping and intervention: 35 rats were randomly divided into 4 groups: normal control group (n = 5), chronic constriction injury (CCI) group (n = 10), low-dose ketamine group (n = 10), and high-dose ketamine group (n = 10). Rats in the normal control group did not undergo any surgery or drug intervention. Rats in the CCI group received intraperitoneal injection of saline (1 mL), and their sciatic nerves were ligated after 10 minutes. Rats in the low-dose ketamine group underwent intraperitoneal injection of ketamine (25 mg/kg) 10 minutes prior to ligation of sciatic nerve; while, rats in the high-dose ketamine group were given intraperitoneal injection of ketamine (50 mg/kg) 10 minutes prior to ligation of sciatic nerve. On the third and the seventh days after surgery, dorsal root ganglion were resected from the sciatic nerve and cut into sections. MAIN OUTCOME MEASURES:  相似文献   

2.
Objective To investigate the changes of phosphorylated extracellular signal-regulated kinase (p-ERK) expression in the immunoreactive cells of the spinal dorsal hom after plantar incision,and explore the effects of intrathecal administration of MEK inhibitor U0126 on physiological pain threshold in rat models with incisional pain.Methods Thirty-two male SD rats were equally randomized into control group (C group),incisional pain group (I group),intrathecal U0126 group (Ugroup) and intrathecal DMSO group (D group).Twenty-μL physiological saline was injected into the rats of the C group and I group,respectively.Ten-μL DMSO and U0126 were injected into the rats in the U group and D group,respectively.Rat models with incisionai pain were induced in the other 3 groups except the C group.Mechanical hyperalgesia were evaluated by paw-pressure before and 2,24 h and 2 d after the inducement.Another 24 rats were treated as the above method and equally divided into 4 groups; the numbers of p-ERK immunoreactive cells in the dorsal horn were quantified to determine the ERK activation 2 and 24 after the model inducement.Results The paw-pressure threshold in I group and D group 2 and 24 h,and 2 d after the incision,and that in U group 2 and 24 h after the incision were significantly decreased as compared with that in C group (P<0.05); that between I group and D group showed no significant difference (P>0.05); that in the U group was obviously higher than that in the I group and D group at the same time points (P<0.05).Significantly increased numbers of p-ERK immunoreactive cells in the I group and D group were observed as compared with those in the C group (P<0.05); those in the U group was obviously decreased as compared with those in the I group and D group at the same time points (P<0.05).Conclusion Plantar incision-induced mechanical hyperalgesia can be prevented by intrathecal injection of U0126 through decreasing the expression of p-ERK positive cells,indicating that ERK pathway in the spinal dorsal horn involves in the incision-induced mechanical hyperalgesia in rats.  相似文献   

3.
Objective To investigate the changes of phosphorylated extracellular signal-regulated kinase (p-ERK) expression in the immunoreactive cells of the spinal dorsal hom after plantar incision,and explore the effects of intrathecal administration of MEK inhibitor U0126 on physiological pain threshold in rat models with incisional pain.Methods Thirty-two male SD rats were equally randomized into control group (C group),incisional pain group (I group),intrathecal U0126 group (Ugroup) and intrathecal DMSO group (D group).Twenty-μL physiological saline was injected into the rats of the C group and I group,respectively.Ten-μL DMSO and U0126 were injected into the rats in the U group and D group,respectively.Rat models with incisionai pain were induced in the other 3 groups except the C group.Mechanical hyperalgesia were evaluated by paw-pressure before and 2,24 h and 2 d after the inducement.Another 24 rats were treated as the above method and equally divided into 4 groups; the numbers of p-ERK immunoreactive cells in the dorsal horn were quantified to determine the ERK activation 2 and 24 after the model inducement.Results The paw-pressure threshold in I group and D group 2 and 24 h,and 2 d after the incision,and that in U group 2 and 24 h after the incision were significantly decreased as compared with that in C group (P<0.05); that between I group and D group showed no significant difference (P>0.05); that in the U group was obviously higher than that in the I group and D group at the same time points (P<0.05).Significantly increased numbers of p-ERK immunoreactive cells in the I group and D group were observed as compared with those in the C group (P<0.05); those in the U group was obviously decreased as compared with those in the I group and D group at the same time points (P<0.05).Conclusion Plantar incision-induced mechanical hyperalgesia can be prevented by intrathecal injection of U0126 through decreasing the expression of p-ERK positive cells,indicating that ERK pathway in the spinal dorsal horn involves in the incision-induced mechanical hyperalgesia in rats.  相似文献   

4.
Male Wistar 7-day-old rats were injected with 40 mg/kg ketamine intraperitoneally, followed by three additional injections of 20 mg/kg ketamine each upon restoration of the righting reflex. Neonatal rats injected with equivalent volumes of saline served as controls. Hippocampal samples were collected at 1, 7 or 14 days following administration. Electron microscopy showed that neuronal structure changed noticeably following ketamine treatment. Specifically, microtubular structure became irregular and disorganized. Quantitative real time-PCR revealed that phosphorylated tau mRNA was upregulated after ketamine. Western blot analysis demonstrated that phosphorylated tau levels at serine 396 initially decreased at 1 day after ketamine injection, and then gradually returned to control values. At 14 days after injection, levels of phosphorylated tau were higher in the ketamine group than in the control group. Tau protein phosphorylated at serine 404 significantly increased after ketamine injection, and then gradually decreased with time. However, the levels of tau protein at serine 404 were significantly greater in the ketamine group than in the control group until 14 days. The present results indicate that ketamine induces an increase of phosphorylated tau mRNA and excessive phosphorylation of tau protein at serine 404, causing disruption of microtubules in the neonatal rat hippocampus and potentially resulting in damage to hippocampal neurons.  相似文献   

5.
BACKGROUND:Ginsenoside extracted from the stem and leaf of ginseng(GSL)and choline have both been shown to improve learning and memory functions; however,further studies are needed to understand the synergistic effects of a combination of both.OBJECTIVE:To verify the combined improved synergistic effects of GSL and choline on learning and memory disorders in rats.DESIGN:Control observation.SETTING:Taishan Medical College.MATERIALS:A total of 150 male Kunming mice weighing(20±2)g and 40 healthy male Wistar rats weighing(220±20)g were provided by the Experimental Animal Department of Jilin University.Animal experimentation received confirmed consent from the local ethic committee.GSL was provided by the Department of Chemistry,Norman Bethune Medical University,and choline was provided by the Third Experiment Factory,Shanghai.METHODS:This study was performed at the Life Science Institute,Taishan Medical College from October 2006 to February 2007.①Scopolamine-induced learning and memory disorders in rats:Forty rats were randomly divided into control group,model group,combination group(400 mg/kg GSL 200 mg/kg choline),GSL(400 mg/kg)group,and choline(200 mg/kg)group,8 rats/group.Rats were perfused and administrated in the morning,once a day for 14 successive days.Rats in the control group and model group were perfused with 20 mL/kg distilled water and underwent Morris water maze spatial resolution test 1 hour after perfusion on the 10th,11th,and 12th days after administration.Rats also underwent passive step-down avoidance test 1 hour after reperfusion on the 13th and 14th days after administration.Thirty minutes prior to experimentation,rats in the remaining three groups were intraperitoneally(I.p)injected with 2 mg/kg scopolamine,and rats in the control group were I.p.injected with 2 mL/kg saline.②Scopolamine-induced learning disorder and memory acquired disorder in mice:Fifty mice were randomly divided into control group,model group,combination group(400 mg/kg GSL 200 mg/kg choline),GSL(400 mg/kg)group,and choline(200 mg/kg)group,with 10 mice/group.Mice were perfused and administrated in the morning,once a day for 9 successive days.Mice in the control group and model group were perfused with 20 mL/kg distilled water and underwent passive step down avoidance test 1 hour after reperfusion on the 8th and 9th day after administration.Twenty minutes prior to training,mice in the remaining three groups were I.p.injected with 2 mg/kg scopolamine,and mice in the control group were I.p.injected with 10 mL/kg saline.③ Sodium nitrite-induced memory consolidation disorder in mice:Grouping,administration,and testing were the same as mentioned above.After training,mice in the remaining three groups were immediately subcutaneously injected with 120 mg/kg sodium nitrite,and mice in the control group were subcutaneously injected with 20 mL/g saline.④Ethanol-induced memory reconsotidation disorder in ice:Grouping,administration,and testing were the same as mentioned above.At 24 hours after training and 20 minutes before retraining,mice in the remaining four groups were perfused with 10 mL/kg ethanol(0.3 volume fraction),and mice in the control group were perfused with 10 mL/kg saline.MAIN OUTCOME MEASURES:Synergistic effects of GSL and choline on learning and memory deficits induced by scopolamine,sodium nitrite,and ethanol in experimental animals.RESULTS:All 40 rats and 150 mice were included in the final analysis.①Synergistic effects of GSL and choline on learning and memory disorders induced by scopolamine in rats:During passive step-down avoidance and Morris water maze spatial resolution tests,the number of error responses and length of maze training in the model group were significantly greater than in the control group(P<0.01); while the number of error responses and length of maze training in the combination group were significantly less than in the model group,GSL group,and choline group(P<0.05-0.01 ).The Q value was>1 after combining administration,which suggests that the combination of GSL and choline had synergistic effects.② Synergistic effects of GSL and choline on learning disorder and memory-acquired disorder induced by scopolamine in mice:During passive step-down avoidance test,the number of error responses in the model group were significantly greater than in the control group(P<0.01); while the number of error responses in the combination group were significantly less than in the model group,GSL group,and choline group(P<0.05-0.01).The Q value was>1 after combining administration,which suggests GSL and choline had synergistic effects.③Synergistic effects of GSL and choline on memory sodium nitrate-induced consolidation disorder in mice:During passive step down avoidance test,the number of error responses in the model group were significantly less than in the control group(P<0.01 ); while the number of error responses in the combination group were significantly less than in the model group,GSL group,and choline group(P<0.05-0.01).The Q value was>1 after combined administration,which suggests GSL and choline had synergistic effects.④Synergistic effects of GSL and choline on ethanol-induced memory reconsolidation disorder in mice:During passive step down avoidance test,the number of error responses in the model group were significantly greater than in the control group(P<0.01); while the number of error responses in the combination group were significantly less than in the model group,GSL group,and choline group(P<0.05-0.01).The Q value was>1 after combined dministration,which suggests GSL and choline had synergistic effects.CONCLUSION:GSL and choline have synergistic effects on learning and memory functions.  相似文献   

6.
BACKGROUND: Studies have reported that nitric oxide synthase (NOS) inhibitor can prolong the latency of hyperbaric oxygen-induced convulsion (HBOC). However, there are very few reports addressing the in-fluence of NOS inhibitor on mental behavior. OBJECTIVE: To investigate behavioral changes after HBOC in gerbils, as well as the influence of NOS in-hibitor. DESIGN, TIME AND SETTING: Randomized experiments were performed in the Laboratory of Hyper-baric Pressure and Diving Physiology, Naval Medical Research Institute of Chinese PLA (Shanghai, China) from March 2005 to June 2007. MATERIALS: Forty male gerbils were randomly divided into five groups: HBOC, saline control, NOS in-hibitor, pressure control, and normal control. Each group contained eight animals. METHODS: In the HBOC group, once depression induction ended, animals were removed from the chamber five minutes after the first appearance of generalized convulsion induced by 0.5 MPa hyperbaric oxygen. Ten minutes before entering the chamber, saline control and NOS inhibitor animals were intraperi-toneally injected with 1 mL saline and 20 mg/kg NG-nitro-L-arginine, respectively. The pressure control group was only exposed to 0.5 MPa. The remaining procedures in these three groups were identical to the HBOC group. The normal control group received no intervention. MAIN OUTCOME MEASURES: Open field test scores in gerbils prior to HBOC, as well as immediately, 24 hours, and 72 hours after decompression ended. RESULTS: HBOC was not detected in either the normal control or the pressure control group, and there were no significant differences in open field test scores prior to and after HBOC (P > 0.05). HBOC occurred in the HBOC, saline control, and NOS inhibitor groups, with significant differences in open field test scores after decompression ended compared to normal control and pressure control groups (P < 0.05–0.01). Com-pared to the HBOC and saline control groups, the NOS inhibitor group exhibited a significantly lower score in the open field test immediately after decompression, and a higher score at 24 and 72 hours (P < 0.05–0.01). CONCLUSION: NOS inhibitor can regulate behavioral changes in gerbils after HBOC. Key Words: behavior; nitric oxide synthase; oxygen-induced convulsion; open field test  相似文献   

7.
Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.  相似文献   

8.
Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.  相似文献   

9.
Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.  相似文献   

10.
Objective To investigate the effect of hypertonic saline on cerebral water content, tumor necrosis factor-α (TNF-α) level and neuronal apoptosis following focal cerebral ischemia-reperfusion (IR) injury in rats and explore the mechanisms involved. Methods Ninety-six rats were randomized equally into 4 groups, namely the shame-operated group, untreated IR injury group, and 4.2% and 7.5% hypertonic saline groups (HS-A and HS-B groups, respectively). In the latter 3 groups, cerebral ischcmia was induced by middle cerebral artery occlusion for 2 h followed by administration of the corresponding treatments. Serum sodium concentration was measured at 5 min before and at 30, 60 and 90 min after the reperfilsion. At 22 h of rcperfusion, the rats were sacrificed after neurological deficit evaluation, and brain edema was assessed by measuring the wet-to-dry weight ratio of the brain tissue. TNF-α expression in the ischemic brain tissue was measured by enzyme-linked immunosorbent assay (ELISA), and the neuronal apoptosis was analyzed using TUNEL assay. Results In the saline-treated rats, serum sodium level increased significantly after saline administration, lasting for 60 min before recovering the normal levels in HS-A group and for over 90 min in HS-B group. Compared with that in the sham-operated group, the brain water content in rats of the IR group increased in both of the hemispheres, but more obviously in the ischemic hemisphere. In the two saline-treated groups, the water content decreased significantly in the bilateral hemispheres, which was especially obvious in the ischemic hemisphere;administration of 7.5% saline resulted in greater water content reduction in the ischemic hemisphere than 4.2% saline. Compared with the IR group, the two saline-treated groups showed significant reduction in TNF-α levels and apoptotic cells in the brain along with decreased neurological deficits. Conclusion Hypertonic saline can ameliorate cerebral focal IR injury by decreasing the cerebral water content, TNF-α level and neuronal apoptosis following the injury.  相似文献   

11.
目的 观察右美托咪定(Dex)复合曲马多对开颅术后病人镇痛和镇静的效果.方法 60例择期开颅手术病人随机分为对照组、Dex 0.2 μg组和Dex 0.4μg组,每组20例.Dex 0.2 μg组和Dex 0.4μg组均于麻醉诱导前10 min静脉泵人Dex(1μg/kg),而后再分别以0.2、0.4 μg/(kg·h)的速率泵注至术后24h.3组均于硬脑膜缝合完毕时静脉注射曲马多(1.5 mg/kg),术毕连接镇痛泵.并根据视觉模拟量表(VAS)评分、镇痛泵总按压次数和Ramsay评分等指标评价3组开颅术后镇痛、镇静的效果.结果 VAS评分:除术后2h外,Dex 0.4 μg组<Dex 0.2μg组<对照组(P<0.05).Ramsay评分:在术后各时间点,Dex 0.2 μg组和Dex 0.4 μg组均显著高于对照组(P<0.05);术后6~24 h,Dex 0.4μg组均显著高于Dex 0.2 μg组(P<0.05).镇痛泵总按压次数:Dex 0.4 μg组<Dex 0.2 μg组<对照组(P<0.05).术后恶心呕吐的发生率:Dex 0.4 μg组明显低于Dex 0.2 μg组和对照组(P<0.05).结论 Dex能提高曲马多的镇痛效果,并可提供良好的镇静作用,减少术后不良反应的发生率.  相似文献   

12.
目的 探讨右美托咪定联合地佐辛对自发性脑出血开颅术后镇静、镇痛的临床疗效。方法 回顾性分析2017年9月至2018年9月开颅血肿清除术治疗的符合标准的56例SICH的临床资料。根据术后镇静、镇痛方式分成观察组(28例)和对照组(28例)。观察组采用右美托咪定联合地佐辛治疗,对照组采用咪达唑仑联合地佐辛治疗。结果 用药后2、6、12、24 h,观察组镇静Ramsay评分、镇痛视觉模拟量表(VAS)评分、恶心呕吐AVS评分、平均动脉压、心率较对照组均明显降低(P<0.05),而SpO2均明显提高(P<0.05)。观察组住院时间[(19.86±3.76)d]较对照组[(23.61±5.78)d]明显缩短(P<0.05)。观察组再出血率(3.57%,1/28)与对照组(10.71%,3/28)无统计学差异(P>0.05)。结论 右美托咪定联合地佐辛对自发性脑出血开颅术后病人具有良好的镇静、镇痛作用,能够稳定术后血流动力学指标,减少住院时间。  相似文献   

13.
目的 观察地佐辛用于术后硬膜外镇痛的临床效果.方法 D组镇痛泵配方地佐辛0.3 mg/kg+1%罗哌卡因100 mg+地塞米松5 mg+生理盐水至100 mL,F组芬太尼3 μg/kg+1%罗哌卡因100 mg+地塞米松5 mg+生理盐水至100 mL.镇痛泵参数:持续输注2 mL/h,PCA量0.5 mL/次,锁定时间15 min.记录术后3 h、6 h、9 h、12 h、24 h、36 h各个时间点的VAS、Ramsay、BCS评分及恶心呕吐、尿潴留、皮肤瘙痒、呼吸抑制等不良反应的发生情况.结果 2组各个时间点VAS、Ramsay比较,差异无统计学意义(P>0.05),2组舒适度评分D组高于F组,F组不良反应发生率高于D组,差异有统计学意义(P<0.05).结论 地佐辛可安全有效的用于术后硬膜外镇痛,且不良反应少.  相似文献   

14.
In this study, we aimed to investigate the preemptive analgesic efficacy of epidural application of fentanly-bupivacaine combination. A total of 60 patients admitted for total abdominal hysterectomy were included in this study after the approval of the ethic committee, and the patients were randomly classified into three groups. An epidural catheter was inserted to all patients through L2-3 or L3-4 space before general anesthesia induction. 2 micrograms/kg fentanyl in 0.25% bupivacaine in 10 ml serum saline was applied to the preemptive analgesia group (Group P) 20 minutes before the incision, and to the post-incisional analgesia group (Group E) 20 minutes after the incision, whereas control group received 10 ml serum saline 20 minutes before the incision through the epidural catheter. Pain scores were assessed with 100 mm Visual Analogue Scale (VAS) and four point Verbal Rating Scale (VRS) at 1., 2., 4., 6., 12., 24., 48. hours postoperatively. First analgesic requirement time and total analgesic consumption for 48 hours were also recorded. The VAS and VRS values in the postoperative 48 hours were significantly lower in Group P compared with the other groups (p < 0.05). First analgesic requirement time was also significantly prolonged in Group P (p < 0.001). Total analgesic consumption in Group P was significantly lower than the other two groups (p < 0.05). As a result we observed that preemptive administration of epidural fentanyl-bupivacaine combination reduces the postoperative pain and analgesic consumption in lower abdominal surgery.  相似文献   

15.
目的探讨采用盐酸纳布啡注射液进行剖宫产术后镇痛对产后抑郁的影响。方法选取2018年1月~2019年1月在我院接受剖宫产术产妇200例为主要研究对象,按随机数字表法将研究对象随机分为观察组和对照组,每组各100例。对照组采用舒芬太尼镇痛,观察组采用盐酸纳布啡注射液镇痛。观察比较两组产妇术后各时点疼痛视觉模拟评分(VAS)、Ramsay镇静评分(RSS)抑郁自评量表(SDS)评分及不良反应。结果观察组产妇术后6h、12h、24h、48h、72h时VAS、RSS评分较对照组低(P<0.05或P<0.01);观察组产妇术后3d、7d、15d、30d、90d时SDS评分均较对照组低(P<0.01);观察组产妇术后不良反应和产后抑郁发生率均较对照组低(P<0.01)。结论剖宫产术后镇痛中采用盐酸纳布啡注射液可减轻产妇术后疼痛降低产后抑郁发生率,不良反应少,安全性高,值得推广。  相似文献   

16.
目的评价丁苯酞治疗分支动脉粥样硬化病脑梗死的临床疗效及安全性。方法采用随机对照设计,将64例急性脑梗死患者,随机分为丁苯酞治疗组(32例)和对照组(32例)。两组患者诊断均采用高木诚等提出的诊断标准进行诊断,全部患者均给予口服阿司匹林、阿托伐他汀钙,静脉滴注奥扎格雷钠。治疗组在常规治疗的基础上使用丁苯酞50 mg·d-1,静脉滴注,连续治疗14d。两组患者均在治疗前后进行神经功能缺损程度评分(NIHSS)和日常生活活动能力评分(BI)。结果两组患者治疗前NIHSS评分差异无统计学意义(P>0.05),治疗后NIHSS评分均较治疗前降低(P<0.05);治疗组治疗后NIHSS评分明显低于对照组(P<0.05)。两组患者治疗前BI评分差异无统计学意义(P>0.05),治疗后BI评分均较治疗前增高(P<0.05);治疗组治疗后BI评分明显高于对照组(P<0.05)。治疗过程中未见不良反应。结论丁苯酞能显著改善分支动脉粥样硬化病脑梗死患者的神经功能缺损及日常生活活动能力,疗效确切,安全性好。  相似文献   

17.
目的 检测抑郁大鼠给予氯胺酮后,前额皮层及海马区组织内IL-1β和IL-6表达的变化.方法 Wistar大鼠雄性20只按照随机方式分为2组,各10只,给予生理盐水的大鼠入对照组(C组),给予10 mg/kg氯胺酮的大鼠为K组.应用行强迫游泳实验15 min的方法建立大鼠抑郁模型.次日,腹腔注射氯胺酮或等体积生理盐水,注射30 min后再次进行强迫游泳实验5 min,记录不动时间.并分别采用Western Blot法和双抗体夹心ABC-ELISA法检测大鼠前额皮层及海马组织中IL-1β和IL 6的表达情况.结果 与对照组比较,应用氯胺酮后大鼠强迫游泳不动时间明显减少(P<0.01),大鼠前额皮层及海马区的IL-1β和IIL-6表达均明显下调(P<0.05).结论 氯胺酮对抑郁大鼠的抗抑郁作用可能与前额皮层及海马IL-1和IL-6的表达下调有关.  相似文献   

18.
目的 探讨氟比洛芬酯对功能神经外科手术患者的超前镇痛效果.方法 ASA Ⅰ~Ⅱ级,20~60岁的功能功能外科手术患者60例,随机分为A组(氟比洛芬脂超前镇痛组)和B组(对照组),各30例.麻醉后,于手术开始前10min,A组缓慢静脉注射氟比洛芬酯50mg,B组静脉注射生理盐水10ml.于术后2,24,48h对疼痛行疼痛程度视觉模拟评分(VAS)和镇静评分,并记录各时间点镇痛药用量.结果 A组在2,24,48h的VAS镇痛评分及静脉自控镇痛(PCIA)用药容积均明显低于B组.两组在各时间点上的镇静评分无显著性差异,两组患者均未出现过度镇静(如昏睡、昏迷).结论 氟比洛芬酯具有良好的超前镇痛效果,适用于功能神经外科手术患者.  相似文献   

19.
背景:全膝关节置换持续的股神经阻滞效果好于单纯镇痛剂治疗(吗啡);而相对于持续的神经阻滞,单次注射法不需要专用的设备、特殊的仪器和专人管理,操作更加简单,费用也更低。 目的:观察单次股神经传导阻滞联合神经康复治疗对缓解全膝关节置换后疼痛、促进功能恢复的作用。 方法:40例全膝关节置换患者分为2组,试验组注射40 mL 2.5 g/L的布比卡因,对照组注射同体积的生理盐水,由指定观察者对患者置换后的疼痛、吗啡用量、走动距离、膝关节最大活动度及疼痛目测类比评分进行比较。 结果与结论:与对照组相比,试验组患者置换后疼痛目测类比评分降低,吗啡用量减少,不良事件减少,卧床时间较短,步行距离较长,关节活动度较大(P < 0.05~0.01)。提示单次神经传导阻滞联合神经康复治疗能够明显缓解全膝关节置换后患者的疼痛,促进其早期下床活动,减少住院天数。  相似文献   

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