奥曲肽对oddi括约肌肌电活动的影响

目的 探讨奥曲肽(sandostatin，SS)对oddi括约肌(sphincter of oddi，SO)肌电活动的影响及其临床意义。方法 32只空腹18h成年健康家免随机分为4组，即静脉注射生理盐水组；皮下注射生理盐水组；小剂量静脉滴注SS组；大剂量皮下注射SS组。两对钩状双极金属电极分别置于乳头及十二指肠浆膜下，使用成都仪器厂RM6240多道生理仪及信号采集处理系统，实验在PBG-1型生理实验屏蔽柜内进行。连续记录SO肌电活动120～150min。结果 对照第1组、第2组用药前后SO肌电活动无明显变化，仍表现为单发、规律的SO锋电位(spike potentials of SO，SPSO)；小剂量静脉滴注SS组给药后2～3min出现规律、间断的SO肌电簇(myoelectronic acfivity of SO，MASO)；大剂量皮下注射SS组给药后2～3min，SO肌电活动消失，进入抑制状态。结论 高浓度的SS可以抑制SO肌电活动，导致SO处于舒张状态；而低浓度维持剂量的SS可以使SO肌电活动处于兴奋状态，导致SO蠕动加快。     

奥曲肽对oddi括约肌肌电活动的影响

目的　探讨奥曲肽 (sandostatin ,SS)对oddi括约肌 (sphincterofoddi,SO)肌电活动的影响及其临床意义。方法　 32只空腹 18h成年健康家兔随机分为 4组 ,即静脉注射生理盐水组 ;皮下注射生理盐水组 ;小剂量静脉滴注SS组 ;大剂量皮下注射SS组。两对钩状双极金属电极分别置于乳头及十二指肠浆膜下 ,使用成都仪器厂RM6 2 4 0多道生理仪及信号采集处理系统 ,实验在PBG 1型生理实验屏蔽柜内进行。连续记录SO肌电活动 12 0～ 15 0min。结果　对照第 1组、第 2组用药前后SO肌电活动无明显变化 ,仍表现为单发、规律的SO锋电位 (spikepotentialsofSO ,SPSO) ;小剂量静脉滴注SS组给药后 2～ 3min出现规律、间断的SO肌电簇 (myoelectronicactivityofSO ,MASO) ;大剂量皮下注射SS组给药后 2～ 3min ,SO肌电活动消失 ,进入抑制状态。结论　高浓度的SS可以抑制SO肌电活动 ,导致SO处于舒张状态 ;而低浓度维持剂量的SS可以使SO肌电活动处于兴奋状态 ,导致SO蠕动加快     

Oddi括约肌肌电活动的基本方式

目的 探讨家兔Oddi括约肌(sphincter of Oddi,SO)肌电活动的基本方式及其生物学意义.方法 32只家兔随机分为4组.第1组(n=8)为空腹组;第2组(n=8)为进食组,空腹18 h后经胃造瘘管注入50 ml牛奶;第3组(n=8)为Nardi test激发实验组,静脉注射1 mg吗啡和1 mg新斯的明;第4组(n=8)为神经阻断组,记录空腹家兔肌电活动30 min后静脉给予山莨菪硷1 mg;两对钩状双极金属电极通过浆膜层分别置于SO及十二指肠,使用RM6240多道生理信号采集处理系统同时记录每一组家兔SO及十二指肠肌电活动,连续记录SO肌电活动120～150 min.结果 空腹状态下家兔SO肌电表现为规律的、单发性的SPSO;进食后家兔SO肌电活动表现为规律的、间断的MASO;Nardi test激发实验后SO肌电活动表现为数个长时间、不间断的SPSO组成的肌电串;阻断神经节后胆碱能神经元后SO肌电活动规律随即消失,120 min后SPSO逐渐恢复到空腹状态.结论 家兔SO肌电活动存在4种基本形式,即空腹状态下SO保持一定基础紧张性的基本张力波;进食后SO开始蠕动将胆汁排入十二指肠的蠕动波;Nardi test激发实验后SO处于持续关闭状态的痉挛波;阻断胆碱能神经元后SO处于松弛状态的舒张波.提示SO并非仅仅存在"非开即闭"两种形式.这对今后有关SO基础研究和临床治疗均具有理论指导意义.     

β2受体阻断剂ICI118551对大鼠鼻内浸润注射小剂量肾上腺素后血压的影响

目的 观察静脉预先注射特异性β2受体阻断剂ICI 118551对大鼠鼻内浸润注射小剂量肾上腺素后血压的影响.方法 成年雄性SD大鼠32只,随机均分为四组:生理盐水+生理盐水组(S组)和ICI 118551+生理盐水组(I组)先分别静脉注射生理盐水0.2 ml和ICI 118551 0.5mg/kg,20 min后在大鼠鼻内浸润注射生理盐水0.2 ml;生理盐水+肾上腺素组(E组)和ICI 118551+肾上腺素组(IE组)先分别静脉注射生理盐水0.2 ml和ICI 118551 0.5mg/kg,20 min后在大鼠鼻内浸润注射1:100 000肾上腺素0.2 ml.记录浸润注射前(基础值)和注射后1、2、3、4、5、6、7、8、9、10min的MAP和HR.结果 与浸润注射前相比,E组在注射后3 min时MAP出现明显下降,并持续至注射后10min(P＜0.05).IE组在注射后6、7 min时MAP上升.S组和I组MAP无明显变化.四组HR均无明显变化.结论 大鼠鼻内浸润注射小剂量肾上腺素可引发低血压,静脉预先注射β2受体阻断剂ICI 118551可预防此类低血压.     

硫化氢对脓毒症大鼠动脉压力反射的影响

目的 探讨硫化氢(H2S)对脓毒症大鼠动脉压力反射(ABR)的作用及机理.方法 盲肠结扎穿刺(CLP)法制作脓毒症大鼠模型,选取47只雄性Spargue-Dawley大鼠随机分为9组:①假手术(SO)+0.9%NaCl(NS)静脉注射组;②SO+硫氢化钠(NaHS)静脉注射组;③CLP+Naris静脉注射组;④SO+人工脑脊液(aCSF)双侧孤束核(NTS)注射组;⑤SO+NariS双侧NTS注射组;⑥SO+安慰剂(DMSO)+Naris组;⑦SO+格列苯脲(Gli)+Naris组;⑧CLP+安慰剂(DMSO)组;⑨CLP+GIi组.分别在给药前、给药后5 min和30 Min 3个时间点对各组大鼠的ABR功能进行测定.结果 ①同一组内不同时相问ABR值的变化结果:与给药前比较,SO+NaHS静脉注射组、CLP+NariS静脉注射组、SO+NaHS双侧NTS注射组及SO+安慰剂+NaHS组给药后5 min和30 minABR值均明显降低(P<0.05,P<0.01),而CLP+Gli组明显升高(P<0.05).②相同时相不同组间ABR值的变化结果:给药前,CLP+NaHS静脉注射组明显低于SO+NS静脉注射组或SO+NaHS静脉注射组(P<0.05);给药后5 min和30 min,CLP+NaHs静脉注射组明显低于SO+NS静脉注射组或SO+NaHS静脉注射组(P<0.05),SO+NaHS静脉注射组明显低于SO+NS静脉注射组(P<0.05);SO+NaHS双侧NTS注射组明显低于SO+aCSF双侧NTS注射组(P<0.01);SO+Gli+NaHS组明显高于SO+安慰剂+NaHs组(P<0.05);CLP+Gli组明显高于CLP+安慰剂组(P<0.05).结论 脓毒症H2S生成增加对ABR功能有降低作用,该作用可能与ATP敏感性钾通道开放有关;脓毒症状态下H2S不仅通过外周静脉系统发挥作用,而且可能通过中枢NTS影响ABR功能.     

黏膜接触电极在家兔Oddi括约肌肌电测量中的应用价值

目的 探讨适合Oddi括约肌（sphincter of Oddi,SO）肌电测量的新方法.方法 两组各15只家兔分别用黏膜接触电极（contact electrode on mucosa,CEM）和浆膜钩状电极（chorion claw electrode,CCE）测量SO肌电活动;另外6只家兔同时使用两种电极同步测量.结果 CEM测量SO肌电成功率高,创伤小,而且记录到的家兔SO肌电波形和CCE相比没有明显的差别.结论 CEM是一种很有价值的测量SO肌电活动的新方法,将来可能用于人体SO功能的研究,为人体内镜诊断SO功能提供了一个新方法.     

维库溴铵对全麻患者脑电熵指数和脑电双频谱指数监测镇静深度的影响

目的观察全身麻醉过程中,维库溴铵对脑电熵指数——状态熵（AE）和反应熵（RE）以及脑电双频谱指数（BIS）的影响。方法ASAⅠ级或Ⅱ级择期手术患者60例,随机分为4组（n=15）：Ⅰ组为对照组,静脉注射生理盐水;Ⅱ组、Ⅲ组、Ⅳ组为试验组,分别静脉注射维库溴铵0．03、0．06、0．12 mg/kg。麻醉诱导采用异丙酚靶控输注（TCI）,当效应室浓度（CE）达到3．5μg/ml时,按组别静脉注射维库溴铵或等容积生理盐水,5 min后静脉注射芬太尼3μg/kg,行气管插管,观察5 min后将Ⅰ组、Ⅱ组、Ⅲ组维库溴铵剂量补足到0．12 mg/kg。记录诱导前即刻、CE达到3．5μg/ml、注射维库溴铵或生理盐水后1、2、3、4、5 min、气管插管前即刻、插管后即刻及插管后1、3、5 min的RE、AE、BIS、HR和MAP。结果与维库溴铵静脉注射前即刻比较,4组静脉注射后各时点RE、SE、BIS、HR、MAP差异无统计学意义（P＞0．05）;4组间静脉注射前后RE、SE、BIS、HR、MAP比较差异无统计学意义（P＞0．05）。与插管前即刻比较,4组插管后即刻及插管后1min时RE、SE、BIS、HR和MAP均升高（P＜0．05或0．01）;与Ⅰ组比较,Ⅱ组、Ⅲ组、Ⅳ组插管后即刻和插管后1 min RE、SE和BIS降低（P＜0．05）,但3组间比较差异无统计学意义（P＞0．05）。结论在深度镇静且无伤害性刺激时,维库溴铵对脑电熵指数和BIS无影响;存在伤害性刺激时（如气管插管）,即使小剂量（0．03 mg/kg）的维库溴铵也可降低脑电熵指数和BIS的升高幅度。     

环腺苷酸-蛋白激酶A在大鼠内毒素性急性肺损伤时血红素加氧酶-1表达上调中的作用

目的 探讨环腺苷酸-蛋白激酶A(cAMP-PKA)在大鼠内毒素性急性肺损伤时血红素加氧酶-1(HO-1)表达上调中的作用.方法 健康清洁级雄性SD大鼠48只,体重180 ～ 220 g,2.5 ～ 3.0月龄,采用随机数字表法,将大鼠随机分为4组(n=12)∶正常对照组(C组)股静脉注射生理盐水(LPS溶媒)0.5 ml,2h后皮下注射生理盐水(H89溶媒)0.5 ml;内毒素性急性肺损伤组(ALI组)股静脉注射10 mg/kg LPS 0.5 ml,2h后皮下注射生理盐水0.5 ml; H89+内毒素性急性肺损伤组(H+ALI组),股静脉注射10 mg/kg LPS 0.5 ml,2h后皮下注射5 mg/kg H89 0.5 ml; H89组(H组)股静脉注射生理盐水0.5 ml,2h后皮下注射5 mg/kg H89 0.5 ml.静脉注射LPS后6h时处死大鼠,取肺组织,行病理学评分,测定肺组织含水量;采用Western blot法测定HO-1和PKA表达;采用荧光定量PCR法测定HO-1mRNA表达.结果 与C组比较,ALI组和H+ALI组肺组织含水量和病理学评分升高,肺组织PKA、HO-1和HO-1 mRNA表达上调(P＜0.05),H组上述各指标差异无统计学意义(P＞0.05);与ALI组比较,H+ALI组肺组织含水量和病理学评分升高,肺组织PKA、HO-1和HO-1 mRNA表达下调(P＜0.05).结论 大鼠内毒素性急性肺损伤时HO-1表达上调的机制与cAMP-PKA信号通路活化有一定关系.     

不同剂量神经节苷脂治疗急性脊髓损伤的临床观察

目的观察不同剂量的神经节苷脂(GM1)对脊髓损伤患者的疗效。方法57例脊髓损伤患者随机分为3组,GM1大剂量治疗组16例,每日给予GM1100mg+生理盐水100ml静脉注射,15d为1个疗程,休息7d,再行第2个疗程,用药剂量同第1个疗程。GM1小剂量组23例,每日给予GM140mg+生理盐水100ml静脉注射,15d为1个疗程,休息7d,再行第2个疗程,用药剂量同第1个疗程。GM1小剂量组23例,每日给予GM140mg+生理盐水100ml静脉注射,15d为1个疗程,休息7d,再行第2个疗程,用药量同第1个疗程。常规组18例:术后仅予常规治疗。结果GM1组治疗后脊髓功能总体进步与常规组无差别,但其截瘫的Frankle二级恢复率及有用恢复率明显高于常规组,而GM1大剂量组的治疗效果好于小剂量组。结论脊髓损伤患者GM1大剂量组的治疗效果好于小剂量组与常规组。     

帕瑞昔布对剖宫产术后病人不同剂量吗啡硬膜外镇痛效果的影响

目的 评价帕瑞昔布对剖宫产术后病人不同剂量吗啡硬膜外镇痛效果的影响.方法 择期行剖宫产手术的病人300例,ASA分级Ⅰ或Ⅱ级,年龄20～40岁,体重54 ～ 89 kg,采用随机数字表法,将其随机分为6组(n＝50):帕瑞昔布联合常规剂量吗啡PCEA组(P1组)、帕瑞昔布联合中剂量吗啡PCEA组(P2组)、帕瑞昔布联合小剂量吗啡PCEA组(P3组),3组各设置生理盐水联合吗啡PCEA对照组(C1组、C2组和C3组).于手术结束时P1组、P2组和P3组静脉注射帕瑞昔布40 ng,C1组、C2组和C3组给予等容量生理盐水.6组术后行吗啡PCEA,C1组和P1组:负荷量为吗啡2.0mg,镇痛泵药物为吗啡3.0 mg;C2组和P2组:负荷量为吗啡1.5mg,镇痛泵药物为吗啡2.0 mg;C3组和P3组:负荷量为吗啡1.0 mg,镇痛泵药物为吗啡1.5 mg;负荷量中均加入0.15％罗哌卡因8ml,所有镇痛泵中药物均加入罗哌卡因150 mg、格拉司琼3 mg和地塞米松5 mg,用生理盐水稀释至100 ml,背景输注速率2 ml/h,PCA量0.5ml,锁定时间15 min.分别记录术毕～术后24h期间静息状态及活动状态时镇痛有效情况,记录恶心呕吐、皮肤瘙痒、呼吸抑制、低血压和嗜睡等不良反应的发生情况.结果 与C1组或G2组比较,P1组或P2组术后活动状态和静息状态镇痛有效率差异无统计学意义(P＞0.05);与C3组比较,P3组活动状态镇痛有效率升高(P<0.01),静息状态镇痛有效率差异无统计学意义(P＞0.05).与P1组和P2组比较,P3组恶心呕吐程度和皮肤瘙痒发生率降低(P<0.01),无一例病人发生呼吸抑制、低血压和嗜睡.结论 静脉注射帕瑞昔布40 mg可增强剖宫产术后小剂量吗啡硬膜外镇痛的效果,而对中等剂量或常规剂量吗啡硬膜外镇痛效果无影响.     

Effect of alcohol on cyclical myoelectric activity of the opossum sphincter of Oddi

Ethyl alcohol may adversely affect pancreatic function by perturbing sphincter of Oddi (SO) or duodenal motor activity. The aim of this study was to identify the effect of ingested alcohol on the SO, duodenal, and gastric myoelectric activity in conscious opossums. In five adult opossums bipolar stranded stainless-steel wire electrodes were implanted on the SO, gastric antrum, and duodenum. After a 2-week recovery period, each animal underwent eight 8-hr recording sessions while fasted and awake. After two fasting cycles of the migrating myoelectric complex, animals were randomly fed either 10 ml of a 30% ethyl alcohol solution or 10 ml of water via an esophageal tube, and recordings continued for 4-6 hr. During the control state, cyclical myoelectric spike activity was recorded from the SO, gastric antrum, and duodenum with a mean +/- SD cycle length of 7.35 +/- 15.0 min, 74.3 +/- 10.1 min, and 94.8 +/- 8.7 min, respectively. With alcohol, SO and duodenal cycle lengths were unchanged while gastric cycle length decreased. However, alcohol effected a significant increase in peak SO spike burst frequency with no corresponding change in gastric or duodenal spike burst frequency. An equivalent volume of water had no influence on sphincter of Oddi myoelectric activity. It is concluded that ingested alcohol induces increased myoelectric activity from the opossum SO, independent of changes in activity of the duodenum or stomach. Since the SO plays a major role in metering bile and pancreatic flow into the duodenum, this may be a factor in alcohol-induced pancreatitis.     

应用重组人生长激素治疗肝硬化腹水大鼠的实验研究

目的探讨应用重组人生长激素(rhGH)对肝硬化腹水大鼠的治疗作用。方法应用四氯化碳皮下注射方法复制大鼠肝硬化模型,60只清洁级雄性SD大鼠随机分为正常对照组(A组),肝硬化 生理盐水注射组(B组),肝硬化 rhGH注射组(C组)。结果 C组大鼠肝功能逐渐好转,腹水消失,生长激素抵抗现象被扭转。结论应用rhGH可以显著改善肝功能,促进腹水消退,且持续时间较长。     

Characterization of substance P effects on sphincter of Oddi myoelectric activity

We examined the effects of substance P (SP) on the myoelectric activity of the opossum sphincter of Oddi (SO). Myoelectric data from the SO in five adult opossums were recorded using thin stainless steel electrodes and computer-assisted analog-to-digital conversion. In fully awake and conscious animals, baseline spikeburst activity during phase I of the MMC occurred at a frequency of 28.6 +/- 3.1 spikebursts (SB) per 20-min period. Intravenous infusion of graded doses of substance P (from 0.5 to 8.0 micrograms/kg) stimulated SO myoelectric activity in a dose-related manner (from 80 +/- 8 to 235 +/- 11 SB/20 min, respectively, P less than 0.05 when compared to baseline). The effect of substance P on SO myoelectric activity was antagonized by administration of the H2-blocker, cimetidine (92.0 +/- 6.1 vs 48.2 +/- 7.0, n = 5, P less than 0.05). Administration of the antimuscarinic drug atropine only slightly affected the SO spikeburst frequency when infused prior to SP (73.0 +/- 10.4 vs 70.8 +/- 8.2, P greater than 0.05). We conclude that SP stimulated the SO spikeburst frequency in a dose-dependent fashion. Cimetidine markedly inhibited the response of the SO to SP but atropine did not. The excitatory effect of substance P on the opossum SO is mediated at least in part by a histaminergic, noncholinergic pathway.     

Prevention of adhesions by sodium chromoglycate, dexamethasone, saline and aprotinin after pelvic surgery

BACKGROUND: The purpose of the present paper was to assess the efficacy of saline, sodium chromoglycate, dexamethasone and aprotinin, in single or in combined use in reducing postoperative pelvic adhesion formation in a rabbit model. METHODS: A standard lesion was performed to induce adhesion formation. Forty-five rabbits were divided into nine study groups. Group 1 was the non-treatment group. In group 2, 3 cm(3) of the rabbits' own serum was instilled i.p. In group 3, 5 mg/kg sodium chromoglycate and 3 cm(3) of the rabbits' own serum were administered i.p. The group 4 rabbits were instilled with 5 mg/kg sodium chromoglycate, 3 cm(3) rabbits' own serum and 1 mg/kg dexamethasone i.p. The group 5 rabbits were injected with 5000 units aprotinin i.m. 2 h before operation and 5 mg/kg sodium chromoglycate, 3 cm(3) of rabbit serum, 1 mg dexamethasone and 5000 units aprotinin instilled i.p. In group 6, 3 cm(3) saline was instilled i.p. Groups 7, 8 and 9 were a repeat of groups 4, 5 and 6 with the exception of replacement of the rabbit serum by 3 cm(3) saline. Animals were evaluated for adhesions 10 days after operation. RESULTS: Macroscopic adhesion scores of all the groups (2-9) were significantly less than scores of the control group (group 1). The macroscopic adhesion scores of group 9 and group 8 were significantly less compared to that of group 7. CONCLUSION: Intraperitoneal instillation of saline and sodium chromoglycate decreased pelvic adhesion formation significantly in a rabbit model. Addition of aprotinin and dexamethasone to these agents gave a further advantage in decreasing pelvic adhesion formation.     

No Enhancement of Sensory and Motor Blockade by Neostigmine Added to Mepivacaine Axillary Plexus Block

Background: Intrathecal neostigmine induces analgesia but also several side effects. Recently, 500 [micro sign]g neostigmine administered intraarticularly was shown to produce postoperative analgesia without side effects. The authors' goal was to determine whether 500 [micro sign]g neostigmine added to mepivacaine in axillary plexus block prolongs postoperative analgesia. In addition, they wanted to determine the incidence of side effects in patients undergoing hand surgery.

Methods: Sixty-nine outpatients scheduled for carpal tunnel syndrome repair with axillary plexus block were randomly assigned to one of three groups that received saline solution in the axillary plexus and subcutaneously (group 1), 500 [micro sign]g neostigmine in the axillary plexus and saline solution subcutaneously (group 2), or saline solution in the axillary plexus and 500 [micro sign]g neostigmine subcutaneously (group 3). Sensory and motor block in the four hand nerve distributions were assessed every 5 min for 30 min. The duration of the sensory and motor blocks were assessed after operation. Side effects were also recorded.

Results: Neostigmine had no effect on sensory and motor block in any of the four nerve distributions, nor did it increase the median duration of sensory block (215 min; range, 120-330 min) compared with group 1 (247 min; range, 190-287 min) or group 3 (236 min; range, 160-280 min). Motor block was slightly shorter (P = 0.045) in group 3 (190 min; range, 135-285 min) compared with group 1 (218 min; range, 145-257 min) and group 2 (215 min; range, 105-343 min). Gastrointestinal side effects occurred in 30% of patients in both neostigmine groups but not in group 1 (P < 0.05).     

No enhancement of sensory and motor blockade by neostigmine added to mepivacaine axillary plexus block.

BACKGROUND: Intrathecal neostigmine induces analgesia but also several side effects. Recently, 500 microg neostigmine administered intraarticularly was shown to produce postoperative analgesia without side effects. The authors' goal was to determine whether 500 microg neostigmine added to mepivacaine in axillary plexus block prolongs postoperative analgesia. In addition, they wanted to determine the incidence of side effects in patients undergoing hand surgery. METHODS: Sixty-nine outpatients scheduled for carpal tunnel syndrome repair with axillary plexus block were randomly assigned to one of three groups that received saline solution in the axillary plexus and subcutaneously (group 1), 500 microg neostigmine in the axillary plexus and saline solution subcutaneously (group 2), or saline solution in the axillary plexus and 500 microg neostigmine subcutaneously (group 3). Sensory and motor block in the four hand nerve distributions were assessed every 5 min for 30 min The duration of the sensory and motor blocks were assessed after operation. Side effects were also recorded. RESULTS: Neostigmine had no effect on sensory and motor block in any of the four nerve distributions, nor did it increase the median duration of sensory block (215 min; range, 120-330 min) compared with group 1 (247 min; range, 190-287 min) or group 3 (236 min; range, 160-280 min). Motor block was slightly shorter (P = 0.045) in group 3 (190 min; range, 135-285 min) compared with group 1 (218 min; range, 145257 min) and group 2 (215 min; range, 105-343 min). Gastrointestinal side effects occurred in 30% of patients in both neostigmine groups but not in group 1 (P < 0.05). CONCLUSIONS: This study suggests that 500 microg neostigmine added to mepivacaine in axillary plexus block does not prolong postoperative sensory block, but it does cause a relatively high incidence of side effects. These two findings raise doubts about the use of neostigmine associated with local anesthetics for plexus neural block.     

The Effect of Different Reduction Mandibuloplasty Types on Lower Face Width and Morphology

Mandibular angle ostectomy (MAO) and mandibular angle-splitting ostectomy (MASO) are the main surgical approaches for the aesthetic correction of a square and broad lower face. However, few data exist on the changes in lower face width and morphology after two different forms of reduction mandibuloplasty. The sample in the current study consisted of 42 Chinese patients: 22 who underwent MAO and 20 who received MASO. The standard frontal and lateral cephalometric radiographs were taken preoperatively and 1 year postoperatively. Some landmarks and reference lines from these radiographs were selected for measurement and evaluation of the changes in lower face width and lateral morphology of the mandible. The results demonstrated that both MAO and MASO can reduce the bigonial distance (MAO group mean, 10.4 mm; MASO group mean, 6.2 mm) and the frontal width of the lower face (MAO group mean, 15.4 mm; MASO group mean, 7.6 mm). However, further comparison showed that lower face width apparently is decreased more by MAO (10.4 mm) than by MASO (6.2 mm). In the lateral radiographs, gonial and mandibular plane angles were found to be significantly increased in MAO patients postoperatively (MAO group mean, 13.3 and 10.0 degrees, respectively), but only slight changes in these two angles were seen after MASO (MASO group mean, 1.6 and 1.5 degrees, respectively). This study suggests that MAO and MSAO can effectively reduce lower face width, but brings about some different aesthetic results.     

大鼠肝缺血及再灌注所致小肠过氧化损伤及丹参的保护作用

目的 观察大鼠肝缺血再灌注小肠过氧化损伤及丹参预处理的保护作用.方法 首先将SD大鼠随机分为正常对照组(CO组)、假手术组(SO组)、缺血再灌注组(IR组)、丹参预处理组(SM组),分别在肝缺血30、45、60 min时取上段空肠进行大体病理学检测;然后在肝缺血45 min条件下,动物亦随机分为4组(CO组、SO组、IR组、SM组),按再灌注后不同时间(0、3、12、24、72 h)分为5个亚组,每组5只.SM组在阻断第一肝门30 min前经尾静脉推注丹参注射液6 g/kg加生理盐水40 ml/kg,其余各组按40 ml/kg给予生理盐水尾静脉注入,SO组开腹后仅解剖肝门,不钳夹肝蒂.分别在再灌注0、3、12、24、72 h取上段空肠行病理学检查、丙二醛(MDA)含量测定、髓过氧化物酶(MPO)活性测定.结果 空肠黏膜损伤评分随肝缺血时限延长而加重;在肝缺血45 min再灌注不同时限点SM组空肠黏膜损伤较IR组明显减轻,且肠组织MDA含量、MPO活性均低于IR组(P<0.05).结论 肝缺血再灌注所致小肠明显淤血性损伤,MDA含量、MPO活性升高,丹参预处理对肝缺血再灌注所致小肠损伤具有保护作用.     

山莨菪碱对梗阻性黄疸心脏的保护作用

目的 观察梗阻性黄疸时山莨菪碱对心脏的保护作用。方法将30只成年Wistar大鼠随机分为假手术组和梗阻性黄疸模型组;模型组包括山莨菪碱治疗组,生理盐水对照组。分别于术后第14、28天测定各组血浆内毒素含量,观察心肌病理、酶组织化学和心率改变及山莨菪碱治疗后的变化。结果生理盐水对照组血浆内毒素水平明显升高,心肌出现变性、局灶坏死、线粒体破损等病理改变,心肌组织琥珀酸脱氢酶、腺苷三磷酸酶活性明显降低(P<0.05),而酸性磷酸酶活性明显增强(P<0.05),心率明显减缓(P<0.05),山莨菪碱治疗组则以上情况均有明显改善(P>0.05)。结论 山莨菪碱对梗阻性黄疸时心脏有保护作用。