生长抑素对膀胱引流式犬胰腺移植 Oddi括约肌及外分泌功能的影响

目的研究人工合成的生长抑素类似物思他宁对膀胱引流式犬胰腺移植后移植物Oddi括约肌(SO)和外分泌功能的影响.方法正常犬和膀胱引流式胰腺移植后犬应用思他宁前后进行SO测压,检测移植后犬应用思他宁前后尿中胰蛋白酶原激活肽(TAP)和淀粉酶水平.结果正常犬SO有规律收缩,基础压为(18.5±2.8)mmHg,收缩频率为(9.7±1.5)次/min,收缩幅度为 (47.1±5.5)mmHg,动力指数为(235.6±56.1).应用思他宁后SO 基础压、收缩频率、收缩幅度和 动力指数分别显著降低为(11.5±4.3)mmHg,(3.8±0.8 )次/min,(22.7±5.3)mmHg和(76.9±16.4),与用药前相比,P均<0.01.移植物SO基础压和收缩频率分别升高为(27.8±2.8)mmHg和(13.1±1.9)次/min,收缩幅度缩小为(8.3±1.8)mmHg,动力指数无明显变化.移植犬应用思他宁后,SO基础压和动力指数分别升高为(35.2±4.2)mmHg和(418.7±81.5),与用药前相比,P均<0.01.收缩频率和幅度无明显变化(P>0.05).用思他宁后尿淀粉酶和TAP水平分别显著降低为( 5 000±350) IU/L和(15.6±3.7) nom/L,与用药前相比,P<0.01.结论生理情况下,思他宁可抑制犬SO运动,胰腺移植后,思他宁对移植物SO起直接激动作用,思他宁还可以降低膀胱引流式犬胰腺移植后尿中的胰蛋白酶原激活肽和尿淀粉酶水平,从而有助于防治移植物胰腺炎.     

三硝酸甘油对胰腺移植犬Oddi括约肌运动的影响

目的 研究三硝酸甘油(GTN)对膀胱引流式犬胰腺移植后移植物Oddi括约肌(SO)功能的影响。方法 对正常犬和膀胱引流式胰腺移植后犬应用GTN前后进行SO测压,并检测犬SO中环磷酸鸟苷(CGMP)水平。结果 正常犬SO基础压为(18.5±2.8)mm Hg(1 mm Hg=1.33kPa),收缩频率为(9.7±1.5)次/分,收缩幅度为(47.1±5.5)mm Hg,动力指数为235.6±56.1。应用GTN后SO基础压、收缩频率、收缩幅度和动力指数分别显著降低为(8.1±2.4)mm Hg,(6.2±1.0)次/分,(21.1±4.0)mm Hg和66.5±22.7,与用药前相比,差异有极显著性(P均<0.01)。移植物SO基础压和收缩频率分别升高为(27.8±2.8)mmHg和(13.1±1.9)次/分,收缩幅度缩小为(8.3±1.8)mm Hg。移植犬应用GTN后,基础压、收缩频率和动力指数分别降低为(20.2±2.7)mm Hg,(7.5±1.4)次/分和98.8±28.5,与用药前相比,差异有显著性(P均<0.05)。应用GTN后,正常犬和移植犬SO中CGMP水平分别为(86.5±15.5)pmol/g和(62.6±12.6)pmol/g,显著高于应用GTN前(P<0.01)。结论 GTN可能通过提高SO组织中CGMP水平抑制正常和移植后犬的SO运动。     

膀胱引流式胰腺移植后Oddi括约肌运动变化的实验研究

目的　研究膀胱引流式胰腺移植后移植物Oddi括约肌功能的变化以及对移植物功能的影响。方法　应用三腔测压管对正常犬、膀胱引流式胰腺移植后犬和离体的犬Oddi括约肌进行测压 ,并检测移植后犬Oddi括约肌的抗反流能力 ,同时监测移植物内外分泌功能。结果　正常犬Oddi括约肌在 ( 18 5± 2 8)mmHg( 1mmHg =0 133kPa)基础压水平上有规律收缩 ,收缩频率为 ( 9 7±1 5 )次 /min ,收缩幅度为 ( 4 7 1± 5 5 )mmHg ,动力指数为 2 36± 5 6。移植后犬胰腺内外分泌功能良好 ,移植物Oddi括约肌失去了正常的收缩规律 ,基础压升高至 ( 2 7 8± 2 8)mmHg ,收缩频率增快至( 13 1± 1 9)次 /min ,但收缩幅度明显缩小至 ( 8 3± 1 8)mmHg ,动力指数无明显变化。胆管残端内压力不随膀胱内压升高而发生变化。结论　膀胱引流式犬胰腺移植后 ,移植物Oddi括约肌丧失了正常的收缩规律 ,基础压升高 ,收缩频率增快 ,但收缩幅度明显缩小 ,仍然具有一定的抗反流能力     

胆囊收缩素对自体胰腺移植犬Oddi括约肌功能的影响

目的研究胆囊收缩素对胰腺移植后移植物Oddi括约肌功能的影响。方法对正常犬和膀胱引流式胰腺移植后犬应用胆囊收缩素前后进行Oddi括约肌测压。结果与正常犬相比 ,应用胆囊收缩素后Oddi括约肌的基础压、收缩频率、收缩幅度和动力指数显著降低 ,分别为 (1 8 5±2 8)mmHg与 (1 0 2± 2 2 )mmHg(P <0 0 1 )、(9 7± 1 5 )次 /min与 (5 0± 1 2 )次 /min (P <0 0 1 )、(4 7± 6 )mmHg与 (1 9± 5 )mmHg(P <0 0 1 )、(2 36± 5 6 )与 (5 0± 1 7) (P <0 0 1 )。移植物Od di括约肌基础压和收缩频率分别升高为 (2 7 8± 2 8)mmHg和 (1 3 1± 1 9)次 /min ,收缩幅度降低为(8± 2 )mmHg。移植犬应用胆囊收缩素后 ,基础压、收缩频率和动力指数分别升高为 (35 5± 5 1 )mmHg ,(1 8 9± 1 9)次 /min和 (5 1 5± 4 2 ) ,与用药前相比 ,P均 <0 0 1。 结论胆囊收缩素可抑制正常犬的Oddi括约肌运动 ,但对移植胰腺的Oddi括约肌起激动作用     

生长抑素对Oddi's括约肌功能的影响

目的: 研究生长抑素类似物施他宁对奥狄括约肌(sphincter of Oddi,SO)功能状态的影响.方法: 通过T管窦道经胆道镜途径顺行插入测压管至SO,低压水灌注系统压力传感器与微机相连记录压力曲线,分析软件进行压力曲线分析.结果: 对SO基础压的作用与用药前差异显著(P<0.01);对SO收缩幅度的影响无显著性意义;对SO收缩间期的影响与用药前比较差异显著(P<0.05);对SO收缩频率的影响与用药前比较差异显著(P<0.05).施他宁倍量输入后10 min SO收缩频率与用药前已无差异,与5 μg/min用药10 min比较差异显著(P<0.05).结论: 施他宁显著降低SO基础压,延长收缩间期且具有剂量依赖性.对收缩频率的影响:低剂量时增加,高剂量时抑制;对收缩幅度的作用:高剂量时收缩幅度下降但无显著性意义.     

红霉素对十二指肠、Oddi括约肌及胆囊收缩力的影响

实验证明,胃、十二指肠、Oddi氏括约肌及胆囊在不消化时,受内源性或外源性吗丁啉(Motilin)的影响而仍有收缩.近年发现红霉素在其治疗剂量时能与吗丁啉受体结合而产生与吗丁淋相似的效果,因此可用以治疗胃肠道功能障碍.但对红霉素促进胃肠平滑肌收缩的有效剂量瞭解甚少.作者用草原犬鼠动物模型做了一系列实验:用不同浓度的红霉素乳糖醛酸盐间断输入后,比较十二指肠、Oddi氏括约肌、胆囊收缩幅度、频率与动力指数的变化.在用0.01及0.1mg/kg剂量滴入后,十二指肠的变化不明显.用1.0及10.0mg/kg剂量后,十二指肠收缩振幅明显加大(P<0.05);而用10mg/kg剂量后十二指肠的收缩振幅又明显大于1.0mg/kg时(P<0.05).十二指肠收缩的频率在0.01及 0.1mg/kg剂量时变化也不明显,而1.0与10mg/kg剂量时也出现相似的增高(P<0.05).相似地,十二指肠的动力指数在丑1.0及10.0mg/kg剂量时也明显高于对照     

一氧化氮与胆囊收缩素对犬Oddi括约肌的作用

目的 探讨一氧化氮和胆囊收缩素(CCK)在犬Oddi括约肌运动调节中的作用.方法 测定正常状态及注射CCK、硝普钠、一氧化氮合酶(NOS)抑制剂N-硝基-L-精氨酸甲酯(L-NAME)时,犬Oddi括约肌的基础压、时相收缩频率、时相收缩幅度;免疫组织化学染色法检测犬Oddi括约肌上NOS阳性神经元的表达情况.计量资料的比较采用t检验.结果 注射0、20 ng/kg CCK后,犬Oddi括约肌基础压、时相收缩频率、时相收缩幅度分别为(27±10)mm Hg(1 mm Hg=0.133 kPa)、(10±3)次/min、(32±8)mm Hg和(61±14)mm Hg、(64±21)次/min、(44±15)mm Hg;注射100 ng/kg CCK后产生最大抑制作用和最大兴奋作用时,犬Oddi括约肌基础压、时相收缩频率、时相收缩幅度分别为(77 +31)mm Hg、(69±18)次/min、(79±14)mm Hg和(140±21)mm Hg、(129±25)次/min、( 173±63)mm Hg.胆总管滴注硝普钠后,犬Oddi括约肌基础压、时相收缩幅度均下降(t =3.706,5.183,P＜0.05).而注射L-NAME后,犬Oddi括约肌基础压、时相收缩幅度均升高(t=5.859,3.588,P＜0.05).结论 20 ng/kg生理剂量的CCK可舒张犬Oddi括约肌,大剂量CCK可兴奋犬Oddi括约肌;一氧化氮对犬Oddi括约肌发挥舒张效应,此效应可能在CCK的抑制通路中发挥重要作用.     

IPC、IPO和IPC-IPO对胰腺冷缺血再灌注损伤保护作用的对比研究

目的对比研究缺血预处理(IPC)、缺血后处理(IPO)以及二者联合应用(IPC-IPO)对胰腺缺血再灌注损伤(IRI)的保护作用。方法建立SD大鼠糖尿病模型,24只糖尿病大鼠用于建立胰腺移植模型,随机分为4组,每组6只:I/R组、IPC组、IPO组和IPC-IPO组,另6只糖尿病SD大鼠为假手术组(SO组),检测各组大鼠再灌注前、后血糖水平以及再灌注后2 h移植胰腺组织中SOD和MDA含量,并采用TUNEL法观察移植胰腺组织细胞凋亡情况。结果各组大鼠再灌注前血糖水平之间的差异均无统计学意义(P>0.05);SO组大鼠再灌注后血糖水平明显高于其他4组(P<0.01);I/R组、IPC组、IPO组和IPC-IPO组大鼠再灌注后血糖水平均比再灌注前明显下降(P<0.05或P<0.01),I/R组又明显高于后3组(P<0.01),而后3组大鼠再灌注后血糖水平间的差异均无统计学意义(P>0.05)。再灌注后IPC组、IPO组和IPC-IPO组大鼠与I/R组比较MDA含量均明显降低(P<0.01),而SOD含量均明显升高(P<0.01);与SO组比较,I/R组、IPC组、IPO组和IPC-IPO组大鼠MDA均明显升高(P<0.01),而SOD含量均明显降低(P<0.01);IPC组、IPO组和IPC-IPO组大鼠MDA及SOD含量的差异无统计学意义(P>0.05)。I/R组、IPC组、IPO组和IPC-IPO组大鼠再灌注后2 h胰腺组织中AI值分别为(47.31±4.52)%、(26.25±3.17)%、(24.73±3.62)%和(25.5±4.15)%,均明显高于SO组的(3.16±0.53)%,P<0.01;IPC组、IPO组和IPC-IPO组大鼠与I/R组比较AI值明显降低(P<0.01);而IPC组、IPO组和IPC-IPO组间AI值的差异均无统计学意义(P>0.05)。病理组织学检查显示,I/R组大鼠胰腺损伤最为明显。结论 IPO和IPC对胰腺的IRI均有相似的保护作用。IPC与IPO联合应用对大鼠胰腺IRI和细胞凋亡的保护作用无叠加效应。     

良性前列腺增生并急性尿潴留后的逼尿肌功能评估及其临床意义

目的评估良性前列腺增生(BPH)并急性尿潴留(AUR)后的逼尿肌功能及其临床意义。方法随机选择38例BPH并AUR患者行膀胱压力-容积和压力-流率测定,分析留置尿管时间、逼尿肌收缩力、逼尿肌无抑制性收缩(DI)、DI幅度、梗阻程度之间的相关性。结果38例患者中,发生DI者22例(57.9%),DI幅度3~176(100±41)cmH2O(1cmH2O=0.098kPa);有随意性逼尿肌收缩者32例(84.2%),明确诊断为膀胱出口梗阻者28例(73.7%);逼尿肌收缩力与留置尿管时间无相关性(r=-0.024,P>0.05),与DI、DI幅度、梗阻程度有相关性(r分别为0.377、0.604、0.473,P分别为<0.05、0.01、0.01);DI与梗阻程度无相关性(r=-0.222,P>0.05),DI幅度与梗阻程度呈显著性正相关(r=0.494,P<0.01)。结论BPH并AUR患者尿动力学检查前无需留置尿管2~3周以上;有DI者的逼尿肌收缩力强于无DI者;膀胱出口梗阻越严重,DI幅度越大,逼尿肌收缩力越强,手术效果越好。     

犬Oddi括约肌狭窄模型的建立及其胆道动力学的变化

目的建立犬Oddi括约肌（sphincter of Oddi,SO）狭窄模型,探讨其胆道动力学的变化。方法禁食16～18h成年杂种犬麻醉后,超声测量胆总管管径。实验组行经腹切开十二指肠,机械性损伤SO致其狭窄;对照组仅行经腹切开十二指肠,术毕饲养。定期检查肝功能,4周后再次麻醉下行超声测量胆总管管径及开腹行SO测压。最后切取SO及周围组织行病理检查。结果实验组术后4周肝功能TBIL、DBIL、GGT、ALP明显高于术前,超声测量胆总管管径大于术前,病理检查发现括约肌组织纤维化,而对照组均无明显变化。与对照组相比,实验组胆总管及SO基础压明显升高,SO收缩幅度降低,收缩频率升高,收缩时间缩短。结论SO狭窄模型成功建立;Oddi括约肌狭窄后其胆道动力学发生明显改变。     

Gastrosphincter of Oddi reflex

Gastric distention is known to stimulate gallbladder contraction as well as gastric acid and pancreatic exocrine secretion by way of neural reflexes. Gallbladder distention, in turn, has been shown to affect sphincter of Oddi motility. Since gastric distention may accompany endoscopic or operative biliary manometry, we tested the hypothesis that gastric distention alters sphincter of Oddi motility. In the prairie dog model, gastric distention with acid (0.1 M hydrochloric acid, pH 1.3) and alkaline (10(-5) sodium hydroxide, pH 8.8) isotonic saline solutions both resulted in significant increases in sphincter of Oddi phasic wave frequency, amplitude, and motility index. Similarly, gallbladder pressure increased during both distention periods, thus confirming the previously described pylorocholecystic reflex. These responses were abolished by systemic pretreatment with atropine, suggesting that this reflex is cholinergically mediated. These data suggest the presence of a gastrosphincter of Oddi reflex whereby gastric distention stimulates sphincter of Oddi motility in the prairie dog. We conclude that gastric distention is an important variable to be controlled when performing endoscopic or operative sphincter of Oddi manometry.     

Ethanol inhibits sphincter of oddi motility

Patients with alcohol-induced liver disease are at increased risk for pigment gallstones, which are known to be particularly associated with biliary stasis. Although the effects of ethanol on the sphincter of Oddi are thought to contribute to alcoholic pancreatitis, the precise effects of ethanol on the biliary component of the sphincter of Oddi are unclear. In the prairie dog the common bile and pancreatic ducts enter the duodenum separately, facilitating pressure measurement in the sphincter choledochus in isolation. We therefore used this model to test the hypothesis that ethanol administration alters sphincter of Oddi motility. Twenty-six male prairie dogs fed a nonlithogenic diet were studied. With the animals under α-chloralose anesthesia, a side-hole pressure-monitored perfusion catheter was positioned in the sphincter of Oddi and femoral arterial and venous catheters were placed. Sphincter of Oddi phasic wave frequency (F), amplitude (A), and motility index (MI = F × A) and arterial blood pressure were monitored at 10-minute intervals before (baseline), during 20-minute intravenous infusions of 15 mg/kg (n = 9), 150 mg/kg (n = 10), and 1.5 g/kg (n = 7) ethanol and for 20 minutes after ethanol infusion. The 15 mg/kg dose of ethanol had no effect, the 150 mg/kg dose tended to reduce sphincter of Oddi motility, and significant reductions in sphincter of Oddi amplitude and motility index were seen at the 1.5 g/kg dose. These data demonstrate that ethanol infusion inhibits both sphincter of Oddi amplitude and motility index and that this effect persists for at least 20 minutes following ethanol infusion. Ethanol may contribute to gallstone formation by altering biliary sphincter motility. Supported by National Institutes of Health grants R29-DK41889 (K.D.L.) and R01-DK44279 (H.A.P.)     

Peptide YY inhibits cholecystokinin-stimulated sphincter of Oddi activity in the prairie dog

Peptide YY (PYY), a recently discovered gut peptide, has been shown to have a number of actions that are antagonistic to the effects of cholecystokinin. This study was designed to determine whether PYY would inhibit cholecystokinin-stimulated sphincter of Oddi activity in the prairie dog. In 12 prairie dogs PYY was infused intravenously at 1, 10, and 100 ng/kg/min, and arterial blood samples were obtained. A dose-response curve was obtained, with the 10 ng/kg/min dose producing serum levels of 725 pg/ml. In seven additional prairie dogs a side-hole, pressure-monitored perfusion catheter was passed into the duodenum through a choledochotomy and positioned in the sphincter of Oddi. A perfusion catheter was also placed in the gallbladder fundus. Sphincter of Oddi and gallbladder pressures were recorded before and during 20-minute infusions of cholecystokinin and then cholecystokinin plus PYY at 10 ng/kg/min. PYY significantly inhibited cholecystokinin-stimulated sphincter of Oddi phasic wave frequency (3.8 +/- 0.2 vs 3.3 +/- 0.4; p less than 0.05) and sphincter of Oddi motility index (26.2 +/- 4.3 vs 18.7 +/- 4.8; p less than 0.025) but did not affect the increase in gallbladder pressure induced by cholecystokinin. These findings are consistent with other known anticholecystokinin effects of PYY. We conclude that PYY may also inhibit sphincter of Oddi activity in the prairie dog by an anticholecystokinin effect, thus reducing flow through the sphincter.     

A new method for correlating pancreatic and biliary duct pressures and sphincter of Oddi electromyography

Myoelectric activity of the sphincter of Oddi and duodenum was correlated with pancreatic and biliary duct pressures in eight opossums, in both the fasted and fed states. Four bipolar electrode pairs were implanted in the sphincter of Oddi and duodenum. A polyethylene T tube was placed in the pancreatic duct. The common duct was cannulated through a small bile duct. This method allowed pressure recording for several weeks and avoided interference with the flow of bile or pancreatic juice into the duodenum. The frequency of slow waves was the same in the sphincter of Oddi and duodenum (19 per minute). The variation in the frequency of spike potentials in the sphincter of Oddi correlated to that of the migrating myoelectric complex in the duodenum. The average frequency of slow waves that have superimposed spike potentials in the sphincter of Oddi and duodenum was 3.0 and 0 in phase 1, 4.7, and 6.2 in phase II, 6.1 and 15.1 in phase III, and 3.4 and 6.3 in phase IV, respectively. The average duration of a migrating myoelectric complex cycle was 92 minutes. After feeding, the interdigestive phases of the migrating myoelectric complex were abolished and substituted by a feeding activity pattern that was characterized by an average number of sphincter of Oddi and duodenum spikes of 6.6 and 10.7, respectively. The mean fasting pressure in the pancreatic and biliary duct was 15 and 13 mmHg, respectively. Pressure changes were of two types--synchronous with respiratory movements and with each sphincter of Oddi spike potential. There was no variation in the baseline pressure during the migrating myoelectric complex phases and the fed state. It is concluded that the sphincter of Oddi of the fasting opossum exhibits cyclic changes in the number of spike potentials that correlate with the migrating myoelectric complex in the duodenum. However, the number and amplitude of spike potentials are different in the sphincter of Oddi and duodenum. There is no change in the baseline pressure during fasting and feeding states, and a temporary pressure elevation synchronic with each sphincter of Oddi spike potential was observed.     

内皮素对Oddi括约肌功能影响的实验研究

目的 ：研究内皮素（ET）对离体Oddi括约肌收缩的直接影响，并对其传导通路进行探讨。方法 ：（1）按累积加药法在K-H液中加入各浓度（0.1～100.0nmol/L）的ET-1，观察Oddi括约肌收缩频率及振幅的变化;（2）加入ET-1抗血清、尼卡地平、BQ-123后，再加入ET-1，测定三者对Oddi括约肌收缩的影响;检测Oddi括约肌PKC的活性。结果 ：ET能收缩静息状态下的Oddi括约肌，其作用强度随ET浓度的增加而增强。随着ET-1浓度的增高，Oddi括约肌细胞胞浆蛋白激酶（PKC）活性也呈增高趋势。尼卡地平对ET所致的Oddi括约肌收缩反应无明显抑制作用，ET抗血清及BQ-123能显著抑制ET所致的Oddi括约肌的收缩。结论 ：ET-1 能明显收缩离体Oddi括约肌，其收缩强度与ET存在量效关系。ET抗血清和ET受体拮抗剂（BQ-123）对ET-1有较强的拮抗作用。PKC参与ET-1引起的Oddi约肌收缩的信号传导。     

A comparison of common bile duct pressures after botulinum toxin injection into the sphincter of Oddi versus biliary stenting in a canine model

BACKGROUND: Botulinum toxin A (Botox) functionally paralyzes the sphincter of Oddi in both animals and humans, resulting in reduced pressures. No study, however, has specifically addressed common bile duct (CBD) pressures after Botox injection into the sphincter of Oddi with regard to treating biliary leaks and fistulae. The goals of this present study are to compare, versus biliary stenting, the change in CBD pressures after Botox injection into the sphincter of Oddi, as well as to evaluate the timing of onset and duration of these effects on sphincteric relaxation. METHODS: After midline laparotomy in 20 mongrel dogs, a pediatric umbilical catheter was inserted into the CBD via a small cholecystotomy and attached to a water-perfused pressure transducer. After baseline CBD pressure readings, a lateral duodenotomy was performed. A total of 100 units of Botox was injected with an endoscopic sclerotherapy needle into all four quadrants of the ampulla. The dogs were randomly divided into four groups to undergo repeat laparotomy at either postoperative day 1 (group I), postoperative day 3 (group II), postoperative day 7 (group III), or postoperative day 14 (group IV). At the time of second laparotomy, a pressure-sensing catheter was reinserted into the CBD and pressures recorded. Each dog then underwent transpapillary biliary stenting with a 7 Fr. x 5 cm Cotton-Leung biliary stent and CBD pressures were again recorded. RESULTS: CBD pressures were significantly lower as compared with baseline for all groups after Botox injection and after biliary stenting (P <0.001) In addition, no significant differences in the degree of CBD pressure reduction were identified between groups I through IV after Botox injection. The measured decrease in CBD pressure from baseline after Botox injection as compared with biliary stenting was significantly different for groups I and II (P <0.05) but not for groups III and IV. CONCLUSION: Botox injection into the sphincter of Oddi results in significant CBD pressure reduction within 24 hours and continues for 14 days. Also, after postoperative day 3, there is no significant difference in the reduction of CBD pressure from baseline between Botox injection and biliary stenting. Based on these findings, Botox injection into the sphincter of Oddi may be a beneficial alternative to biliary stenting for the treatment of biliary leaks and fistulae.     

犬胆囊、Oddi括约肌电活动和胆囊胆总管压力的同步检测

目的探讨同步检测犬胆囊、Oddi括约肌肌电和胆囊、胆总管压力的实验方法。方法采用多通道生理仪同步记录麻醉后犬的胆囊和Oddi括约肌的肌电图以及胆囊、胆总管压力。剖腹显示肝、胆、胃及十二指肠,用7F静脉深穿管经肝穿刺进入胆囊腔内作为测压通道,再将一对铂金电极缝在胆囊底部浆膜上。把另一条7F静脉深穿管制作成带一对铂金电极的胆总管测压和Oddi括约肌肌电检测通道。结果Oddi括约肌峰电位为0．18～0．20mV,频率为2～5次／min;其慢波电位0．06～0．08mV,频率为8～10次／min,峰电位往往在某次慢波电位的基础上突然出现。胆囊肌电不明显。胆囊的压力为7～9cmH2O,胆总管压力为11～15cmH2O。结论同步检测Oddi括约肌肌电活动与胆囊、胆总管压力的实验方法是可行的,有利于研究Oddi括约肌肌电活动与胆囊及胆总管压力的关系,但是对于记录在体胆囊的肌电活动方法需要进一步改进。     

Sphincter of Oddi response to caerulein after endoscopic sphincterotomy for papillary stenosis

Using a percutaneous transhepatic cholangioscopy (PTCS) catheter, sphincter of Oddi motility was measured in a patient with papillary stenosis secondary to bile duct stones. Prior to sphincterotomy, intramuscular injection of 20 micrograms caerulein did not inhibit pathological contraction waves of the sphincter of Oddi or relieve abdominal pain. Endoscopic sphincterotomy of the lower segment of the sphincter of Oddi resulted in recovery of the normal response to caerulein, i.e. relaxation of the sphincter of Oddi. This observation indicates that the pathological contraction and lack of relaxation to cholecystokinin in a patient with papillary stenosis is due to high common bile duct pressure. The measurement of motility of sphincter of Oddi via the PTCS route is useful in diagnosing motor disorders in the sphincter of Oddi and is helpful in deciding to perform endoscopic sphincterotomy.     

乌司他丁治疗老年重症急性胰腺炎的临床观察

目的观察乌司他丁(Ulinastatin,UTI)对早期老年重症急性胰腺炎(severe acute pancrea-titis,SAP)的临床疗效。方法69例老年SAP患者随机分成两组:UTI组38例,应用乌司他丁治疗;对照组31例,采用奥曲肽治疗。结果组内比较,白细胞计数第10d较第1d明显降低(P<0.05),血清淀粉酶及CT所示胰腺坏死范围第5d、第10d的结果较第1d明显降低和缩小(P<0.05),且与患者的临床表现相一致。但组间比较无统计学差异(P>0.05)。UTI组治疗有效率为86.8%(33/38),并发症发生率为63.2%(24/38);奥曲肽组治疗有效率为90.3%(28/31),并发症发生率为54.8%(17/31)。两组比较均无统计学差异(P>0.05)。结论乌司他丁治疗早期老年SAP有肯定的疗效。