0.25%5—氟脲嘧啶胰被膜下灌注抑制胰腺外分泌的研究

通过动物模型的制作探讨了在急性出血坏死性胰腺炎时,清除坏死胰组织后,在胰被膜下局部灌注抗代谢药5-FU与静脉滴注5-FU,对抑制胰腺外分泌淀粉酶含量的动态变化。结果表明,胰被膜下局部灌注5-FU犬组(A组)在48小时末血清淀粉酶和主胰管插管胰液淀粉酶的含量分别降至49±13、189±31苏氏单位;静脉滴注5-FU犬组(B组)在48小时末分别降至46±28、198±28苏氏单位(P>0.05),提示胰被膜下局部灌注5-FU使之与有生机的胰组织直接接触,抑制胰腺外分泌同样能达到静脉途径给药的目的。     

犬急性水肿型胰腺炎胰液外引流模型的制备及胰腺外分泌功能的观察

目的建立犬急性水肿型胰腺炎胰液外引流模型,观察胰腺外分泌的功能。方法健康杂种犬12只,分为对照组和胰腺炎组,每组6只。制备犬胰液外引流模型后24h,5%牛磺胆酸钠(0.5mL/kg)1mL/min胰管逆行注射制备急性水肿型胰腺炎模型。每12h收集胰液一次,测定胰液的分泌量,胰液中淀粉酶、脂肪酶、总蛋白、pH值和主要电解质含量。制模后在不同时段采血,检测血中的淀粉酶、脂肪酶的浓度。取胰腺组织行病理学检查。结果成功建立犬急性水肿型胰腺炎胰液外引流模型。胰腺炎组胰液分泌量,胰液中淀粉酶、脂肪酶、总蛋白、HCO3-含量和pH值低于对照组(P0.05),Cl-高于对照组(P0.05)。胰液中的Na~+、K~+、Ca~(2+)、Mg~(2+)胰腺炎组与对照组差异无统计学意义(P0.05)。结论本模型适用于急性水肿型胰腺炎胰腺外分泌功能的研究。     

质子泵抑制剂对犬胰腺外分泌功能影响的研究

目的 探索质子泵抑制剂（proton pump inhibitor,PPI）对犬胰腺外分泌功能的影响。方法健康成年犬24只平均随机分成4组：对照组（A组）、对照给药组（B组）、胰腺炎组（C组）、胰腺炎给药组（D组）。A组和B组制备犬胰液外引流模型,C组和D组制备犬急性水肿型胰腺炎胰液外引流模型。采用5%牛磺胆酸钠（0.5 mL/kg）以1 mL/min胰管逆行注射制备急性水肿型胰腺炎模型。B组和D组建模成功后立即给予泮托拉唑（0.7 mg/kg+生理盐水50 mL,q12 h）,A组和C组给予等量的生理盐水。各组每12 h收集胰液一次,并测量胰液的分泌量,胰液中的淀粉酶、脂肪酶、总蛋白含量和pH值。胰腺组织送病理学和电镜检查。结果 B组与A组比较,胰液的分泌量,胰液中淀粉酶、脂肪酶的浓度和pH值在第1天和第2天均降低（P ＜0.05）。胰液中总蛋白的含量第1天B组和A组无明显统计学差异（P ＞0.05）,第2天B组低于A组（P ＜0.05）。D组与C组比较,胰液的分泌量,胰液中淀粉酶、脂肪酶、总蛋白的浓度和pH值无明显变化（P ＞0.05）。D组和C组在不同时间段的血淀粉酶、脂肪酶浓度无明显差别（P ＞0.05）。病理学检查未见明显的差别。电镜下可见PPI作用后胰腺腺泡细胞内酶原颗粒增多。结论 质子泵抑制剂能够明显抑制正常犬的胰腺外分泌,但对急性水肿型胰腺炎犬的胰腺外分泌功能影响不大。     

谷氨酸受体拮抗剂在严重烧伤大鼠脑组织中的作用

目的 探讨烧伤后谷氨酸对脑组织的影响及谷氨酸受体拮抗剂的作用。方法 采用30％TBSAⅢ度烧伤大鼠模型,伤后2、6、12和24h测定了脑水含量、脑组织K^ 、Na^ 、Ca^2 、Mg^2 和-氧化氮(NO)代谢产物NO2^-／NO3^-浓度,在光镜和电镜下进行形态学和组织化学研究。结果 烧伤后脑水含量升高,脑组织Na^ 、Ca2^ 、NO2^-／NO3^-浓度高于对照组;脑内ATP酶减少;电镜观察毛细血管内皮细胞、神经细胞及胞浆部分线粒体肿胀,毛细血管壁出现胞饮泡。给予谷氨酸受体拮抗剂D-2-氨基-7-磷庚酸脂(D—AP7),可使脑水含量、脑组织Na^ 、Ca^2 、NO2^-／NO3^-浓度降低,毛细血管壁胞饮泡减少,神经细胞肿胀减轻。结论 烧伤后脑微血管通透性增加、组织细胞有缺血性改变和水肿发生。烧伤后脑组织形态及代谢变化与谷氨酸过量释放有关。兴奋毒性作用通过其受体介导,谷氨酸受体拮抗剂D—AP7可减轻烧伤后脑损伤。     

改良式胰肾联合移植1例并文献复习

目的探讨改良式胰肾联合移植治疗2型糖尿病合并终末期肾病的移植效果。方法为1例2型糖尿病合并终末期肾病患者行改良式胰肾联合移植,其中移植胰腺的外分泌采用胰液空肠内引流术式,将供胰十二指肠节段与受体上段空肠直接行侧侧吻合。结果术后围手术期移植肾稳定泌尿,3800～4500ml/24h,3d后血清肌酐降至正常水平。术后胰腺功能恢复顺利,血、尿淀粉酶逐渐下降并稳定在正常范围,空腹血糖也于术后10d恢复至正常值范围以内。切口一期愈合,于术后两周出院。随访27个月移植肾功能正常,胰腺功能正常,未发生血栓、胰瘘、胰腺炎、排斥反应等并发症。结论改良式胰肾联合移植技术简单、安全,胰液经空肠引流更接近消化生理,是治疗糖尿病合并终末期肾病的有效手术方式。     

手术前期大剂量快速静脉输注佳乐施时血清钾的变化

目的 前瞻性研究手术前期大剂量快速静脉输注佳乐施时血清钾的变化及其影响因素。方法 选择中上腹部手术患者30例，随机分为佳乐施组（GEL组）和对照组，每组15例。硬膜外穿刺完毕后，抽取第一次标本，作为基础值，佳乐施组开始输注佳乐施10ml/kg，半小时内输完，取第二次标本（T30min），再输注佳乐施10ml/lkg，1小时内输完，取第次标本（T90min），之后30分钟（T120min)及90分钟（T180min)分别取第4、第5次标本，检测血清电解质Na^ 、K^ 、Cl^-、Ca^2 、Mg^2 ；pH值、渗透压、红细胞压积；尿电解质Na^ 、K^ 、Cl^ 、Ca^2 、Mg^2 ；红细胞内电解质K^ 、Mg^2 。对照组以生理盐水代替佳乐施，操作方法同实验组。结果 快速大量静脉输注佳乐施，血清K 呈进行性下降。 结论 手术期间大量快速静脉输注佳乐施可能发生血钾降低。     

胰肾联合移植术: 附19例报告

摘要：目的 探讨胰肾联合移植术中药物的应用方法，以取得良好的术后效果。方法 19例胰肾联合移植受者，术中用药如下；以白蛋白（清蛋白）作为主要血管扩容剂，平均用量为1.5~2.0g/kg；电解质溶液输注量为30~50mL/kg；用异搏定（5mg/12h）、前列腺素E1 （100μg/12h）以减少移植器官的保存损伤；用生长抑素（3mg/12h）抑制移植胰腺外分泌功能。结果 19例受者移植胰腺通血后5~10min分泌含高淀粉酶（平均为20 800U/L）的胰液，供肾血管开放后2~10min，输尿管有尿液流出。术后2~4d肾功恢复，术后1.5h至9d停用胰岛素。结论 胰、肾联合移植术中合理应用白蛋白、血管扩张剂和生长抑素对移植胰、肾功能有良好作用。     

改良式胰液肠腔引流胰十二指肠及肾一期联合移植(附二例报告)

目的 研究改良式胰液肠腔引流胰十二指肠及肾一期联合移植的效果、术式、用药量及并发症。方法 对2例1型糖尿病并发尿毒症患者施行改良式胰液肠腔引流胰十二指肠及肾一期联合移植，术后早期应用他克莫司(FK506)、霉酚酸酯(MMF)、皮质激素和抗胸腺细胞球蛋白(ATG)进行免疫治疗。监测胰腺、肾功能恢复。结果 2例患者术后第3—5天肌酐、尿素氮恢复正常，术后第5—10天停用胰岛素，移植胰腺分泌功能正常。例1术后第7天出现FK506中毒，尿量减少，经调整FK506用量及血液透析过度，术后第25天肾功能恢复正常；例2术后第20天并发消化道出血，使用生长抑素及基因重组凝血因子Ⅶa等治疗痊愈。随访3—24个月，移植胰和移植肾功能均正常，一般情况良好。结论 改良式胰液肠腔引流胰十二指肠及肾一期联合移植是治疗胰岛素依赖型糖尿病合并肾功能衰竭的较好术式，优质供体及良好配型可减少并发症的发生。     

维拉帕米提高移植胰功能的研究

目的 :研究同种异体胰腺移植中应用维拉帕米提高移植胰的功能。方法 :将 2 0头健康小型猪 ,随机分成A、B两组 ,每组 10头 ,两组均作带十二指肠袢的同种异体胰腺移植 ,除B组供体标本灌注及术后加用维拉帕米外 ,两组围手术期处理均相同。结果 :2 0头猪中 18头及其移植胰存活两周以上 ,A、B组中各有 1例术后第 1天血栓形成致移植胰功能丧失。术后 1～ 3d两组C 肽有所下降 ,第 5天开始回升 ,维持 2w以上。两组同一时段比较B组C 肽高于A组 ,P <0 .0 5。术后第三天起 ,两组胰液淀粉酶开始升高 ,维持 2w以上 ,两组同一时段比较B组高于A组 ,P <0 .0 5。结论 :胰腺移植中供体器官灌注和术后使用维拉帕米可明显改善移植胰的功能。     

门、肠引流式胰肾一期联合移植5例报告

目的:总结胰腺内分泌门静脉引流、外分泌肠腔引流式（PE）一期胰、肾联合移植的临床经验。方法：对5例1型糖尿病并发尿毒症患者施行PE一期胰、肾联合移植术的临床资料及手术技术和非手术性并发症的预防进行回顾性分析。结果：5例手术均获成功，其中3例恢复良好，2例围手术期死亡，分别死于胰漏感染和FK506药物中毒。存活者术后3d血肌酐、尿素氮恢复正常;术后7d停用胰岛素，移植胰内、外分泌功能正常。结论：PE引流式胰腺移植在生理、代谢和免疫学等方面更具优势和合理性;PE式将是胰腺移植优先选择的术式;加强围手术期管理有助于减少术后并发症，取得良好疗效。     

Cellular electrolyte and volume changes induced by acidosis in the rabbit proximal straight tubule.

Cellular acidosis induced either by high Pco2 or by low HCO3- concentrations has been shown to cause cell swelling in isolated, lumen-collapsed, S2 segments of the rabbit proximal tubule (Sullivan et al., Am J Physiol 1990; 258: F831-F839). The swelling is not followed by a volume regulatory response. The ionic basis of the swelling has been investigated by measurement of the cellular K+, Na+, and Cl- content (electron probe) and HCO3- concentration (pH-sensitive fluorescent dye). Cell content of K+, Na+, and Cl- was expressed as a ratio to P content. Exposure to 15% CO2 increased K/P from 0.98 to 1.16, Cl/P from 0.14 to 0.20, and Na/P from 0.09 to 0.11. Cell (HCO3-) increased from 22 to 32 mM. Reduction in bath (HCO3-) from 25 to 5 mM reduced cell (HCO3-) from 24 to 8 mM and increased K/P from 0.75 to 0.90. Na/P fell from 0.13 to 0.09, and Cl/P fell from 0.15 to 0.12. Thus, swelling resulting from acidosis induced by high CO2 was accompanied by an accumulation of K+, Cl-, and HCO3-; that resulting from acidosis induced by a fall in (HCO3-) was combined with an accumulation of K+ and an unidentified anion. To determine if the swelling induced by a fall in pH might be coupled with depolarization of the basolateral membrane, the effect of 1 mM barium was tested. Barium caused cell volume to increase 10.2%. Cell pH rose from 7.38 to 7.56, K/P increased from 0.63 to 0.73, Na/P did not change, and Cl/P rose from 0.17 to 0.20. Cell (HCO3-) increased 10.4 mM. When the pH of the barium-treated tissue was reduced to 7.02 by raising Pco2, additional cell swelling and accumulation of K+ occurred. The effect on cell volume of a reduction of bath (HCO3-) from 25 to 5 mM at constant bath pH was determined. Cell pH was not altered. Cell volume decreased 3% initially and then returned to the control level. When the bath (HCO3-) was restored to 25 mM, cell volume increased 3.9% and then returned to the baseline. Thus, volume regulation was not impaired. It was concluded that a fall in cell pH induces swelling, and this is coupled with an accumulation of K+. This is probably the result of a pH effect on barium-sensitive and barium-insensitive K+ conductance pathways. The nature of the anions that balance the gain in K+ depends on the means used to induce acidosis.     

全麻非心脏手术患者羟乙基淀粉130/0.4电解质注射液与羟乙基淀粉130/0.4氯化钠溶液容量治疗效果的比较:多中心、前瞻、随机、双盲、对照研究

目的 比较全麻非心脏手术患者羟乙基淀粉(HES) 130/0.4电解质注射液与HES130/0.4氯化钠溶液容量治疗的效果.方法 择期全麻非心脏外科手术(神经外科手术除外)患者242例,年龄18～64岁,体重指数18～29 kg/m2,性别不限,ASA分级Ⅰ或Ⅱ级,采用随机数字表法,将患者随机分为试验组和对照组:麻醉诱导后经1h静脉输注6％ HES 130/0.4电解质注射液或6％HES130/0.4氯化钠溶液15ml/kg.于HES输注前和输注结束后15 min时取动脉血样,行血气分析,记录pH值、BE、HCO3-、电解质(K+、Na+、Cl-、Mg2+);测定Hct、Hb、血液生化指标(ALT、AST、Cr、BUN和血糖)、凝血功能指标,记录电解质和血液生化指标异常有临床意义的发生情况、血管活性药物的使用情况,与研究药物有关不良事件(凝血酶原时间延长、活化部分凝血活酶时间延长和高氯血症)的发生情况和术中液体出入量.结果 试验组和对照组最终完成91例和95例.两组液体用量和尿量比较差异均无统计学意义(P＞0.05).与对照组比较,试验组输注结束后15 min时pH值、BE、HCO3-、K+、Mg2+升高,Na+、Cl-降低(P＜0.05),Hb和Hct差异无统计学意义(P＞0.05);与输注前比较,输注结束后15 min时对照组BE、HCO3 -、Mg2+、Hb和Hct降低,Cl-升高,试验组Na+、Mg2+、Hb和Hct降低,Cl-升高(P＜0.05).试验组血钾、血氯异常有临床意义的发生率明显低于对照组(P＜0.05).两组血管活性药物使用率、与研究药物有关的不良事件发生率、生化指标异常有临床意义的发生率比较差异无统计学意义(P＞0.05).结论 与6％HES 130/0.4氯化钠溶液比较,6％ HES 130/0.4电解质注射液扩容效能无差异,但能更好地维持机体电解质和酸碱平衡.     

离子与离子通道在精子获能中的调控机制

哺乳类动物精子膜上的离子通道,包括Ca2+、Na+、K+、Cl-和HCO3-等通道,在精子获能过程中发挥各自重要的作用。精子获能过程通过Ca2+、HCO3-、活性氧等信号分子,激活可溶性腺苷酸环化酶,在环磷酸腺苷(cAMP)、Ca2+以及胞内pH协作下,经cAMP/蛋白激酶A(PKA)和酪氨酸磷酸化信号转导途径促进精子发生获能相关生物效应。     

Effect of hypothermia on pancreatic acinar cells in rats.

This study was designed to evaluate the effects of direct pancreatic surface cooling on the exocrine pancreas. We measured the changes in serum amylase levels, pancreatic water, amylase and cathepsin B as a lysosomal enzyme, content, histological changes of acinar cells, and the subcellular distribution of cathepsin B after 1-2- and 3-hours of direct pancreatic cooling in rats. In addition, we evaluated the in-vivo amylase and cathepsin B output stimulated by caerulein, in-vitro lysosomal and mitochondrial fragility as well as the pancreatic adenylate energy metabolism. 2-hours cooling showed slight yet significant changes, but 3-hours cooling caused most significant changes including hyperamylasemia, increased pancreatic amylase content and very mild histological changes. Furthermore, 3-hours cooling caused a remarkable redistribution of cathepsin B activity from the lysosomal fraction to the heavier zymogen fraction, and colocalization of the lysosomal enzyme with the digestive enzyme, the impaired amylase and cathepsin B output into pancreatic juice stimulated by caerulein as well as the accelerated fragility of lysosomes and mitochondria, and impaired pancreatic adenylate energy metabolism. These results indicate the impaired exocrine pancreatic functions induced by direct pancreatic cooling injury induced by cooling as shown in the other models of experimental pancreatitis. Moreover, this cooling model of pancreatitis seems to be useful in understanding the early events in the pathogenesis of acute pancreatitis, and we must take these "cold" injuries of exocrine pancreas into considerations, particularly in the pancreas transplantation and in other major abdominal surgeries where the pancreas is exposed to cooling.     

Factors affecting metabolic and electrolyte changes after reperfusion in liver transplantation

BACKGROUND: The metabolic and electrolyte changes were evaluated after various durations of cold and warm ischemia times to correlate ASA status with hemodynamic changes that may affect the severity of the reperfusion syndrome. PATIENTS AND METHODS: Sixty-one patients who underwent liver transplantation (OLT) were monitored by arterial pH, PaO2, PaCO2, HCO2, BE, K+, Ca2+, Na+, GL, and serial Ht at three specific times: after the skin incision (baseline), 10 minutes before reperfusion (T2), and 10 minutes after reperfusion (T3). Changes in metabolic parameters were correlated with ASA status, hemodynamic changes, time of OLT, as well as cold and warm ischemia times. RESULTS: The pH in ASA IV patients was significantly lower at T1 and T3, and PCO2 higher in ASA V at T1. A significant correlation was observed between pH, PaCO2, HCO3-, BE, Na+, Ca2+, and glucose with the phase of the procedure. The pH and HCO3- decreased significantly from T1 and T2, increasing during T3. Ca2+ fell from T1 to T2 increasing in T3. Mean glucose and sodium levels increase from T1 to T3. Mean BE dropped from T1 to T2 and increased at T3 without a significant correlation between the metabolic parameters in any phase of the study and the cold or warm ischemia times. Patients with a high ASA status showed an increased risk for cardiovascular collapse after reperfusion. CONCLUSIONS: Patients with advanced ASA status are more prone to metabolic and acid-base disturbances during reperfusion, without any relation to the cold or warm ischemia times. High ASA status shows an increased risk for cardiovascular collapse after reperfusion.     

Physiologic studies of urinary drained pancreaticoduodenal grafts in humans.

Exocrine function of urinary drained pancreas transplants (UDP) as determined by measurements of urinary pancreatic metabolites was assessed in 15 recipients. Normal UDP showed significantly higher levels (P less than 0.05) of urinary amylase, (42,931 +/- 5135 U/liter), HCO3 (27.12 +/- 3.18 meq/liter), and pH 7.83 +/- 0.15) than nine other recipients of enteric drained pancreas transplants with corresponding values of 168.00 +/- 2.00 U/liter, 3.20 +/- 0.20 meq/liter, and 6.08 +/- 0.27. These urinary metabolites dropped significantly (P less than 0.02) during rejection to 13,576 +/- 3446 U/liter, 19.22 +/- 5.74 meq/liter, and 7.06 +/- 0.14, respectively. These changes preceded elevation of blood sugar levels by 2-3 days. During rejection episodes, pancreatic grafts failed also to excrete bicarbonate and amylase significantly in response to secretion stimulation (P less than 0.05) contrary to nonrejecting pancreata. It is concluded that decreases in urinary amylase, HCO3, and pH observed with and without secretin stimulation are simple markers of pancreatic rejection.     

猪全胰十二指肠移植排斥反应的早期诊断

目的 探讨移植胰腺分泌的胰液中肿瘤坏死因子（ＴＮＦ－α）水平、淀粉酶流量和受者的血糖水平在排斥反应早期诊断中的意义。方法 采用全胰切除的猪行全胰十二指肠移植，第１组受者不用免疫抑制剂；第２组受者应用甲泼尼龙＋雷公藤多甙片；第３组受者应用环孢素Ａ＋雷公藤多甙＋甲泼尼龙。观察受者的空腹血糖、胰液淀粉酶流量和ＮＴＦ－α水平。结果 第１组受者移植后第４ｄ胰液和淀粉酶流量下降，第８ｄ停止；第２组受者的胰液和     

Direct surface cooling of the exocrine pancreas in the rat.

A study was carried out to evaluate the effects of direct cooling on the exocrine pancreas. Changes in amylase and cathepsin B release, and in the subcellular distribution of amylase and cathepsin B were measured after 1, 2 and 3 h of direct pancreatic cooling in rats. Cooling for 2 and 3 h caused significant hyperamylasaemia and increased pancreatic amylase content, but minimal histological change. Furthermore, 3 h of cooling caused marked redistribution of cathepsin B activity from the lysosomal fraction to the heavier zymogen fraction, and co-localization of lysosomal and digestive enzymes; amylase and cathepsin B output into pancreatic juice after caerulein stimulation were also reduced. These results show that direct pancreatic cooling impairs exocrine function and implicate lysosomal enzymes in the pathogenesis of pancreatic injury, in agreement with results from other models of experimental pancreatitis.     

The effect of cyclosporine on exocrine function of the rat pancreas--an in vitro study.

We have studied the effect of cyclosporine on the exocrine pancreas of rats submitted to treatment with different parenteral doses (15, 30, 50 mg/kg/day) for different time periods (7 and 30 days). Serum amylase levels, pancreas weight, and total pancreatic amylase and protein content showed a dose-dependent decrease. Basal amylase secretion from isolated lobules remained unchanged. Furthermore, the pancreatic lobules from animals under cyclosporine treatment exhibited a decreased response to bethanechol stimulation. Our data suggest that cyclosporine produces a toxic effect on exocrine pancreatic function.     

Cytoplasmic pH regulation in canine renal proximal tubule cells

The precise mechanisms by which the mammalian kidney proximal tubule transports H+ and HCO3- and regulates cytosolic pH (pHi) remain in doubt, though both a H+-ATPase pump and Na+/H+ exchange at the luminal membrane are known to function in the export of protons. The mechanisms of HCO3- transport are less clear though recent reports suggest an important role for an electrogenic Na+/HCO3- symport in the basolateral membrane. The importance of chloride-dependent bicarbonate transport is unknown. In the present studies, the pH-sensitive fluorescent dye, bis-(carboxyethyl)-carboxyfluorescein (BCECF) has been used to study pHi changes in suspensions of canine proximal tubule cells following acidification or alkalinization of the cytosol. Cells were acid-loaded to pH 6.5 by exposure to the H+/K+ ionophore, nigericin. Following removal of nigericin, pHi returned to basal levels (pHi = 7.1) when the cells were resuspended in a buffer containing 100 mM Na+. This recovery was blocked by removal of Na+ or addition of 0.2 mM amiloride to the cell suspension. In the presence of 0.2 mM amiloride and Na+, partial excretion of the acid load occurred if the buffer also contained HCO3-/CO2, but this effect was blocked by the removal of Na+ or the addition of 1 mM 4-acetomido-4'-isothiocyano-2,2'-stilbene disulfonic acid (SITS). When cell membrane potential was monitored in these experiments using the potential-sensitive fluorescent dye, bis-(1,3-dibutylbarbiturate) trimethine oxonol, the increase in pHi seen in the presence of Na+ was found to be electroneutral, whereas when that occurred in the presence of Na+, amiloride and HCO3-/CO2 was associated with membrane hyperpolarization.(ABSTRACT TRUNCATED AT 250 WORDS)