大鼠重症急性胰腺炎肺泡巨噬细胞的活化和调控作用

目的 观察巨噬细胞中p38蛋白活化激酶对大鼠重症急性胰腺炎肺损伤的影响.方法 假手术组仅胆胰管注射生理盐水0.1 ml/100 g;5%的牛黄胆酸(0.1 ml/100 g)逆行注射到SD大鼠的胆胰管内,造成重症急性胰腺炎(SAP)分为SAP组和SB03580组(SB203580,0.5 mg/kg,静注).在6 h剖杀大鼠,查腹水,抽血检测血清淀粉酶(AMS)和肿瘤坏死因子(TNF)-α和白细胞介素(IL)-6[酶联免疫吸附试验(ELISA)法];同时分别离心收集全肺肺泡巨噬细胞,免疫组织化学检测肺组织及其巨噬细胞中p38 MAPK的表达,同时检测肺组织中的TNF-α和IL-6;光镜下检测胰腺组织损害.结果 SAP组及SB组中AMS在6 h分别为(4865.12±890.35)IU/L和(2918.24±614.58)IU/L,差异有统计学意义.血清TNF-α分别为(106.59±43.71)ng/L和(76.43±38.43)ng/L;IL-6是(2203.76±640.85)ng/L和(1254.76±459.35)ng/L,差异有统计学意义(P<0.01).肺组织中的TNF-α和IL-6的升高与血中的一致.光镜下,胰腺组织内可见炎细胞浸润、充血、水肿和坏死;在SAP组中肺组织及其巨噬细胞中p38 MAPK强烈表达,TNF-α和IL-6的表达一致,SB治疗组表达下降.结论 TNF-α和IL-6在重症急性胰腺炎肺损伤起着重要作用;肺泡巨噬细胞中p38 MAPK表达对TNF-α和IL-6的转录和合成起重要作用.     

合并室间隔缺损的大动脉转位所致肺动脉高压的可逆性程度及其分子机制

目的 探讨合并室间隔缺损(VSD)的完全性大动脉转位(TGA)所致肺动脉高压的可逆性程度及其分子机制.方法 24例平均肺动脉压力大于30 mmHg(4.0 kPa)病儿,其中大动脉转位伴室间隔缺损10例,单纯室间隔缺损14例.在体外循环开始前取其右中叶肺组织,标本经HE及弹力纤维染色,评估肺血管病变程度.ELISA检测标本中eNOS、iNOS、ET-1、ET-AR、ET-BR、MMP-2、MMP-9及TIMP的表达情况.结果 两组病儿年龄、身高、体重、VSD大小、术前肺动脉压力筹异均无统计学意义,而血红蛋白浓度、主动脉及肺动脉内氧饱和度及术后肺动脉压力下降值筹异明显,P<0.05.两组肺标本Heath-Edwards分级0～Ⅱ级,ELISA检测发现TGA组的eNOS及MMP-2表达,分别为(280.13 ±101.92)ng/mg和(31.68±15.36)ng/mg,明显低于单纯VSD组的(488.41±249.6)ng/mg和(69.28±49.12)ng/mg,P<0.05.两组iNOS、ET-1、ET-AR、ET-BR、MMP-9及TIMP表达差异无统计学意义.结论 NOS系统、ET系统及MMP/TIMP系统的失衡参与TGA合并VSD者的肺高压形成过程,相对于单纯VSD者,TGA者肺循环的高氧合状态使MMP-2和eNOS表达下调,在一定程度上影响肺动脉高压的进展及其肺血管病变的可逆性程度.     

糖皮质激素受体对内毒素性急性肺损伤大鼠的保护作用及机制

目的 探讨糖皮质激素受体(glucocorticoid receptor,GR)在内毒素急性肺损伤(acute lung injury,ALI)中的作用及机制.方法 SD雄性大鼠84只,随机数字表法分为5组:Control组,仅注射生理盐水;脂多糖(lipopoIysaccharide,LPS)组,经尾静脉注射LPS 5 mg/kg;地塞米松(dexamethasone,DEX)+LPS组,注射LPS前30 min腹腔注射Dex 6 mg/kg;米非司酮(RU486)组,皮下注射GR拮抗剂RU486 20 mg/kg,90 min后经尾静脉注射生理盐水;RU486+Dex+LPS组,按照上述顺序分别注射RU486、Dex和LPS.Control组和RU486组6 h后,其余3组分别在1、3、6 h各时间点处死.检测各组大鼠支气管肺泡灌洗液(brobehoalveolar lavage fluid,BALF)中蛋白浓度,肺水系数(1ung index,LI),肺组织的病理变化,凋亡指数(apoptosis index,AI)以及肺组织中p38MAPK的活化状态及表达.结果 与Control组BALF中蛋白浓度(49±5)g/L、LI(2.36±0.14)、AI(12.0±1.7)%相比,LPS组分别为(77±9)g/L、5.93±0.44、(43.9±3.1)%(P＜0.05),HE染色显示肺组织炎症和损伤严重.与LPS组相比,Dex+LPS组分别为(54±4)g/L、3.77±0.48、(32.7±2.7)%(P＜0.05),且肺组织损伤程度减轻,应用GR抑制剂RU486后,Dex的肺保护作用消失.另外,LPS组肺组织中磷酸化p38MAPK(p-p38MAPK)的表达与Control组相比显著升高(P＜0.05);与LPS相比,Dex+LPS组p-p38MAPK表达下调(P＜0.05),而RU486+Dex+LPS组的表达上调(P＞0.05).结论 糖皮质激素受体在内毒素导致的急性肺损伤中发挥着重要的作用.激素活化的GR可能通过抑制p38MAPK的活化/磷酸化抑制肺组织细胞的凋亡,缓解肺损伤的程度.     

骨髓间充质干细胞对急性胰腺炎大鼠p38丝裂原活化蛋白激酶信号通路表达的影响

目的 观察骨髓间充质干细胞(MSCs)对急性胰腺炎(AP)大鼠p38丝裂原活化蛋白激酶(p38MAPK)信号通路的影响,探讨其减轻胰腺炎的作用机制.方法 采用腹腔注射L-精氨酸建立大鼠AP模型.SD大鼠随机分4组:AP未治疗组(24只);MSCs移植组(24只);p38MAPK抑制组(24只)和正常对照组(6只).流式细胞术检测MSCs表面标记物;逆转录-聚合酶链反应(RT-PCR)方法检测胰腺组织p38MAPK mRNA表达变化;同时观察组织形态学改变.结果 (1)未治疗组大鼠在建模后1h时胰腺组织p38MAPK mRNA表达显著升高并达到顶峰(P＜0.01);移植MSCs后表达明显降低,与正常对照组比较,差异无统计学意义(P＞0.05).(2)未治疗组血清炎性因子水平分别为:肿瘤坏死因子(TNF)-α(614.8 ±54.6)ng/L、白细胞介素(IL)-1(3040.5±506.4)ng/L、IL-17(4.5±0.4)U/L,胰腺组织中性粒细胞趋化因子(CINC)和单核粒细胞趋化因子(MCP-1)染色阳性率均明显升高(P＜0.05);移植MSCs后,CINC、MCP-1染色阳性率显著下降,血清炎性因子水平分别为:TNF-α( 277.5±60.8)ng/L、IL-1( 1056.2±563.1)ng/L、IL-17(1.2±0.4)U/L,两组比较差异有统计学意义(P＜0.05).(3)胰腺组织苏木素-伊红(HE)染色显示,未治疗组有大量炎性细胞浸润,胰腺细胞破坏明显,腺体结构紊乱,而移植组仅见少量炎性细胞浸润,细胞偶有破坏,排列整齐,结构有序.结论 急性胰腺炎时,胰腺组织内p38MAPK mRNA表达上调,胰腺组织损伤严重.MSCs移植可以明显抑制p38MAPK mRNA表达,降低胰腺组织内趋化因子和血清炎性因子水平,从而减轻胰腺损伤.     

异丙酚对IL-1β诱导人脐静脉内皮细胞通透性增高的影响

目的 评价异丙酚对IL-1β诱导人脐静脉内皮细胞(HUVECs)通透性增高的影响.方法 原代分离培养HUVECs并用免疫磁珠法进行纯化.免疫荧光法检测内皮细胞VE-钙粘素的表达.使用Transwell系统检测HUVECs单层通透性,以每孔2× 105个内皮细胞接种于12孔Transwell系统嵌套膜上层,待生长至汇合后3d时以两种方式干预细胞.采用随机数字表法,将细胞分为6组(n=36):对照组不作任何处理,其余5组分别以1、2、5、10和20 ng/ml IL-1β干预24h;采用随机数字表法,将细胞分为5组(n=30):对照组不作任何处理,其余4组分别先以0、10、50和100 μnol/L异丙酚预处理30 min,再以10 ng/ml IL-1β干预24h.采用随机数字表法,将细胞分为3组(n=18):对照组不作任何处理,其余2组分别以50 μmol/L异丙酚处理30 min,再以10 ng/ml IL-1β干预24h或30 min.采用Western blot法检测HUVECs occludin蛋白、磷酸化p38丝裂原活化蛋白激酶(p38 MAPK)及p-p38 MAPK的表达水平.结果 与对照组比较,5、10和20 ng/ml IL-1β呈浓度依赖性地增加HUVECs通透性(P＜0.05或0.01).10、50和100 μnol/L异丙酚可呈浓度依赖性地抑制IL-1β诱导HUVECs通透性增加(P＜0.01).IL-1β可下调HUVECs occludin蛋白表达,激活p38 MAPK信号通路,异丙酚可抑制IL-1β诱导的HUVECs occludin蛋白表达下调和p38 MAPK信号通路激活(P＜0.01).结论 异丙酚可减轻IL-1β诱导HUVECs通透性增高,与抑制p38 MAPK信号通路激活有关.     

氯胺酮对大鼠全肝缺血/再灌注后肺损伤的保护作用及机制

目的 观察10 mg/kg氯胺酮对于大鼠全肝缺血/再灌注诱发的急性肺损伤保护作用及其机制.方法 30只9～10周龄雌性SD大鼠以区组随机法随机分为3组(每组10只),假手术组(Sham组),全肝缺血/再灌注组(IR组)以pringle's法阻断门静脉和肝动脉30 min后再灌注1h.全肝缺血/再灌注氯胺酮预处理组(Ket组),以10 mg/kg氯胺酮于全肝血流阻断前20 min经尾静脉注射预处理.测定各组肺组织干湿重比值(W/D比值);血清中天冬氨酸氨基转移酶(AST)、血清丙氨酸氨基转移酶(ALT)含量;逆转录/实时聚合酶链式反应( RT-PCR)法测定肺组织中血清肿瘤坏死因子-α(TNF-α)mRNA、细胞间黏附分子-1( ICAM-1 )mRNA含量;Western blot法测定肺组织中核因子-kb( NF-kJ )/P65含量;各组肺组织HE染色后病理评分.结果 血清AST、ALT含量:IR组[AST:(91±25)U/ml,ALT:(67.0±19.4) U/ml]和Ket组[AST:(85±12) U/ml,ALT:(51.3±9.9) U/ml]均高于Sham组[AST:(29±9) U/ml,ALT:(7.8±2.7) U/ml] (P＜0.05).血清TNF-α、ICAM-1含量:IR组[TNF.α:(23.1±4.8) μg/L,ICAM-1:(34±9)μg/L]和Ket组[TNF-α:(19.1+5.8)μg/L,ICAM-1:(41±7) μg/L]均高于Sham组[TNF-α:(8.7±2.4) μg/L,ICAM-1:(13±5)μg/L](P＜0.05).而Ket组和IR组之间无统计学差异(P＞0.05).W/D比值:IR组(6.9±1.7)和Ket组(5.1±1.1)高于Sham组(3.7±0.7)(P＜0.05),IR组高于Ket组(P＜0.05).肺组织中TNF-α mRNA、ICAM-1 mRNA和NF-kb/P65含量:IR组[TNF-α mRNA:(2.91±0.49)μg/L,ICAM-1 mRNA:(2.39±0.58) μg/L,NF-kb/P65:(1.97±0.17) μg/L]高于Sham组[TNF-αmRNA:(1.75±0.29) μg/L,ICAM-1 mRNA:( 1.63±0.33) μg/L,NF-kb/P65:(1.06±0.24) μg/L]和Ket组[TNF-α mRNA:(2.19±0.52) μg/L,ICAM-1 mRNA:(1.78±0.28)μg/L,NF-kb/P65:(1.33±0.30μg/L](P＜0.05).Sham组和Ket组之间无统计学差异(p＞0.05).肺组织病理评分:Sham组低于IR组和Ket组(P＜0.05),Ket组低于IR组(P＜0.05).相关性:TNF-α mRNA与NF-kb/P65正相关,R=0.849(P＜0.05),ICAM-1 mRNA与NF-kb/P65正相关,R=0.639(P＜0.05).结论 10 mg/kg氯胺酮20 min前预处理对于全肝缺血/再灌注肺损伤有保护作用.     

p38丝裂原活化蛋白激酶在罗哌卡因致SH-SY5Y细胞凋亡中的作用

目的 评价p38丝裂原活化蛋白激酶(p38MAPK)在罗哌卡因致SH-SY5Y细胞凋亡中的作用,以探讨罗哌卡因诱发神经毒性的机制.方法 采用随机数字表法,将SH-SY5Y细胞随机分为4组(n=18):正常对照组(C组)、10 μmol/L p38MAPK特异性抑制剂SB203580组(SB组)、3 mmol/L罗哌卡因组(R组)、10 μmol/L SB203580+3 mmol/L罗哌卡因组(SB+R组).C组在细胞培养液中继续培养；SB组在含10 μmol/L SB203580培养液中孵育；R组在含3 mmol/L罗哌卡因的培养液中孵育；SB+R组在含10 μmol/L SB203580的培养液中孵育30 min后,用含3mmol/L罗哌卡因的培养液继续孵育.各组细胞培养或罗哌卡因孵育4 h后采用流式细胞仪检测细胞内活性氧(ROS)水平和细胞凋亡率,采用Western blot法检测p38MAPK和磷酸化p38MAPK(p-p38MAPK)的表达,采用MTT法检测细胞活力.结果 与C组比较,R组和SB+R组ROS水平升高,p-p38MAPK表达上调,细胞活力降低,细胞凋亡率升高(P＜0.01),SB组上述指标差异无统计学意义(P＞0.05)；与R组比较,SB组p-p38MAPK表达下调,细胞活力升高,细胞凋亡率降低(P＜0.01).四组p38MAPK表达水平差异无统计学意义(P＞0.05).结论 罗哌卡因致SH-SY5Y细胞凋亡作用的机制部分与p38MAPK的激活有关.     

P38MAPK信号通路在失血性休克复苏诱发急性肺损伤小鼠HO-1表达上调中的作用

目的 探讨p38分裂原激活蛋白激酶(p38MAPK)信号通路在失血性休克复苏诱发急性肺损伤小鼠血红素加氧酶1(HO-1)表达上调中的作用.方法 SPF级野生型小鼠C3H/HeN32只32只,10～12周龄,体重20～25 g,随机分为4组(n=8),假手术组(S组):只进行手术操作;失血性休克复苏组(HSR组):股动脉放血,至MAP为40 mm Hg,通过放血和回输血液维持MAP 35～45mmHg,60 min后回输全部血液和等失血量的乳酸钠林格氏液复苏;FR167653组(FR组):静脉注射p38MAPK抑制剂FR167653 5 mg/kg;FR+HSR组:于放血前30 min静脉注射FR167653 5 mg/kg.复苏后6 h处死小鼠,取肺组织,观察病理学结果,并进行病理学评分,计算肺湿/干重比,检测肺组织髓过氧化物酶(MPO)、IL-10、IL-6和HO-1水平以及p38MAPK的激活水平.结果 与S组比较,HSR组肺组织病理学评分、肺湿/干重比、MPO、IL-6、IL-10、HO-1和p38MAPK的激活水平升高,HSR+FR组肺组织病理学评分、肺湿/干重比和HO-1表达水平升高(P＜0.01),FR组上述指标差异无统计学意义(P＞0.05);与HSR组比较,HSR+FR组肺组织病理学评分、肺湿/干重比、MPO、IL-6、IL-10、HO-1和p38 MAPK激活水平降低(P＜0.01).结论 p38MAPK信号通路介导了失血性休克复苏诱发急性肺损伤小鼠HO-1的表达上调.     

一氧化氮吸入预测肺动脉高压的可逆性

目的通过超声心动图评价一氧化氮(NO)吸入预测肺动脉高压患者肺血管病变的可逆性。方法对50例即将进行心脏手术的肺动脉高压患者行超声心动图检查,检测吸入10~20ppm NO 15min前后与术后1月肺动脉血流动力学的参数变化,包括肺血管阻力(PVR)、肺动脉平均压(PAMP)、肺动脉收缩压(PASP)和肺循环血流量(PVCO)。结果与吸入NO前比较,39例肺血管反应阳性的患者吸入NO 15min、1月后PVR、PAMP、PASP明显降低(P0.01),术后监护室停留天数为(1.34±0.38)d,术后1月患者恢复良好。11例肺血管反应阴性患者在吸入NO前后肺动脉血流动力学指标差异无统计学意义,术后监护室停留天数为(2.95±0.93)d,术后1月仍无改善,甚至有2例患者肺血管参数有所增高。结论初步结果显示吸入NO可以作为预测肺动脉高压患者血管参数可逆性的手段。     

静脉应用抑肽酶对大鼠肺移植模型缺血再灌注损伤的作用

目的 探讨静脉应用抑肽酶对肺移植后肺缺血再灌注损伤的作用和机制.方法 利用移植肺冷缺血14 h建立的大鼠肺移植缺血再灌注损伤模型,考察抑肽酶对缺血再灌注损伤的影响,并检测细胞因子等指标探讨机制.结果 抑肽酶组较对照组移植肺氧合好、湿干比小,同时支气管肺泡灌洗液中白细胞介素(IL)-2[(113±32)μg/L和(162±43)μg/L,P＜0.05]、血清中IL-8[(7.26±1.01)ng/L和(9.43±0.97)ng/L,P＜0.05]和肿瘤坏死因子(TNF)-α[(152.3±36.4)ng/L和(211.6±52.7)ng/L,P＜0.05]、肺组织中髓过氧化物酶活性[(2.36±0.62)U/g和(3.98±0.36)U/g,P＜0.05]都显著降低.结论 静脉应用抑肽酶能够减轻缺血再灌注损伤,机制可能包括:减少IL-2的释放、抑制TNF-α活化和IL-8产生,抑制中性粒细胞的聚集、激活和脱颗粒.     

Vasopressor hormone response following mesenteric traction during major abdominal surgery

Background : We investigated the vasopressor hormone response following mesenteric traction (MT) with hypotension due to prostacyclin (PGI₂) release in patients undergoing abdominal surgery with a combined general and epidural anesthesia. Methods : In a prospective, randomized, placebo-controlled study we administered 400 mg ibuprofen (i.v.) in 42 patients scheduled for abdominal surgery. General anesthesia was combined with epidural anesthesia (T4-L1). Before as well as 5, 15, 30, 45, and 90 min after MT we recorded plasma osmolality, hemodynamics and measured 6-keto-PGFlα (stabile metabolite of PGI₂), TXB₂ (stabile metabolite of thromboxane A₂) active renin, and arginine vasopressin (AVP) plasma concentrations by radioimmunoassay. Catecholamine levels were assessed by high-pressure liquid chromatography (HPLC) with electrochemical detection. Results : Following MT, arterial hypotension occurred along with a substantial PGI₂ release. This was completely abolished by ibuprofen administration. Although plasma levels of 6-keto-PGF_1α (1133 (708) vs. 60 (3) ng/L, median (median absolute deviation), P=0.0001, placebo vs. ibuprofen) remained significantly elevated, blood pressure was restored within 30 min after MT in the placebo group. At the same point in time plasma concentrations of TXB² (164 (87) vs. 58 (1) ng/L, P=0.0001), epinephrine (46 (33) vs. 14 (6) ng/L, P=0.001), AVP (41 ± (18) vs. 12 (7) ng/L, P=0.0004), and active renin (27 (12) vs. 12 (4) ng/L, P = 0.001) were significantly higher in placebo-treated patients. Conclusion : Under combined general and epidural anesthesia arterial hypotension following MT due to endogenous PGI₂ release is associated with enhanced release of AVP, active renin, epinephrine and thromboxane A₂, presumably contributing to hemodynamic stability within 30 min after MT.     

A Teaspoon Pump for Pumping Blood with High Hydraulic Efficiency and Low Hemolysis Potential

Abstract: Virtually all blood pumps contain some kind of rubbing, sliding, closely moving machinery surfaces that are exposed to the blood being pumped. These valves, internal bearings, magnetic bearing position sensors, and shaft seals cause most of the problems with blood pumps. The original teaspoon pump design prevented the rubbing, sliding machinery surfaces from contacting the blood. However, the hydraulic efficiency was low because the blood was able to "slip around" the rotating impeller so that the blood itself never rotated fast enough to develop adequate pressure. An improved teaspoon blood pump has been designed and tested and has shown acceptable hydraulic performance and low hemolysis potential. The new pump uses a nonrotating "swinging" hose as the pump impeller. The fluid enters the pump through the center of the swinging hose; therefore, there can be no fluid slip between the revolving blood and the revolving impeller. The new pump uses an impeller that is comparable to a flexible garden hose. If the free end of the hose were swung around in a circle like half of a jump rope, the fluid inside the hose would rotate and develop pressure even though the hose impeller itself did not "rotate"; therefore, no rotating shaft seal or internal bearings are required.     

Microspheres Based Detoxification System: A New Method in Convective Blood Purification

Abstract: A variety of protein-bound or hydrophobic substances, accumulating as a result of pathologic conditions such as exogenous or endogenous intoxications, are removed poorly by conventional detoxification methods because of low accessibility (hemodialysis), insufficient adsorption capabilities (hemosorption), low efficiency (peritoneal dialysis), or economic limitations (high-volume plasmapheresis). Combining advantages of existing methods with microspheric technology, a module-based system was designed. Major operating parameters of the latter can be modified to allow for adjustment to individual clinical situations. An extracorporeal blood circuit including a plasmafilter is combined with a secondary high-velocity plasma circuit driven by a centrifugal pump. Different microspheric adsorbers can be combined in one circuit or applied in sequence. Thus, a prolonged treatment can be tailored using specially designed selective adsorber materials. Comparing this system with existing methods (high-flux hemodialysis, molecular adsorbent recycling system), results from our in vitro studies and animal experiments demonstrate the superior efficiency of substance removal.     

Is the recovery profile of mivacurium independent of the rate of decay of its plasma concentration in patients with normal plasma cholinesterase activity?

Background: The duration of action of muscle relaxants is poorly correlated to the rate of decay of their plasma concentration. The plasma concentration of mivacurium may rapidly decrease below its active concentration because of the extensive hydrolysis of mivacurium. By inflating a tourniquet on one upper limb for 3 min after the administration of atracurium, mivacurium or vecuronium, we studied the influence of the initial decline of their plasma concentration on their effect. Methods: In 50 patients anaesthetised with thiopental, isoflurane and fentanyl, the effect of bolus doses of 0.15 or 0.25 mg . kg^?1 mivacurium (MIV 15, MIV 25), 0.3 or 0.5 mg . kg^?1 atracurium (ATR 30, ATR 50) and 0.06 or 0.1 mg . kg^?1 vecuronium (VEC 06, VEC 10) were measured on both arms (evoked response of the adductor pollicis to train-of-four stimulation every 12 s), a tourniquet being applied on one arm just before and during 3 min after the muscle relaxant bolus. Results: Tourniquet inflation of 3 min almost abolished the neuromuscular effect of mivacurium. In the vecuronium groups and in the ATR 50 group, tourniquet inflation did not modify the maximum degree of depression of the twitch response. Also, the duration of action of vecuronium was unaffected by the tourniquet. In the ATR 30 group, times to return of the twitch response to 25% (duration 25%) and 75% (duration 75%) of control response were significantly shorter in the cuffed arm, 23 min vs 27 min, and 41 min vs 45 min, respectively. In the ATR 50 group, only duration 25% was significantly shorter in the cuffed arm (41 min vs 45 min). Conclusion: The results suggest that the rate of decline of the plasma concentration of mivacurium is so rapid, that a very low and almost clinically ineffective concentration is present as soon as 3 min after its administration. The results also indicate that the recovery from a mivacurium-induced neuromuscular blockade is not influenced by the rate of decay of its plasma concentration in patients with genotypically normal plasma cholinesterase.     

Membranes in Artificial Organs

Abstract: Membrane processes play a pivotal and enabling role in modern replacement therapy for acute and chronic organ failure and in the management of immunologic diseases. In fact, virtually all contemporary extracorporeal blood purification methods employ membrane devices, and the next generation of artificial organs and tissue engineering therapies are almost certain to be similarly grounded in membrane technology. In this short essay, we comment on the similarities and differences among synthetic membranes and their natural counterparts and also provide a critical overview of the demographics and technology of hemodialysis, hemofiltration, apheresis, oxygenation, and emerging membrane technologies and applications.     

Tissue perfusion in relation to cardiac output during continuous positive-pressure ventilation and administration of propranolol or verapamil

Background : Our objective was to determine whether administration of propranolol or verapamil modifies the hemodynamic adaptation to continuous positive-pressure ventilation (CPPV), in particular the regional distribution of cardiac output (CO).
Methods : General hemodynamics and regional blood flows assessed by microsphere technique (15 (μm) were recorded in 16 anesthetized pigs during spontaneous breathing (SB) and CPPV with 8 cm H₂O end-expiratory pressure (CPPV8) before and after intravenous administration of propranolol (0.3 mg · kg⁻¹ followed by 0.15 mg · kg⁻¹ · h⁻¹, n=8) or verapamil (0.1 mg · kg⁻¹ followed by 0.3 mg · kg⁻¹ · h⁻¹, n=8).
Results : CPPV8 depressed CO by 25% without shifts in its relative distribution with the exception of a noteworthy increase in adrenal perfusion. Propranolol increased arterial blood pressure, and due to a fall in heart rate, CO dropped by 25%. The kidneys and, to a lesser extent, the splanchic region and central nervous system received increased fractions of the remaining CO at the expense of skeletal muscle flow. Similar patterns were seen during SB and CPPV8 such that the combination of propranolol and CPPV8 depressed CO by 50%. The circulatory effects of verapamil were less evident but myocardial perfusion tended to increase.
Conclusions : The combination of propranolol or verapamil with CPPV does not result in any specific hemodynamic interaction in anesthetized pigs, except that the combined effect of propranolol and CPPV may severely reduce CO.     

Volatile anaesthetics reduce adhesion of blood platelets under low-flow conditions in the coronary system of isolated guinea pig hearts

Background : Inhibitory effects of volatile anaesthetics on platelet aggregation have been demonstrated in several studies. However, the influence of volatile anaesthetics on intracoronary platelet adhesion has not been elucidated so far.
Methods : Isolated hearts of guinea pigs were perfused with buffer in the absence or presence of volatile anaesthetics (0.5 and 1 MAC) at constant coronary flow rates of 5 ml/min for 25 min, then 1 ml/min for 30 min and again 5 ml/min for 10 min. Before, during and after low-flow perfusion, a bolus of human platelets was applied into the coronary system. To simulate thrombogenic conditions, 0.3 U/ml human thrombin was infused during low-flow perfusion and reperfusion. The number of platelets sequestered to the endothelium was calculated from the difference between coronary in- and output of platelets. The myocardial production of lactate and consumption of pyruvate and coronary perfusion pressure were also determined.
Results : At a flow rate of 5 ml/min only about 3% of the applied platelets did not emerge from the coronary system, in any group. In contrast, 13.1±1.2% (mean±SEM) of infused platelets became adherent in low-flow perfusion in the control group without anaesthetic. The adherence was reduced with each 1 MAC isoflurane (to 6.2±1.2%), sevoflurane (to 4.4±0.9%) or halothane (to 3.2±1.5%) (each P <0.05 vs. control). Volatile anaesthetic, 0.5 MAC, did not inhibit platelet adhesion to a statistically significant extent in any case. Perfusion pressure and metabolic parameters were not statistically different between the control and the hearts exposed to anaesthetics.
Conclusion : Volatile anaesthetics in a concentration of 1 MAC can reduce the adhesion of platelets in the coronary system under reduced flow conditions. This action does not arise from vasodilation or inhibition of ischaemic stress.     

Bariatric Surgery in Some "Central and East-European (former Eastern bloc)"Countries - Current Status and Prediction for the Next Millennium

Background: Obesity is increasing globallly, including in the formerly "Eastern Bloc" countries. Methods: A survey was made of obesity and bariatric surgery. Results: In the 8 East and Central European countries studied, with total population 300 million, roughly 43% of the population was overweight (BMI 25-30), 23% obese (BMI > 30), with about 15 million people morbidly obese (BMI > 40). From 0-10 morbidly obese individuals/100,000/year undergo bariatric surgery. Conclusion: Most countries were found to provide inadequate treatment for obesity.The majority of the morbidly obese are not treated effectively. However, health-care awareness of obesity and bariatric surgeons are slowly increasing.     

Dilemma of Membrane Biocompatibility and Reuse

Abstract: Numerous articles have been published on the multiple use of dialyzers and on the effect of different reprocessing chemicals and techniques on the dialyzer biocompatibility and performance. The results often appear contradictory, especially those comparing standard biocompatibility parameters. Despite this confusion, a discerning review of the published works allows certain limited conclusions to be drawn. Reprocessing of used hemodialyzers changes the biocompatibility profile of a dialyzer as defined by the parameters complement activation. leukopenia, and cytokine release. The effect of reprocessing depends on the chemicals and reprocessing technique applied and also on the type of membrane polymer being subjected to the reprocessing procedure. Reports of pyrogenic reactions indicate that the flux of the membrane also influences how suitable it is for safe reuse. An increased risk of allergic and pyrogenic reactions appears to be associated with dialyzer reuse. Furthermore, there has been a lack of investigations into the immunologic effect of the layer of adsorbed and chemically altered proteins that remains on the inner surface of reprocessed dialyzers. We conclude that the clinical benefit of dialyzer reuse cannot be generally accepted from a biocompatibility point of view.     

Synergistic interaction between the effects of propofol and midazolam with fentanyl on phrenic nerve activity in rabbits

Background: It has been shown that the depressive effects of both propofol and midazolam on consciousness are synergistic with opioids, but the nature of their interactions on other physiological systems, e. g. respiration, has not been fully investigated. The present study examined the effect of propofol and midazolam alone and in combination with fentanyl on phrenic nerve activity (PNA) and whether such interactions are additive or synergistic. Methods: PNA was recorded in 27 anaesthetised and artificially ventilated rabbits. In three groups, propofol, fentanyl and midazolam were administered intravenously in incremental doses to construct dose-response curves for the depressant effects of each one on PNA. In another two groups, the effect of pretreatment with either fentanyl 1 μg · kg^?1 i. v. or midazolam 0.05 mg · kg^?1 i. v. on the effects of propofol and fentanyl respectively on PNA were studied. Results: Propofol and fentanyl caused a dose-dependent depression of PNA with complete abolition at the highest total doses of 16 mg · kg^?1 i. v. and 32 μg · kg^?1 i. v., respectively. In contrast, midazolam in incremental doses to a total of 0.8 mg · kg^?1 reduced mean PNA by 63%, but approximately 12% of PNA remained at a total dose as high as 6.4 mg · kg^?1. The mean ED₅₀s, calculated from dose-response curves, were 5.4 mg · kg^?1, 3.9 μg · kg^?1 and 0.4 mg · kg^?1 for propofol, fentanyl and midazolam, respectively. Initial doses of either fentanyl 1 μg · kg^?1 i. v. or midazolam 0.05 mg · kg^?1 i. v. acted synergistically with subsequent doses of either propofol or fentanyl to abolish PNA at total doses of 8 mg · kg^?1 and 8 μg · kg^?1, respectively. Conclusion: Fentanyl has a synergistic interaction with both propofol and midazolam on PNA and hence potentially on respiration.