丙酮酸腹膜透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用

目的：研究丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器的保护作用。方法：雄性SD大鼠40只,随机分为4组（n=10）。大鼠按全身血容量的45％经股动脉放血制作失血性休克模型。单纯静脉复苏组（VR组）于休克1h后回输失血及2倍失血量的乳酸钠林格液行静脉复苏,其余3组在上述静脉复苏基础上,分别腹腔注射生理盐水（DPR组）、乳酸钠透析液（L组）、丙酮酸钠透析液（P组）20ml行腹腔复苏,时间30min。分别于休克前（O时）及休克后60（静脉复苏前）、180（腹腔复苏后1h）、360rain（腹腔复苏后4h）用PICCO心肺容量监测仪监测大鼠平均动脉压（MAP）;激光多普勒血流仪测定休克后180min和360min肝、肾和小肠黏膜血流量;生化法测定休克前及休克后180、360min血丙氨酸转氨酶（ALT）、二胺氧化酶（DAO）活性和肌酐（cr）水平;干／湿比重法测定休克后180、360min肝、肾、肠各组织含水率。结果：失血性休克后各组MAP骤降至（35±5）mmHg;休克后60min时,各组大鼠MAP无明显差异（P〉0．05）。腹腔复苏后,与VR组比较,L和P组均能显著提高失血性休克大鼠MAP（P〈0．05）,降低血ALT、Cr和DAO水平,减轻肝、肾、肠组织含水率,提高腹腔脏器血流量（P〈0．05或P〈0．01）,在失血后360min时,P组的上述变化较其余复苏组更为显著。结论：丙酮酸腹腔透析液对大鼠失血性休克静脉液体复苏后腹腔脏器具有保护作用。     

Effectors of hypercarbia during experimental pneumoperitoneum.

Hypercarbia occurs during laparoscopy with carbon dioxide (CO2) insufflation. This may be due to increased ventilatory dead space after expansion of the peritoneal cavity with impairment of diaphragmatic excursion, or to increased absorption of CO2 from the peritoneum. To separate these effects, the authors examined the consequences of different insufflating gases and of diminished tissue perfusion on hypercarbia and dead space during pneumoperitoneum. Helium was chosen as an alternate insufflating gas because it is both inert and minimally absorbed. Eight swine (18 to 20 kg) were anesthetized, paralyzed, and mechanically ventilated at constant minute volume. Pneumoperitoneum with helium was maintained at 15 mm Hg for 45 minutes. After desufflation and stabilization for 1 hour, pneumoperitoneum was repeated with CO2. The sequence was again repeated after hemorrhagic shock to constant mean arterial pressure of 50 mm Hg. Data was analyzed by analysis of variance; significance levels are P < 0.01 unless otherwise listed. Arterial PCO2 increased significantly with CO2 insufflation within 15 minutes in normotensive animals and within 30 minutes during hypotension. Arterial pH decrease with CO2 pneumoperitoneum was significant in both groups at 30 minutes. Mixed venous PCO2 also increased with CO2 pneumoperitoneum within 30 minutes. Hypotension did not alter these changes. No significant changes were seen with helium pneumoperitoneum. Neither helium nor CO2 pneumoperitoneum significantly altered dead space. The authors make the following conclusions: 1) Absorption of CO2 from the abdomen during CO2 pneumoperitoneum produces respiratory acidosis, which is not seen with helium insufflation; 2) Pneumoperitoneum does not significantly increase dead space with either gas; 3) Transperitoneal absorption of CO2 is only partly related to perfusion because significant hypercarbia occurs during hemorrhagic shock.     

高渗氯化钠高氧液对失血性休克家兔血乳酸和动脉血气的影响

目的:观察高渗氯化钠高氧液对失血性休克家兔动脉血气和血乳酸值的影响，评价其对失血性休克的早期救治效果。方法:制备高渗氯化钠溶液(HS)、生理盐水高氧液（NSO）和高渗氯化钠高氧液(HSO)。30只雄性家兔制备失血性休克模型［于10min内使平均动脉压（MAP）降至40mmHg（1mmHg＝0.133kPa），维持60min］，随机分为NSO，HS，HSO组3个治疗组。分别按6mL/kg剂量5min内静脉输入NSO,HS和HSO。记录休克前后及给药后心率（HR）、呼吸（RR）、MAP及尿滴（UD），测定休克前、休克60min，给药后30，60，120min时血乳酸（BL）和动脉血气值。最后观察尸肺，测定肺系数。结果:HS和HSO组均显著地改善MAP，HR和UD，降低BL，改善代谢性酸中毒,肺系数明显低于NSO组。HSO与NSO及HS比较，能更显著地降低血BL，提高动脉血氧饱和度（SaO2）和动脉血氧分压（PaO2）。结论:HSO较HS和NSO能更显著地降低血BL,提高SaO2和PaO2，对失血性休克的早期救治具有较高的使用价值。     

电视胸腔镜在穿透性胸腹联合伤中的应用

目的探讨电视胸腔镜诊治穿透性胸腹联合伤的价值。方法全麻，双腔气管插管，胸腔镜探查损伤情况。损伤轻微者可行胸腔镜辅助胸壁小切口治疗。胸壁、胸膜腔出血行电凝止血、缝合止血、凝血块清除，多数膈肌裂伤可同时修补，出血、裂伤脏器可行修补或切除治疗。损伤严重者中转开胸、开腹探查。结果全组18例，电视胸腔镜辅助胸壁小切口完成胸部手术15例（膈肌修补15例，肋间动脉止血8例，肺修补2例，肺楔形切除2例，凝固性血胸清除2例），中转开胸3例（膈肌修补3例，心脏修补1例，食管修补1例，肺叶切除2例）。经胸行腹腔诊治13例（肝脏修补1例，脾脏切除1例，胃修补1例，膈疝还纳3例，探查7例），开腹诊治5例（胰腺修补1例，肝脏修补1例，脾脏切除1例，胃修补2例，大网膜及肠系膜修补3例）。1例多脏器穿透伤患者，虽经开胸、开腹治疗，但终因失血性休克、循环衰竭、DIC死亡。手术时间45～220min，（125±44）min；术中出血量500～10000ml，（1089±582）ml；术后24h胸腔引流量100～350ml，（234±75）ml；术后胸管留置时间2～5d，平均2．5d；术后排气时间1～4d，平均2d。12例门诊随访3～12个月，平均6个月，无与外伤相关的并发症发生。结论恰当地选择病例，电视胸腔镜辅助胸壁小切口诊治穿透性胸腹联合伤安全，疗效可靠。     

多沙普仑对犬失血性休克等容输血后血流动力学的影响

目的：观察多沙普仑对犬失血性休克等容输血后血流动力学的影响。方法：犬分为对照组和多沙普仑组（只数均＝５）。股动脉快速放血３０ｍｌ／ｋｇ，造成严重休克模型，３０分钟后等容输血。多沙普仑组输血后立即静脉注射多沙普仑２ｍｇ／ｋｇ。用Ｓｗａｎ－Ｇａｎｚ漂浮导管等方法分别于休克、输血前后测定血流动力学参数。结果：休克后５分钟、３０分钟ＭＡＰ、ＣＯ、ＣＩ、ＳＶ、ＬＶＳＷ、ＬＶＳＷＩ明显下降，ＳＶＲ明显增高。输血后１５分钟，多沙普仑组已恢复到休克前水平，但对照组则未能恢复。结论：多沙普仑能促进失血性休克等容输血后循环功能的恢复。     

Effects of naloxone on splanchnic perfusion in hemorrhagic shock

Endogenous opiate peptides are released in early hemorrhagic shock and may mediate hypotension during hypovolemia. We compared the effects of naloxone alone versus incomplete volume resuscitation on survival and splanchnic blood flow. Dogs were bled to a MAP of 35 mm Hg for 2 hours. In eight dogs, shed blood was returned; eight dogs received naloxone (2 mg/kg bolus and 2 mg/kg/hr in 0.5 ml/kg/hr normal saline) with no shed blood returned. Seven dogs received normal saline alone without shed blood or naloxone and served as untreated controls. Untreated dogs survived a mean of 18.6 minutes. All other dogs survived for 180 minutes. Naloxone and shed blood were equally effective in improving hepatic and renal blood flow; gastric, intestinal, pancreatic, and splenic blood flow remained unchanged from shock values in both groups. These data indicate that in the face of hypovolemia naloxone improves survival and blood flow (ml/min/gm) to splanchnic organs despite no return of shed blood.     

A novel method of peritoneal resuscitation improves organ perfusion after hemorrhagic shock

BACKGROUND: After resuscitation from hemorrhagic shock, intestinal microvessels constrict leading to impairment of blood flow. This occurs despite restoration and maintenance of central hemodynamics. Our recent studies have demonstrated that topical and continuous exposure of the gut microvasculature to a clinical solution (Delflex; Fresenius Medical Care), as a technique of direct peritoneal resuscitation (DPR), reverses the postresuscitation vasoconstriction and hypoperfusion to a sustained dilation and hyperperfusion. We hypothesize that initiation of DPR simultaneously with resuscitation from hemorrhagic shock enhance organ blood flow to all tissues surrounding the peritoneal cavity as well as distant organs. METHODS: Male Sprague-Dawley rats were anesthetized, intubated and cannulated for monitoring of hemodynamics and for withdrawal of blood. Rats were hemorrhaged to 50% of mean blood pressure for 60 minutes prior to resuscitation with shed blood plus 2 volumes of saline. Animals were randomized for intraperitoneal therapy with 30 mL saline (group 1, n = 9), or Delflex (group 2, n = 9). Whole organ blood flow was measured by colorimetric microsphere technique with phantom organ at baseline, after completion of resuscitation, and at 120 minutes postresuscitation. Replenishment of the dwelling intraperitoneal saline or Delflex was performed in (group 3, n = 8), and (group 4, n = 8), respectively at 90 minutes postresuscitation, and a single whole organ blood flow was performed at 120 minutes postresuscitation. RESULTS: Direct peritoneal resuscitation caused a significant increase in blood flow to the jejunum (35%), ileum (33%), spleen (48%), and pancreas (57%), whereas a marked increase in blood flow was detected in the lung (111%), psoas major muscle (115%), and diaphragm (132%), as compared with the saline treated animals in group 1. At 120 minutes postresuscitation, organ blood flow returned to the prehemorrhagic shock baseline level in all organs irrespective of peritoneal therapy. Replenishment of the intraperitoneal solution in group 3 and 4, enhanced blood flow to the liver, kidneys, and diaphragm. CONCLUSIONS: Direct peritoneal resuscitation enhanced blood flow to organs incited in the pathogenesis of multiple organ failure that follows hemorrhagic shock.     

缝隙连接在兔失血性休克复苏诱发肺损伤中的作用

目的 评价缝隙连接在兔失血性休克复苏诱发肺损伤中的作用.方法 健康家兔24只,体重1.5～2.2 kg,经股动脉放血制备失血性休克模型.随机分为2组(n=12),传统治疗组(A组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3);辛醇组(B组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3),同时腹腔注射99.5%辛醇5 mmol/kg.然后两组回输全部放血及等放血量的乳酸钠林格氏液后静脉输注乳酸钠林格氏液2.5 ml·kg-·h-1 150 min(T4).于放血前(T1)、模型制备成功即刻(T2)、T3、T4时记录左心室收缩压(LVSP)和HR,记录复苏期间兔的病死情况.于T时处死,测定肺组织Na+-K+-ATP酶和Ca2+-ATP酶的活性,计算肺通透性指数和肺湿重/干重(W/D)比,光镜下观察肺组织病理学结果.结果 与A组比较,B组T3时HR和LVSP降低,T4时LVSP升高,HR降低,Na+-K+-ATP酶和Ca2+-ATP酶活性升高,肺通透性指数降低,肺组织W/D比和病死率降低(P＜0.05或0.01).B组肺组织病理学损伤程度较A组明显减轻.结论 缝隙连接参与了兔失血性休克复苏诱发肺损伤.     

肝肺撞击伤伴失血后CO2气腹对兔肺血流量的影响

目的 探讨肝肺撞击伤伴失血后CO22气腹对兔肺血流量(PBF)的影响及其机制.方法 制作创伤性失血兔模型,按不同失血量(6、12、22 ml/ks体重)及CO2腹压(5、10、15 mm Hg)将新西兰大白兔按随机数字表分为9组(Ⅰ～Ⅸ,n=6).采用彩色微球法观察建立气腹前、气腹0.5、2 h及撤去气腹后0.5 h肺血流量的变化和死亡率.结果 未建立气腹时,随失血量的递增,肺血流量持续下降显著(P<0.05).建立15mm Hg气腹压下实验组PBF下降明显,5 mm Hg腹压下实验组PBF增加显著,而在10 mm Hg腹压下,6 ml/kg体重失血量时PBF增加,当失血量达12 ml/kg体重失血量时,PBF下降.随着气腹时间的延长,能存活组PBF均下降(P<0.05).撤除气腹后,6 ml/kg体重失血量组PBF与气腹前无统计学意义(P>0.05),而12 ml/kg体重失血量组PBF低于气腹前水平(P<0.05).结论 一定气腹压力(<10mm Hg)对创伤伴失血性(<12ml/kg体重)自主呼吸兔的肺血流量的影响是可逆的;但过高气腹压力(15 mm Hg)以及重度失血(40%)建立气腹将导致致死性后果.     

Gallbladder and gastrointestinal motility after hemorrhagic shock

The alterations in fasting gallbladder and gastrointestinal motility during hemorrhagic shock were investigated. Eight opossums implanted with a gallbladder cannula, gastrointestinal bipolar electrodes, and a carotid catheter were subjected to hemorrhagic shock of 30 mm Hg for 60 minutes by the removal of arterial blood. Shed blood was reinfused after the shock period. Fasting gallbladder volume and gastrointestinal electrical activity were studied before, immediately after, and 24 hours after hemorrhagic shock. Control measurements demonstrated a slow-wave frequency maximal in the duodenum (18.1 +/- 1.1 waves/min), with a plateau in the proximal third of the small bowel, decreasing thereafter. The migrating motor complex (MMC) had a duration of 118 +/- 28 minutes. The average volume of the gallbladder before shock was 5.4 +/- 1.5 ml. Gallbladder volume fluctuated with the MMC, being maximal during phase I and minimal in phase III. The volume of blood removed to reduce mean arterial pressure to 30 mm Hg was 45 +/- 5 ml/kg. Immediately after the shock and blood reinfusion, slow-wave frequency decreased by 40% in the antrum and 25% in the small bowel. The MMC was of shorter duration (91 +/- 22 minutes; p less than 0.05), and gallbladder volume increased to 7.0 +/- 1.7 ml (p less than 0.05). Fluctuations in gallbladder volume during the MMC were absent. Twenty-four hours after shock, slow-wave frequency, MMC, and gallbladder volume had returned to normal and were not different from control measurements. Ischemic damage to the gastrointestinal tract is postulated as the cause of gallbladder dysfunction and altered intestinal motility after hemorrhagic shock.     

L-FABP and NGAL are novel biomarkers for detection of abdominal injury and hemorrhagic shock

IntroductionDelayed diagnosis of abdominal injuries and hemorrhagic shock leads to secondary complications and high late mortality in severely traumatized patients. The liver fatty acid-binding protein (L-FABP) is expressed in intestine, liver and kidney; the neutrophil gelatinase-associated lipocalin (NGAL) in colon and kidney. We hypothesized that l-FABP is an early biomarker for abdominal injury and hemorrhagic shock and that l-FABP and NGAL are specific markers for detection of liver and/or kidney injuries.Patients and MethodsTraumatized patients with an age ≥18 years and an abdominal injury (AIS_abd≥2), independently from Injury Severity Score (ISS), were prospectively included from 04/2018 to 05/2021. 68 patients had an abdominal injury (“Abd”) and 10 patients had an abdominal injury with hemorrhagic shock (“HS Abd”). 41 patients without abdominal injury and hemorrhagic shock but with an ISS ≥ 25 (“noAbd”) were included as control group. Four abdominal subgroups with isolated organ injuries were defined. Plasma l-FABP and NGAL levels were measured at admission (ER) and up to two days post-trauma.ResultsAll patient groups had a median ISS≥25. In ER, median l-FABP levels were significantly higher in “HS Abd” group (1209.2 ng/ml [IQR=575.2–1780.3]) compared to “noAbd” group (36.4 ng/ml [IQR=14.8–88.5]), and to “Abd” group (41.4 ng/ml [IQR=18.0–235.5]), p<0.001. In matched-pair-analysis l-FABP levels in the group “Abd” were significantly higher (108.3 ng/ml [IQR=31.4–540.9]) compared to “noAbd” (26.4 ng/ml [IQR=15.5–88.8]), p = 0.0016. l-FABP correlated significantly with clinical parameters of hemorrhagic shock; the optimal cut-off level of l-FABP for detection was 334.3 ng/ml (sensitivity: 90%, specificity: 78%). Median l-FABP-levels were significantly higher in patients with isolated liver or kidney injuries and correlated significantly with AST, ALT and creatinine value. Median NGAL levels in the ER were significantly higher in “HS Abd” group (115.9 ng/ml [IQR=90.6–163.8]) compared to “noAbd” group (58.5 ng/ml [IQR=41.0–89.6],p<0.001) and “Abd” group (70.5 ng/ml [IQR=53.3–115.5], p<0.05). The group “Abd” showed significant higher median NGAL levels compared to “noAbd”, p = 0.019. NGAL levels correlated significantly with clinical parameters of hemorrhagic shock.Conclusion:L-FABP and NGAL are novel biomarkers for detection of abdominal trauma and hemorrhagic shock. l-FABP may be a useful and promising parameter in diagnosis of liver and kidney injuries, NGAL failed to achieve the same.     

6％的羟乙基淀粉-高渗盐水在失血性休克狗复苏时的作用

背景血流动力学和全身氧输送的变化无法反映内脏低灌注，从而导致无法认识到对失血性休克的处理不足。液体复苏后扩容对改善失血性休克时全身和局部的氧供是必不可少的。我们假设，与传统的代血浆相比，应用少量的扩容剂7．5氯化钠／6％羟乙基淀粉（hydroxyethyl starch．hypertonic saline，HHES）溶液，可能提供较少的全身氧输送和胃血流灌注。我们为失血的狗进行临床上严重出血时常用的固定量液体单次输注，分别观察HHES、乳酸林格液（1actatedRinger，LR）和6％羟乙基淀粉（hydroxyethyl starch，HES）溶液对血管内扩容、早期全身氧合和胃灌注的影响。方法30只狗，出血30ml／kg，保持平均动脉压在40～50mmHg，持续45分钟后，分3组进行复苏：LR组（n=10），输注3倍出血量的液体；HES组（平均分子量130KDa，替代级0．4）（n=10），输注出血量等量的液体；HHES组（n=10），以4ml／kg的速度输注。测定血管内容量增加情况（用Evans蓝和血红蛋白稀释）、血流动力学、全身氧合、静动脉CO2分压差（Pv-aco2）和胃黏膜-动脉血CO2分压差（Pco2间隙）变化，测定时间点为基础值、出血45分钟后以及液体复苏5分钟、45分钟、90分钟时。结果由于HHES的高扩容效力增加了血容量，但它对血管内容量的扩张作用是各溶液中最小的（P〈0．05）。3种溶液对血流动力学影响相同，但相对于LR组和HES组，HHES组相混合静脉血Po，更低，全身氧合、Pv-aco2和胃黏膜Pco2间隙更大（P〈0．05）。结论对狗进行按血压调节的失血性休克和固定容量的复苏，尽管HHES有高效扩容作用，但相比LR和HES，由于输注量受限，它的血管内容量扩充能力较小，全身氧合和胃血流灌注较差。     

多沙普仑纳络酮对失血性休克犬等容输血后血流动力学的影响

目的：在实验犬中观察多沙普化、纳络酮对失血性休克等容输血后血流动力学的影响。方法：实验犬分为对照组、多沙普化组和纳络酮组，每组５条，三组动物均以动脉快速放血３０ｍｌ／ｋｇ、造成严重失血性休克模型，３０ｍｉｎ后等容输血，多沙普仑组和纳络酮组分别于输血后立即静脉注射多潲普仑２ｍｇ／ｋｇ或纳络酮０．０１５ｍｇ／ｋｇ，采用Ｓｗａｎ－Ｇａｎｚ漂浮导管及心脏电脑监护仪等手段分别于动物休克、等容输血前后测定血流     

腹腔复苏对失血性休克家兔血乳酸和酸碱平衡的影响

目的 观察腹腔复苏对失血性休克家兔血乳酸(BL)浓度、酸碱平衡状态,探讨其在失血性休克救治中的作用.方法 21只雄性家兔随机分为三组,腹腔复苏组(A组)、常规静脉复苏组(B组)、正常对照组(C组).A、B组于10 min内使MAP降至40 mm Hg,维持60 min后,在20 min内静脉回输放出的血液和两倍于放血量的复方乳酸钠进行液体复苏,并于血液和液体复苏的同时,A组腹腔内注射120 ml临床用透析液,而B、C组腹腔注入等量生理盐水对照.观察休克前后与复苏后的MAP,测定动脉血pH、HCO-3、BE、BL.复苏后180 min,取门静脉血测定BL浓度,然后静脉注射空气处死家兔.结果 复苏后30、60、90 min,A组MAP高于B组(P＜0.01).复苏后60、180min时A组静脉血和复苏后180 min门静脉血BL值明显低于B组(P＜ 0.05),pH、HCO3、BE分别高于B组(P＜0.05或P＜0.01).且A组在复苏后180 min与C组相应值相近,同时也接近休克前水平.结论 腹腔复苏对失血性休克的早期救治具有一定的实用价值.     

A method to attenuate pneumoperitoneum-induced reductions in splanchnic blood flow

OBJECTIVE: To determine if increasing nitric oxide bioactivity by inclusion of ethyl nitrite (ENO) in the insufflation admixture would attenuate pneumoperitoneum-induced decreases in splanchnic perfusion. SUMMARY BACKGROUND DATA: Organ blood flow is reduced during pneumoperitoneum and can contribute to laparoscopy-associated morbidity and mortality. Previous attempts to control such decreases in flow have been ineffective. METHODS: Laser-Doppler flow probes were placed on the liver and right kidney of anesthetized pigs. After a baseline recording period, animals were insufflated to a final intraperitoneal pressure of 15 mm Hg. Group one received CO2 (standard practice), whereas group 2 received CO2 plus 100 ppm ENO. Insufflation was maintained for 60 minutes and then the abdomen was manually deflated; monitoring was continued for another 60 minutes. RESULTS: CO2 insufflation (n = 5) cut liver blood flow in half; liver flow remained at this level throughout the postinsufflation period. Inclusion of 100 ppm ENO (n = 6) attenuated both the acute and prolonged blood flow decreases. Statistical modeling of the data showed that, on average, liver blood flow was 14.3 U/min higher in the ENO pigs compared with the CO2 group (P = 0.0454). In contrast, neither treatment significantly altered kidney blood flow (P = 0.6215). CONCLUSION: The data indicate that ENO can effectively attenuate pneumoperitoneum-induced blood flow decreases within the peritoneal cavity. The result suggests a novel therapeutic method of regulating hemodynamic changes during laparoscopic procedures.     

Increased Insufflation Pressure Enhances the Development of Liver Metastasis in a Mouse Laparoscopy Model

Despite the widespread use of laparoscopic techniques for colorectal cancer surgery, little is known about the potential risk of liver metastasis following CO2 pneumoperitoneum. We investigated the effect of different insufflation pressures and durations of CO2 pneumoperitoneum on the growth of liver metastasis in a mouse model. Six- to 7-week old male BALB/C mice were intraportally inoculated with 2×104 Colon 26 cells and randomly allocated to receive either CO2 pneumoperitoneum at different pressures (5 mmHg, 10 mmHg, or 15 mmHg), xiphoid-pubic laparotomy, or no treatment other than tumor cell inoculation. Mice undergoing pneumoperitoneum or laparotomy were then subdivided by the duration of treatment (30 minutes or 60 minutes). Cancer nodules on the liver surface from a total of 122 mice were evaluated on the 14th postoperative day. Similar to full laparotomy, CO2 pneumoperitoneum at 10 mmHg and 15 mmHg for 60 minutes, and pneumoperitoneum at 15 mmHg for 30 minutes significantly promoted the growth of cancer nodules on the liver surface. Enhancement of tumor growth was influenced by increased insufflation pressures (p < 0.05) rather than the prolonged length of pneumoperitoneum (p = 0.53) without significant interaction (p = 0.49). These results suggest that an increased insufflation pressure promotes the growth of liver metastases as well as laparotomy in this animal model.     

不同二氧化碳气腹压力对家兔心肌细胞的影响

目的　研究不同CO2 气腹压力对家兔心肌超微结构的影响。方法　 1 8只健康家兔 ,随机分为三组。A组气腹压力 1 0mmHg ,B组 1 5mmHg ,C组 2 0mmHg。用氯胺酮和地西泮肌注麻醉。测定气腹前和气腹后 30、6 0min的MAP、CVP ,HR ,测定同一时点的内皮素 (ET)、洋地黄物质(EDLS)和心肌酶谱。实验结束 ,取左室内壁心肌组织行电镜观察。结果　 (1 )血液动力学变化 :三组的HR组内、组间比较均无差异。CVP组内比较 ,三组气腹前与气腹后 30、6 0min ,差异非常显著(P <0 0 1 ) ;组间比较 ,气腹后 30、6 0min ,A组与B组、C组差异显著 (P <0 0 5 ) ,B组与C组间无差异。MAP组内比较 ,C组气腹前与气腹后 6 0min差异显著 (P <0 0 5 ) ;组间比较 ,A组与C组、B组与C组间差异显著 (P <0 0 5 )。 (2 )EDLS :组内组间均无差异 ,但气腹后 30、6 0min时的血浆水平比气腹前增加。 (3)ET :组内组间均无差异 ,但组内比较总体呈下降趋势。 (4 )心肌酶谱 :心肌酶随气腹时间的延长和压力的升高呈上升趋势。乳酸脱氢酶 (LDH) :B组气腹前与气腹后 6 0min比较差异显著 (P <0 0 5 )。天冬氨酸转移酶 (AST) :B组气腹前与气腹后 6 0min比较差异显著 (P <0 0 5 )。 (5 )心肌超微结构的变化 :A、B、C三组动物心肌组织均有不同程度的超微结     

A study on the mechanism of development of acute gastric ulcer in hemorrhagic shock--with special reference to the relation of PGE2 and noradrenaline levels in the gastric mucosa and changes in gastric mucosal blood flow

Changes in gastric mucosal blood flow in acute gastric ulceration associated with hemorrhagic shock were investigated for their relationship to gastric mucosal PGE2 and NA in rats which were deprived of 24 ml/kg of blood. The results were: 1. Gastric mucosal blood flow and NA were decreased by 65% and 25% respectively at 30 minutes after hemorrhage. Gastric mucosal PGE2 was 26% increased at 30 minutes after exsanguination and then showed a marked decrease. 2. Administration of NA resulted in an 100% increase of gastric mucosal PGE2. However, animals receiving NA at 20 or 50 minutes after hemorrhage gave values for gastric mucosal PGE2 which were not different from those of non-NA-treated animals at 30 and 60 minutes after hemorrhage. 3. Pre-treatment with PGE2 suppressed the reduction in both gastric mucosal blood flow and NA and the development of ulcer, whereas pre-treatment with indomethacin accelerated them. These results suggest that the increase in gastric mucosal PGE2 in early shock might represent a phenomenon of adaptation to decreased blood flow, implicating adrenergic activation as one of causative factors, and the decrease in gastric mucosal PGE2 in late shock might be construed as the result of impaired synthesis of PGE2 due to persistent hypoxia and be one of the possible factors for ulcers.     

The effects of intraabdominally insufflated carbon dioxide on hepatic blood flow during laparoscopic surgery assessed by transesophageal echocardiography

Conflicting results have been published about the effects of carbon dioxide (CO(2)) pneumoperitoneum on splanchnic and liver perfusion. Several experimental studies described a pressure-related reduction in hepatic blood flow, whereas other investigators reported an increase as long as the intraabdominal pressure (IAP) remained less than 16 mm Hg. Our goal in the present study was to investigate the effects of insufflated CO(2) on hepatic blood flow during laparoscopic surgery in healthy adults. Blood flow in the right and middle hepatic veins was assessed in 24 patients undergoing laparoscopic surgery by use of transesophageal Doppler echocardiography. Hepatic venous blood flow was recorded before and after 5, 10, 20, 30, and 40 min of pneumoperitoneum, as well as 1 and 5 min after deflation. Twelve patients undergoing conventional hernia repair served as the control group. The induction of pneumoperitoneum produced a significant increase in blood flow of the right and middle hepatic veins. Five minutes after insufflation of CO(2) the median right hepatic blood flow index increased from 196 mL/min/m(2) (95% confidence interval (CI), 140-261 mL/min/m(2)) to 392 mL/min/m(2) (CI, 263-551 mL/min/m(2)) (P < 0.05) and persisted during maintenance of pneumoperitoneum. In the middle hepatic vein the blood flow index increased from 105 mL/min/m(2) (CI, 71-136 mL/min/m(2)) to 159 mL/min/m(2) (CI, 103-236 mL/min/m(2)) 20 min after insufflation of CO(2). After deflation blood flow returned to baseline values in both hepatic veins. Conversely, in the control group hepatic blood flow remained unchanged over the entire study period. We conclude that induction of CO(2) pneumoperitoneum with an IAP of 12 mm Hg is associated with an increase in hepatic perfusion in healthy adults.     

CO2气腹对糖尿病兔胰腺功能影响的实验研究

目的探讨二氧化碳（CO2）气腹对糖尿病兔胰腺功能的影响。方法利用四氧嘧啶制作糖尿病兔模型,建立不同压力气腹,观察气腹前和气腹后0、2、6及12h各时间点血糖、淀粉酶、胰岛素、C肽、胰腺组织SOD活性及MDA含量的变化。结果气腹结束后,血糖、淀粉酶、胰岛素、C肽浓度和MDA含量较气腹前上升（P〈0.05）,SOD活性较气腹前下降（P〈0.05）。气腹结束后12h,10mmHg（1mmHg=0.133kPa）气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量与气腹前比较差异无统计学意义（P〉0.05）,15mmHg气腹组血糖、淀粉酶、胰岛素、C肽浓度和MDA含量仍较气腹前升高（P〈0.05）;SOD活性在2组均未恢复至气腹前水平（P〈0.05）。10mmHg和15mmHg气腹组相应时相之间,血糖和胰岛素变化差异无统计学意义（P〉0.05）,淀粉酶、C肽浓度、MDA含量和SOD活性变化差异有统计学意义（P〈0.05）。结论CO2气腹对糖尿病兔胰腺功能有损伤作用,损伤程度与气腹压力相关,较低的气腹压引起的胰腺损害更易逆转。