弱激光照射对早期内毒素血症大鼠胃黏膜的效应

目的 探讨弱激光照射对早期内毒素血症(endotoxemia, ETM)大鼠胃黏膜变化的效应.方法 采用脂多糖(LPS)静脉注射法建立ETM疾病模型.60只SD大鼠随机分为对照组、内毒素损伤组和弱激光照射组,每组20只.弱激光组在注射LPS 30 min后以SLT半导体激光治疗仪对大鼠的股动、静脉和耳部血管同时进行照射,治疗参数为波长650 nm、功率5 mW,一次性垂直照射30 min.在ETM形成1、2、4、6 h后,检测胃液pH值,观察胃黏膜组织病理学变化.结果 胃液pH值在ETM形成6 h内尚未发生变化,但此时大鼠胃黏膜已有组织学改变,主要表现为胃黏膜上皮细胞损伤、脱落,局部充血、水肿、渗出及炎性细胞浸润;经弱激光照射后胃黏膜炎性反应明显减轻.结论 这种SD大鼠早期ETM疾病模型在6 h内胃液pH值未发生变化,但胃黏膜已有形态学变化,弱激光照射可减轻早期的病理损伤.     

肝病时的肠源性内毒素血症

肝硬变、重型及慢性病毒性肝炎等肝病患者多伴有肠源性内毒素血症（gutdririedendotoxemia,GET）,其可加重肝损害及促发各种并发症并与肝病互为因果。韩德五[1]记提出肝功衰竭发病机制的内毒素血症假说,认为GET是肝功能衰竭发生的物质基础。1内毒素（LPS）和GET1．ILPSLPS存在于革兰阴性（G－）细菌细胞壁外层,在细胞死亡细胞壁崩解时释放或活菌以发泡形式将其释出。其化学成分为脂多糖（LPS）,由三层组成。外层为O-特异多糖,代表细菌特异抗原;中层为R-核心多糖,为细菌类属的共同抗原;内层为类脂A,有较恒定的分子结构…     

内毒素血症的实验诊断方法学进展

内毒素是革兰氏阴性细菌的脂多糖,也是重要的热源质,可引起人机体内广泛的生物学作用和病理学反应,近几年随着细胞分子免疫学和分子生物学技术的快速发展,对内毒素的抗原结构、单克隆抗体的制备、临床诊断及其致病机理等方面取得了许多重大的进展,本文就内毒素检测研究的进展做一综述。     

烧伤内毒素血症研究的若干进展

感染是烧伤后最常见的并发症,成为首要的致死原因。特别是革兰氏阴性杆菌如绿脓杆菌、大肠杆菌等侵袭所致脓毒症,对患者生命威胁极大。而此类细菌所产生的致病因子——内毒素在其发病中可能起着举足轻     

论内毒素血症的治疗对策

科学家与细菌的较量 ,有相当多的工作表现在与细菌毒素的抗争。细菌毒素主要分为外毒素 (exotoxin)和内毒素 (endotoxin) ;一些危害人类健康的重要致病菌如白喉和破伤风等细菌的外毒素 ,随着其抗毒素和类毒素的相继研制成功和有效应用 ,已不再使人谈虎色变 ;如今对细菌毒素的抗     

肝硬化患者小肠黏膜超微结构改变与内毒素血症

目的:研究肝硬化患者小肠黏膜超微结构的改变与血浆内毒素水平的关系。方法:40例肝硬化患者,10例健康志愿者分别按常规内镜下活检术取小肠黏膜行透射电镜观察其超微结构,并分别以鲎实验法检测血浆内毒素水平;分析小肠黏膜超微结构改变与血浆内毒素水平之间的关系。结果:40例肝硬化患者中,22例患者的小肠黏膜出现超微结构改变,发生率为55%,透射电镜下表现为小肠黏膜上皮微绒毛减少、变短,肠黏膜上皮细胞核固缩,肠黏膜紧密连接间隙增宽以及线粒体肿胀。Child-PughA、B、C级组小肠黏膜超微结构改变的发生率分别为20%(3/15),61.5%(8/13),91.7%(11/12),P<0.01。肝硬化患者与健康志愿者的血浆内毒素分别为(0.452±0.113)Eu/mL,(0.045±0.021)Eu/mL,P<0.01;肝硬化伴与不伴小肠黏膜超微结构改变者的血浆内毒素分别为(0.815±0.213)Eu/mL,(0.321±0.233)Eu/mL,P<0.01。结论:肝硬化患者存在小肠黏膜超微结构的改变,其发生率随肝硬化程度的加重而增高;伴有小肠黏膜超微结构改变的肝硬化患者血浆内毒素水平增高,提示小肠黏膜超微结构改变是...     

肝硬化肠源性内毒素血症的研究进展

肝硬化患者由于脾功能亢进,机体免疫功能减退而抵抗力低下,门体静脉间侧支循环的建立,增加了病原微生物进入血液循环的机会,故极易并发感染而出现内毒素血症[1],长期内毒素升高可导致细胞因子反应,引起肝脏持续性损害,加速肝病的恶化.现就肝硬化肠源性内毒素血症的研究进展综述如下.     

内皮素与梗阻性黄疸时内毒素血症的相关研究

梗阻性黄疸时发生的肠源性内毒素学症可导致围手术期患者死亡率增高。肝网状内皮系统是清除内毒素的主要场所，梗阻性黄疸时其功能下降是主要原因。内皮素作为体内最强的缩血管因子，对维持肝网状内皮系统血运起重要作用。本实验通过观察梗阻性黄疸模型大鼠内皮素（ET）、内毒素（LPS）含量的变化，初步探讨梗阻性黄疸时肝网状内皮系统血液动力学变化对肠源性内毒素含量的影响机制。     

流行性出血热与内毒素血症的关系

本文报道用稀释加热的毛细管法检测55例出血热患者血浆内毒素,结果26例阳性(47.3%),16例重症病例15例阳性(93.8%),且与出血表现及急性肾功能衰竭的程度相平行,提示内毒素血症参与出血热的中间发病过程。最后对内毒素血症产生的可能因素进行了讨论。     

动态监测胃黏膜内pH值对胆源性胰腺炎外科治疗的价值

目的探讨胃黏膜内pH值对胆源性胰腺炎病情预后评估及在决定手术冶疗中应用的价值。方法对确诊的146例胆源性胰腺炎患者经鼻插入胃黏膜二氧化碳张力计（TRIP-NGS导管）测定胃黏膜内pH值，每隔12小时测定一次，并进行APACHEⅡ评分，将2组数据与外科治疗进行相关分析。结果①pH值变化反映胆源性胰腺炎病情发展变化，与器官衰竭数呈负相关；②外科干预治疗与内科治疗比较差异有统计学意义（P〈0．05）；③pHI〉7．25与pH〈7．25患者开腹手术病死率和细菌培养阳性率比较差异有统计学意义（P〈0．05）。结论pH值对胆源性胰腺炎外科治疗有指导意义。外科处理原则是：①胆道无梗阻，以内科保守治疗为主；②伴胆道梗阻，先行经内镜十二指肠乳头括约肌切开术、经内镜鼻胆管引流术、B超导引引流、腹腔灌洗等，如胆道引流不畅或pH值持续下降，则开腹手术。     

Effect of ranitidine on gastric intramucosal pH in critically ill patients

Objective: To determine whether ranitidine a) increases the values of gastric intramucosal pH (pHi) in critically ill patients, as determined by tonometry; b) reduces the variability of these measurements. Design: Prospective, double blind, randomized, placebo-controlled study. Setting: General Intensive Care Unit of a teaching hospital. Patients: Twenty-five critically ill, mechanically ventilated patients requiring arterial catheter and nasogastric tube. Interventions: Tonometer placement; blind, random administration of intravenous ranitidine (50 mg) or placebo. Measurements and main results: Tonometer saline PCO₂ (PCO₂i), arterial blood gases, gastric juice pH and pHi were determined immediately before, and 2, 4, 6 and 8 h after, ranitidine (12 patients) or placebo (13 patients). Ranitidine significantly increased gastric juice pH, but did not affect PCO₂i or pHi; pHi was 7.34 ± 0.14 before ranitidine, and 7.30 ± 0.12, 7.31 ± 0.11, 7.31 ± 0.14 and 7.31 ± 0.12 – 2, 4, 6 and 8 h, respectively, after ranitidine administration (p = 0.55). Ranitidine did not modify the coefficients of variation of PCO₂i or pHi, either. No significant changes in gastric juice pH, PCO₂i or pHi were observed in the placebo group. Conclusions: In critically ill patients, ranitidine has no effect on pHi values, and does not increase the reproducibility of pHi measurements. Received: 24 October 1996 Accepted: 22 October 1997     

Effect of sucralfate on gastric intramucosal pH in critically ill patients

Objective: To determine whether sucralfate administration affects the tonometric measurement of gastric intramucosal pH (pHi). Design: Non-randomized observational study. Setting: General intensive care unit of a teaching hospital. Patients: Twenty critically ill, mechanically ventilated, consecutively admitted patients requiring an arterial catheter and nasogastric tube. Interventions: Tonometer placement and sucralfate administration. Measurements and main results: We simultaneously determined tonometer saline PCO₂ (PCO₂i), arterial blood gases, pH of gastric juice and pHi. These parameters were evaluated immediately before sucralfate administration, and 2 h and 4 h after. We did not detect any change in either PCO₂i or pHi after sucralfate administration (PCO₂i: basal 6.4 ± 1.7, 2 h 6.3 ± 1.7, 4 h 6.3 ± 1.7; pHi: basal 7.35 ± 0.13, 2 h 7.36 ± 0.12, 4 h 7.36 ± 0.12). Conclusions: Sucralfate does not affect the tonometric measurement of PCO₂i and pHi. Received: 21 August 1996 Accepted: 18 April 1997     

The effects of prostacyclin on gastric intramucosal pH in patients with septic shock

Objective To investigate whether infusing prostacyclin (PGI₂) in patients with septic shock improves splanchnic oxygenation as assessed by gastric intramucosal pH (pHi).Design Interventional clinical study.Setting Surgical ICU in a university hospital.Patients 16 consecutive patients with septic shock according to the criteria of the ACCP/SCCM consensus conference all requiring norepinephrine to maintain arterial blood pressure.Interventions All patients received PGI₂ (10 ng/kg·min) after no further increase in oxygen delivery could be obtained by volume expansion, red cell transfusion and dobutamine infusion. The results were compared with those before and after conventional resuscitation. The patients received continuous PGI₂ infusion for 3–32 days.Measurements and results O₂ uptake was measured directly in the respiratory gases, pHi was determined by tonometry. Baseline O₂ delivery, O₂ uptake and pHi were 466±122 ml/min·m², 158±38 ml/min·m², and 7.29±0.09, respectively. While O₂ uptake remained unchanged, infusing PGI₂ increased O₂ delivery (from 610±140 to 682±155 ml/min·m²,p<0.01) and pHi (from 7.32±0.09 to 7.38±0.08,p<0.001) beyond the values obtained by conventional resuscitation. While 9 of 11 patients with final pHi>7.35 survived, all patients with final pHi<7.35 died (p<0.01).Conclusions Infusing PGI₂ in patients with septic shock increases pHi probably by enhancing blood flow to the splanchnic bed and thereby improves splanchnic oxygenation even when conventional resuscitation goals have been achieved.Presented in part at the 13th International Symposium on Intensive Care and Emergency Medicine, Brussels, March 1993     

Validity of gastric intramucosal pH (pHi) for circulatory evaluation in pediatric patients

Objective.To determine if the measurement of gastricintramucosal pH (pHi) is useful for evaluation of circulatory status ofcritically ill pediatric patients. Design.Prospective clinicalstudy. Setting.General intensive care unit in a universityhospital. Patients.Seven pediatric patients (mean age: 2 y.o.);six post-cardiac surgery, one receiving barbiturate therapy.Interventions.Tonometric catheters were placed via nasogastricapproach. pHi was measured after confirmation of the catheter positionby X-ray. Measurements and main results.Saturation of venousblood oxygen (SvO₂), arterial keton body ratio (AKBR), serumlactate level and pHi were evaluated simultaneously. No patientssurvived with pHi below 7.22; pHi above 7.11 significantly correlatedwith SvO₂ values (r= 0.814, p< 0.001);pHi below 7.11 did not show any significant correlation withSvO₂. Whereas SvO₂ values of under 40% weredistributed in the pHi range from 7.11 to 7.19, pHi below 7.11 occurredwhen SvO₂ values were more than 40%. AKBR and serumlactate level did not correlate with pHi. Conclusion.pHi can bea useful parameter for evaluating the circulatory status of criticallyill pediatric patients; it allows reliable evaluation of splanchnic andperipheral perfusion.     

Influence of alveolar ventilation changes on calculated gastric intramucosal pH and gastric-arterial PCO2 difference

Objective: To evaluate the influence of changes in alveolar ventilation on the following tonometry-derived variables: gastric intramucosal CO₂ tension (PtCO₂), gastric arterial CO₂ tension difference (P_gapCO₂), gastric intramucosal pH (pHi) and arterial pH-pHi difference (pH_gap). Design: Clinical prospective study. Setting: A medical intensive care unit in a university hospital. Patients: Ten critically ill, mechanically ventilated patients requiring hemodynamic monitoring with pulmonary artery catheter. Interventions: Gastric tonometer placement. A progressive increase in tidal volume (V_T) from 7 to 10 ml/kg followed by an abrupt return to baseline V_T level. Measurements and main results: Tonometer saline PtCO₂ and hemodynamic data were collected hourly at various V_T levels: H0 and H0' (baseline V_T = 7 ml/kg), H1 (V_T = 8 ml/kg), H2 (V_T = 9 ml/kg), H3 (V_T = 10 ml/kg), H4 (baseline V_T). During the “hyperventilation phase” (H0-H3), pHi (p < 0.01) and pH_gap (p < 0.05) increased but P_gapCO₂ remained unchanged. Cardiac output (CO) was not affected by ventilatory change. During the “hypoventilation phase” (H3-H4), pHi fell from 7.27 ± 0.11 to 7.23 ± 0.09 (p < 0.01) and P_gapCO₂ decreased from 16 ± 5 mmHg to 13 ± 4 mmHg (p < 0.05). V_T reduction was associated with a significant cardiac output elevation (p < 0.05). Conclusions: PaCO₂ and PtCO₂ are similarly influenced by the changes in alveolar ventilation. Unlike pHi, the P_gapCO₂ is not affected by ventilation variations unless CO changes are associated. Received: 15 June 1998 Final revision received: 21 October 1998 Accepted: 16 November 1998     

脑出血患者胃粘膜pH值与氧输送变化的临床意义

目的初步探讨脑出血患者胃粘膜ｐＨ值（ｐＨｉ）及氧输送（ＤＯ２）改变与急性应激性胃粘膜病变（ＡＳＧＬ）的关系。方法对７例脑出血患者进行胃粘膜ｐＨ、ＤＯ２和胃潜血测定。结果成活组４例中,在监测开始时ｐＨｉ与ＤＯ２都在正常范围内,而死亡３例中ｐＨｉ都明显减低,但ＤＯ２减低不明显。随着治疗,死亡组ｐＨｉ明显下降,与成活组２４小时、４８小时相比,差异显著（Ｐ＜００１）;成活组ＤＯ２逐渐下降,而死亡组ＤＯ２有增高趋势。有４例病人出现了ＡＳＧＬ,死亡组３例均出现了严重的消化道出血。结论监测ｐＨｉ对判断组织氧合及预后有重要意义,与ＤＯ２结合起来对治疗有具体的指导意义。但因ｐＨｉ与ＤＯ２不完全依赖,在部分病人中,仅以提高ＤＯ２为治疗原则是不够的。     

胃黏膜pH监测对重度急性颅脑外伤患者的临床意义

目的探讨重度急性颅脑外伤患者胃黏膜pH值(pHi)及其衍生指标PgapCO2和pHgap的变化与重度急性颅脑外伤患者脑外并发症(应激性溃疡出血和多器官功能障碍综合征)及近期预后之间的关系。方法队列研究2002-11～2003-12收治的重度急性颅脑外伤患者共41例,入院予以常规治疗。用自动空气张力计法每小时测一次PgCO2,共测24h。入院当时及入院后8、16、24h测动脉血气,应用S/5监护仪自动计算胃pHi及其衍生指标PgapCO2、pHgap。将一次或一次以上胃pHi值<732者归为降低组,≥732者归为正常组。根据1周内是否存活,分为存活组和死亡组。每日观察胃液隐血。连续7d每日进行SOFA评价和MOF评分。结果胃pHi正常组23例,降低组18例。死亡12例。胃pHi降低组与正常组1周内病死率、胃液隐血阳性发生率、MODS发生率、SOFA评分和MOF评分的差别有统计意义(P<001或P<005)。存活组与死亡组的胃液隐血阳性发生率和MODS发生率的差别有统计意义(P<005和P<001)。存活组与死亡组入院时PgapCO2差别有统计意义(P<001)。入院24h两组PgCO2、PgapCO2、pHi和pHgap差别均有统计意义(P<005或P<001)。结论入院24h内胃pHi及其衍生指标PgapCO2、pHgap的异常对重度急性颅脑外伤的脑外并发症及其近期预后有预警作用。     

动静脉血pH和二氧化碳分压差与胃粘膜pH监测组织氧合相关性的实验研究

目的：探讨反应组织氧合状况简便易行而有实用价值的指标。方法：用致病性大肠村菌活菌液制备兔感染性休克模型（实验组１０只,对照组６只注射等量生理盐水）,观察实验组与对照组在种菌前,种菌后０．５,１．０,１．５,２．０和２．５平均动脉压（ＭＡＰ）,胃粘膜ｐＨ值（ｐＨｉ）和动,静脉血ｐＨ（ａ－ｖｐＨ）及二氧化碳分压差（ｖ－ａＰＣＯ２）的变化及其相关性。     

机械通气患者早期肠内营养与胃黏膜pH值监测的临床应用

目的 观察早期肠内营养及胃黏膜pH值(pHi)监测对重症监护病房(ICU)中非胃肠道外伤或手术需机械通气患者的疗效.方法 通过连续监测40例患者术后7 d内pHi的变化,并根据生命体征和肠鸣音的恢复情况分别于术后12～72 h内(早期)给予肠内营养(25例)和静脉营养(15例),比较两组7 d内脱机成功率及机械通气时间.结果 肠内营养组7 d内脱机成功率明显高于静脉营养组[76%(19/25)比40%(6/15),P<0.05],机械通气时间则明显短于静脉营养组[(4.30±0.01)d比(8.22±0.02)d,P<0.05];肠内营养组术后7 d pHi较1 d时增加(7.39±0.03比7.28±0.01,P<0.05),且明显高于静脉营养组(7.30±0.02,P<0.05).此外,肠内营养组较静脉营养组恢复排气时间明显缩短[(47.08±8.33)h比(67.03±8.03)h,P<0.05].结论 pHi监测是反映危重病患者胃肠黏膜血液灌注及氧合状态的敏感指标;早期实施肠内营养可以改善患者胃肠黏膜血液灌注,从而有效防止肠道细菌移位的发生,提高脱机成功率并缩短时间;只要胃肠道功能正常,应尽早实施肠内营养支持.     

失血性休克时胃粘膜内pH与组织氧合监测的实验研究

目的 进一步探讨粘膜内pH与值肠粘膜组织氧合的关系。方法 以失血性休克大鼠为模型,根据胃内PCO2和同时测得的动脉血HCO3^-浓度,通过Henderson-Hasselbalch公式间接测定胃粘膜内pH(pHi),同时测定动脉血,混合静脉血,门静脉乳酸（Lacp)及动脉血,混合静脉血气分析。结果 失血性休克时,pHi与门静脉乳酸（Lacp)显降低,两呈线性关系（r=-0.88),pHi的降低不仅与胃肠粘膜的氧合障碍有关,同时还与全身组织氧合不足有关,失血性休克时,pHi的降低与胃肠粘膜的病理性损害一致。结论 pHi的变化可早期反映肠道及全身组织氧合情况,可作为重症监护的一个重要指标。