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Endotracheal tube fire induced by electrocautery during tracheostomy--a case report. 气管切开术中电灼致气管管起火1例。
Pub Date : 2002-12-01 DOI: 10.6955/AAS.200212.0209
Chih-Cheng Wu, Ching-Hui Shen, W. Ho
Airway fire resulting from ignition of the endotracheal tube (ETT) caused by electrocautery during tracheostomy is a severe and possibly fatal event, and should be avoided. An 88-year-old male because of respiratory failure received elective tracheostomy for ventilatory support on which prolonged dependence was anticipated. Unfortunately, flame was noted to jet out from the trachea incision just after a single burst of electrocautery to coagulate a bleeder in the trachea tissue nearby the incision. After primary management, including extinguishing the flame and evaluation of the tracheal injury by bronchoscope, a tracheostomy tube was inserted smoothly without causing hypoxemia or hemodynamic instability. The patient stood this ordeal of fire well without related sequelae and was returned from the intensive care unit (ICU) to the general ward two weeks later. From this accident, we recommend that, besides emphasis on lowering of the inspired oxygen concentration (FiO2) and careful use of electrocautery during the tracheostomy procedure, special attention should be paid to the integrality of ETT cuff. It serves as a barrier to prevent oxygen leaking out from the trachea to be exposed to the sparks of electrocautery while the surgical procedure is under way, and thus it plays a significant role in the avoidance of airway fire induced by electrocautery.
气管切开术中由电灼引起的气管内管着火是一种严重且可能致命的事件,应避免发生。一位88岁男性患者因呼吸衰竭接受择期气管切开术以获得通气支持,预期长期依赖。不幸的是,在一次电灼之后,火焰从气管切口喷出,使切口附近的气管组织中的出血点凝固。初步处理后,包括扑灭火焰和支气管镜评估气管损伤,气管造瘘管顺利插入,没有引起低氧血症或血流动力学不稳定。病人很好地经受住了这场大火的折磨,没有留下任何后遗症,两周后从重症监护室(ICU)回到普通病房。从这次事故中,我们建议在气管切开术中,除了强调降低吸入氧浓度(FiO2)和小心使用电切外,还应特别注意ETT袖带的完整性。在手术过程中,它作为一个屏障,防止氧气从气管中泄漏出来,暴露在电灼的火花中,因此它在避免电灼引起的气道火灾中起着重要的作用。
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引用次数: 8
Oral clonidine reduces myocardial ischemia in patients with coronary artery disease undergoing noncardiac surgery. 口服可乐定可减少冠心病非心脏手术患者心肌缺血。
Pub Date : 2002-12-01
Young-Chen Yin, Lok-Hi Chow, Cheng-Ming Tsao, Chi-Chun Chu, Mei-Yung Tsou, Kwok-Hon Chan, Shen-Kou Tsai

Background: To access the clinical effect of clonidine on reduction of myocardial ischemia events in patients with history of coronary artery disease undergoing noncardiac surgeries.

Methods: Sixty ASA class III patients with coronary artery disease were allotted at random to two groups in a prospective, double-blind study to receive either clonidine (3 micrograms/kg) or placebo (control group) 90 minutes before arrival at the operating room. Continuous EKG monitoring (Holter monitor) was performed to analyze the ST segment in lead II, V2 and V5 during the preoperative (since late hours the night before operation), intraoperative and early postoperative periods (total monitoring time = 24 hours). The episode of myocardial ischemia defined as the magnitude of ST segment depression of at least 1 mm, occurring 60 ms after the J point and persisting for three minutes or more was recorded. Perioperative hemodynamic data were analyzed with two-way ANOVA with repeated measures. Student's t-test for unpaired data was used for analysis of demographics. Chi-square test was used for ST segment changes. Results are expressed as mean +/- SD and P < 0.05 was considered to be statistically significant.

Results: In the control group, 9 patients (30%) were noted to have episodes of ischemia preoperatively, 7 patients (23.3%) intraoperatively, and 12 patients (40%) postoperatively. The occurrence of myocardial ischemia peaked in the early postoperative period (P < 0.05). On the contrary, in the clonidine group, 10 patients (33.3%) saw ischemic episodes preoperatively, 3 patients (10%) intraoperatively and 5 patients (16.7%) postoperatively. The incidence of myocardial ischemia in clonidine group was significantly lower than that in placebo group in intraoperative and postoperative periods. The mean arterial pressure was significantly lower in some clonidine-treated patients during perioperative periods (P < 0.05). A number of patients in clonidine group suffered from drowsiness (66.7%) after operation (P < 0.05), but they could be easily aroused. In regard to dryness of mouth, nausea and vomiting clonidine and control groups did not differ much (P > 0.05). Demerol consumption was significantly lower in clonidine group (43.7 +/- 4.6 mg) than in control group (76.3 +/- 3.7 mg, P < 0.05).

Conclusions: We conclude that premedication with oral clonidine can significantly reduce the incidence of perioperative myocardial ischemia in patients with CAD undergoing noncardiac surgeries. The incidence of myocardial ischemia in these patients is rather high during perioperative period, which deserves our exceptional caution.

背景:探讨可乐定对有冠心病史的非心脏手术患者减少心肌缺血事件的临床效果。方法:60例ASA III级冠心病患者在一项前瞻性双盲研究中随机分为两组,在到达手术室前90分钟接受可乐定(3微克/公斤)或安慰剂(对照组)。术前(术前深夜起)、术中及术后早期(总监测时间= 24小时)连续心电图监测(霍尔特监护),分析II导联、V2导联、V5导联ST段。记录心肌缺血发作,定义为ST段下降幅度至少1mm,发生在J点后60ms,持续3分钟以上。围手术期血流动力学资料采用重复测量的双因素方差分析。非配对数据的学生t检验用于人口统计学分析。ST段变化采用卡方检验。结果以均数+/- SD表示,P < 0.05为有统计学意义。结果:对照组术前出现缺血9例(30%),术中出现缺血7例(23.3%),术后出现缺血12例(40%)。术后早期心肌缺血发生率最高(P < 0.05)。相反,可乐定组术前出现缺血发作10例(33.3%),术中出现缺血发作3例(10%),术后出现缺血发作5例(16.7%)。可乐定组术中、术后心肌缺血发生率均显著低于安慰剂组。部分患者围手术期平均动脉压明显降低(P < 0.05)。可乐定组术后出现嗜睡的患者较多,占66.7% (P < 0.05),但易被唤醒。在口干、恶心、呕吐方面,可乐定组与对照组差异无统计学意义(P > 0.05)。可乐定组杜冷丁消耗量(43.7 +/- 4.6 mg)显著低于对照组(76.3 +/- 3.7 mg, P < 0.05)。结论:术前口服可乐定可显著降低冠心病非心脏手术患者围手术期心肌缺血的发生率。围手术期心肌缺血发生率较高,值得我们格外注意。
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引用次数: 0
Personnel exposure to waste sevoflurane and nitrous oxide during general anesthesia with cuffed endotracheal tube. 人员暴露于废弃七氟醚和氧化亚氮在全身麻醉与气管插管。
Pub Date : 2002-12-01 DOI: 10.6955/AAS.200212.0185
Shou-Huang Li, Shou-Nan Li, Hui-Ya Shih, H. Yi, Chin-Yuan Chiang
BACKGROUNDWaste anesthetic gases may have adverse effects on the health of operating room personnel. To reduce the risk of exposure, the United States National Institute of Occupational Safety and Health (US-NIOSH) recommends a time-weighted average (TWA) of 25 ppm (part-per-million) for nitrous oxide (N2O) and a ceiling of 2 ppm for sevoflurane (SEV). This study investigated the concentrations of these two gases in the atmosphere of operating room to which the working personnel (anesthetists) were exposed during anesthetic practice.METHODSAn extractive Fourier transform infrared (FTIR) spectrometer, with an optical path length of 10 meters, was used to monitor the concentrations of waste general anesthetics in the operating rooms. The FTIR in application could simultaneously determine the concentrations of several gases in a near real-time manner, which helped to accurately obtain the varying concentrations of gases in different anesthetic condition. The sampling Teflon tube of the FTIR was conveniently installed in the breathing zone of the anesthetic personnel to obtain the personal exposure concentrations of N2O and SEV.RESULTSNitrous oxide (N2O) and sevoflurane (SEV) concentrations for five surgeries in four different operating rooms were determined. In normal condition during maintenance, the SEV concentrations as measured were less than 2 ppm but the average N2O concentration was greater than 25 ppm. In addition, in three abnormal or specific conditions, the N2O and SEV concentrations increased dramatically. Firstly, at the end of maintenance (right before emergence), peak concentrations of 751 ppm for N2O and 26 ppm for SEV were measured. These unusually high concentrations resulted from flushing the tubing of the anesthetic machine to speed up the emergence of wakefulness of the patient from anesthesia. Secondly, when the cuff of the endotracheal tube was not well inflated or unserviceable, peak concentrations of 631 ppm for N2O and 32 ppm for SEV were measured. Thirdly, malfunction of or loose connection (or disconnection) between the anesthetic machine and the exhaust venting system of operating theater almost doubled the N2O and SEV concentrations.CONCLUSIONSTo decrease the exposure of the operating personnel to waste anesthetics, minimization of the use of N2O is recommended. Besides, the three extraordinary conditions as disclosed in this study were tubing flushing, illy managed endotracheal tube cuff and disconnection of scarvenging system, the first of which sometimes is unavoidable but the last two of which should be avoided.
背景:废弃麻醉气体可能对手术室人员的健康产生不利影响。为了减少接触风险,美国国家职业安全与健康研究所(US-NIOSH)建议,一氧化二氮(N2O)的时间加权平均值(TWA)为25 ppm(百万分之一),七氟醚(SEV)的上限为2 ppm。本研究调查了工作人员(麻醉师)在麻醉过程中所接触的手术室大气中这两种气体的浓度。方法采用提取式傅里叶变换红外光谱仪(FTIR),光程长度为10 m,监测手术室中废全麻的浓度。应用中的FTIR可以同时近实时地测定几种气体的浓度,有助于准确地获得不同麻醉条件下气体的不同浓度。将FTIR的特氟龙采样管方便地安装在麻醉人员的呼吸区,以获得N2O和SEV的个人暴露浓度。结果测定4个不同手术室5例手术中氧化亚氮(N2O)和七氟醚(SEV)浓度。在正常维护状态下,SEV浓度测量值小于2ppm,而N2O平均浓度大于25ppm。此外,在三种异常或特殊条件下,N2O和SEV浓度均显著升高。首先,在维护结束时(出现之前),测量了N2O的峰值浓度为751 ppm, SEV的峰值浓度为26 ppm。这些不寻常的高浓度是由于冲洗麻醉机的管道以加速病人从麻醉中苏醒。其次,当气管插管袖带充气不良或无法使用时,测量N2O和SEV的峰值浓度分别为631 ppm和32 ppm。第三,麻醉机与手术室排气系统之间的故障或连接松动(或断开)几乎使N2O和SEV浓度增加一倍。结论为减少手术人员对废麻药的接触,建议尽量减少N2O的使用。此外,本研究披露的三种异常情况分别是气管冲洗、气管套管管理不当和清除系统断开,前者有时是不可避免的,后两者应避免。
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引用次数: 21
Metastatic hepatocellular carcinoma of the right atrium causing right ventricular outflow tract obstruction during induction of anesthesia--a case report. 右心房转移性肝细胞癌致麻醉诱导时右心室流出道梗阻1例报告。
Pub Date : 2002-12-01
Shih-Yen Peng, Chih-Cheng Wu, Chung-Pei Chang, Shih-Kuei Peng, Wai-Meng Ho

Metastatic hepatocellular carcinoma (HCC) to the right atrium occurs rarely and may lead to lethal perioperative complications. A 61-year-old female who was about to undergo operation for resection of a right intraatrial tumor thought possibly to be metastatic hepatocellular carcinoma met with sudden protrusion of the tumor from the right atrial wall that sank into the right ventricle during induction of anesthesia. Right ventricular outflow tract obstruction developed and was quickly diagnosed by transesophageal echocardiography. Emergent cardiopulmonary bypass was rushed on the spot and the surgery was completed smoothly. Here we discuss the possible causes of the event and we recommend that special attention should be paid to the anesthetic techniques and proper precaution should be taken in the face of such a risky surgery.

转移至右心房的肝细胞癌(HCC)很少发生,可导致致命的围手术期并发症。1例61岁女性,因右侧心房肿瘤疑似转移性肝细胞癌,在麻醉诱导下,肿瘤突然从右心房壁突出,陷入右心室。右心室流出道梗阻发生后,经食管超声心动图迅速诊断。现场紧急进行体外循环,手术顺利完成。在此,我们讨论了该事件的可能原因,并建议在面对这种危险的手术时应特别注意麻醉技术和采取适当的预防措施。
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引用次数: 0
The analgesic effect of nalbuphine and its long-acting prodrug, nalbuphine pivalate, in rats. 纳布啡及其长效前药哌酸纳布啡对大鼠的镇痛作用。
Pub Date : 2002-12-01 DOI: 10.6955/AAS.200212.0191
Kuan-Ting Chen, O. Hu, S. Ho, Yu-Wen Chen, Jhi-Joung Wang
BACKGROUNDNalbuphine is an opioid-analgesic with agonist-antagonist properties. Recently, we have synthesized a nalbuphine prodrug, nalbuphine pivalate. The aim of the present study was to evaluate the analgesic effect and the analgesic duration of this prodrug.METHODSForty-eight male Sprague-Dawley rats (4 groups, n = 12 in each group) were used. Rats in group 1 received nalbuphine HCl 25 mumol/kg (in saline) intramuscular injection; rats in group 2 received nalbuphine pivalate 25 mumol/kg (in sesame oil) intramuscular injection, whereas those in groups 3 and 4 received saline and sesame oil respectively. The analgesic effects of testing agents were evaluated using the cold ethanol tail-flick test (-30 degrees C).RESULTSBoth nalbuphine HCl and nalbuphine pivalate demonstrated significant analgesic effects. The analgesic duration of nalbuphine HCl was 2 h while that of nalbuphine pivalate was 30 h.CONCLUSIONSNalbuphine pivalate has a very long duration of analgesic action. This fascinating finding is worth further evaluation.
纳布啡是一种具有激动-拮抗剂特性的阿片类镇痛药。最近,我们合成了一种纳布啡前药,私家纳布啡。本研究的目的是评价该前药的镇痛效果和镇痛持续时间。方法雄性Sprague-Dawley大鼠48只,分为4组,每组12只。1组大鼠给予盐酸纳布啡25 μ mol/kg(生理盐水)肌内注射;第2组大鼠肌肉注射盐酸纳布啡25 μ mol/kg(麻油中),第3组和第4组大鼠分别注射生理盐水和麻油。采用冷乙醇甩尾试验(-30℃)评价试验剂的镇痛作用。结果盐酸纳布啡和哌酸纳布啡均有明显的镇痛作用。盐酸纳布啡的镇痛时间为2 h,而哌酸纳布啡的镇痛时间为30 h。结论哌酸纳布啡的镇痛作用持续时间很长。这一有趣的发现值得进一步评价。
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引用次数: 3
Long-term opioid treatment: the role of pain facilitatory system. 长期阿片类药物治疗:疼痛促进系统的作用。
Pub Date : 2002-09-01 DOI: 10.6955/AAS.200209.0105
Chih-Shung Wong
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引用次数: 0
Soft-tip intubating stylet. 软尖插管风格。
Pub Date : 2002-09-01
Hwa-Kou King

Endotracheal intubation using a laryngoscope is the most rapid and usually the easiest means to ensure a patent airway. It has therefore earned its popularity in anesthesia and other acute health care practices. However, intubation by conventional technique is not always successful as at times direct vision of the glottis/vocal cords is impossible during laryngoscopy. Thus, acute airway obstruction remains a constant problem in all acute health care practices. To deal with this challenge, we have developed a new technique incorporating a modified Satin-Slip intubating stylet (Mallinckrodt Medical, St. Louis, MO, USA). First, cut the plastic sheath of the stylet at its distal end and push the sheath forward about one and a half inches. The soft plastic tip of the malleable stylet is then allowed to protrude from the endotracheal tube (ETT). When visualization of the glottic aperture is not possible, one simply places the soft plastic tip of the stylet under the epiglottis and advances it forward, and the tip will eventually enter the larynx. The ETT is then advanced off the stylet into the trachea. This new technique works very well in our experiences. It can be performed quickly with readily available inexpensive equipment. Our favorable experience leads us to believe it is one of the most promising additions to the current recommended alternatives.

使用喉镜进行气管插管是确保气道通畅的最快速和最简单的方法。因此,它在麻醉和其他急性保健实践中获得了普及。然而,传统的插管技术并不总是成功的,因为有时喉镜检查无法直接看到声门/声带。因此,急性气道阻塞仍然是一个持续的问题,在所有急性卫生保健实践。为了应对这一挑战,我们开发了一种新技术,其中包括一种改良的缎面滑动插管样式(Mallinckrodt Medical, St. Louis, MO, USA)。首先,剪掉发卡末端的塑料护套,将护套向前推进1.5英寸。然后允许可锻铸针的软塑料尖端从气管内管(ETT)中伸出。当无法看到声门孔时,可以简单地将软的塑料尖端放在会厌下并向前推进,尖端最终会进入喉部。然后将气管插管从柱头推进到气管内。根据我们的经验,这项新技术效果很好。它可以用现成的廉价设备快速完成。我们良好的经验使我们相信它是目前推荐的替代方案中最有希望的补充之一。
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引用次数: 0
GTPCH is not a rate-limiting factor for hemorrhagic shock-induced hepatic nitric oxide biosynthesis. GTPCH不是出血性休克诱导的肝一氧化氮生物合成的限速因素。
Pub Date : 2002-09-01
Ching-Rong Cheng, Chun-Jen Huang, Yen-Ta Lu, Yung-Wei Hsu, Peishan Tsai, Nuan-Yen Su, Jeffrey W Skimming

Background: Hemorrhagic shock upregulates inducible nitric oxide (NO) synthase (iNOS) expression and the resultant NO overproduction. Liver is one of the major organs that is responsible for increased NO production after trauma-hemorrhage and resuscitation. Guanosine triphosphate cyclohydrolase I (GTPCH) is the rate-limiting enzyme for the synthesis of tetrahydrobiopterin (BH4), a necessary co-factor for iNOS activity. Very little is known about the effects of hemorrhagic shock on hepatic GTPCH expression.

Methods: Fifteen male Sprague-Dawley rats were randomly assigned to one of three groups, i.e. a sham instrumented (Sham) group, a sustained hemorrhagic shock (HS) group, and a hemorrhagic shock with resuscitation (HS/RES) group (n = 5 in each group). Controlled hemorrhagic shock was induced and the mean arterial pressure (MAP) was kept between 40-45 mmHg for sixty minutes in both HS and HS/RES groups. Then resuscitation with infusion of shed autologous blood and normal saline was performed in HS/RES group. Microdialysis probes were put in the liver and the right atrium for collection of serial samples. NO concentrations in dialysate samples were measured using chemiluminescence. Hepatic iNOS and GTPCH mRNA concentrations were analyzed using semiquantitative reverse transcription and polymerase chain reaction (RT-PCR).

Results: Hemorrhagic shock induced both the hepatic and circulating NO biosynthesis as well as hepatic iNOS mRNA expression. Resuscitation with shed blood/normal saline normalized this upregulation. However, no difference was found in mean hepatic GTPCH mRNA concentrations between groups in this experiment.

Conclusions: We provide the evidence that hemorrhagic shock-induced NO biosynthesis involves upregulation of iNOS transcription in liver tissue and GTPCH transcription is unaffected by either hemorrhagic shock or resuscitation. Furthermore, microdialysis is an ideal technique for serial sampling and that events can be followed.

背景:失血性休克上调诱导型一氧化氮(NO)合成酶(iNOS)表达并导致NO过量产生。肝脏是创伤出血和复苏后负责增加一氧化氮产生的主要器官之一。鸟苷三磷酸环水解酶I (GTPCH)是合成四氢生物蝶呤(BH4)的限速酶,BH4是iNOS活性的必要辅助因子。目前对失血性休克对肝脏GTPCH表达的影响知之甚少。方法:15只雄性Sprague-Dawley大鼠随机分为假手术(sham)组、持续性失血性休克(HS)组和失血性休克复苏(HS/RES)组(每组n = 5)。HS组和HS/RES组均诱导控制性失血性休克,平均动脉压(MAP)保持在40-45 mmHg之间60分钟。HS/RES组给予自体血滴注及生理盐水复苏。在肝脏和右心房放置微透析探针,收集系列样品。采用化学发光法测定透析液样品中的NO浓度。采用半定量反转录和聚合酶链反应(RT-PCR)分析肝脏iNOS和GTPCH mRNA浓度。结果:失血性休克诱导肝脏和循环NO生物合成及肝脏iNOS mRNA表达。出血复苏/生理盐水使这种上调正常化。但各组肝脏GTPCH mRNA平均浓度无显著差异。结论:我们提供的证据表明,失血性休克诱导的NO生物合成涉及肝组织中iNOS转录的上调,GTPCH转录不受失血性休克或复苏的影响。此外,微透析是一种理想的连续采样技术,可以跟踪事件。
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引用次数: 0
The effect of anesthetic techniques on hemostatic function in arthroscopic surgery: evaluation by thromboelastography. 麻醉技术对关节镜手术止血功能的影响:血栓弹性成像评价。
Pub Date : 2002-09-01
Go-Shine Huang, Jen-Huei Chang, Meei-Shyuan Lee, Chia-Chun Wu, Shu-Pi Lin, Shinn-Long Lin, Chih-Shung Wong

Background: Anesthetic techniques are known to affect blood hemostasis, which may be responsible for the pathogenesis of postoperative venous thromboembolism. The purpose of this study was to evaluate the effect of general and spinal anesthesias on blood hemostasis using thromboelastography.

Methods: Forty patients undergoing arthroscopic knee surgery were enrolled for study and randomly allocated to one of two groups, to receive either general (GA; n = 20) or spinal anesthesia (SA; n = 20). In addition to thromboelastography, prothrombin and activated partial-thromboplastin time, and haematocrit and platelet count were also examined concurrently. Blood was sampled and examined before anesthesia to provide the baseline data (Time 1). Three more evaluations were performed at different time, i.e., twenty minutes after induction of anesthesia and just prior to skin incision (Time 2), thirty minutes after skin incision (Time 3), and three hours after surgery (Time 4).

Results: There were no intra- or inter-group differences noted as comparing the measured parameters obtained prior to, during, or three hours after surgery.

Conclusions: From the present study, we do not find any individual anesthetic technique which would have effect on the hemostasis of patients who received diagnostic arthroscopic surgery.

背景:已知麻醉技术会影响血液止血,这可能是术后静脉血栓栓塞的发病机制。本研究的目的是评估全身麻醉和脊髓麻醉对血栓弹性成像止血的影响。方法:选取40例膝关节关节镜手术患者进行研究,随机分为两组,接受普通(GA)治疗;n = 20)或脊髓麻醉(SA;N = 20)。除了血栓弹性成像,凝血酶原和活化的部分凝血活酶时间,红细胞压积和血小板计数也被同时检查。麻醉前抽血并检查以提供基线数据(时间1)。在不同时间进行三次评估,即麻醉诱导后20分钟和皮肤切口前(时间2),皮肤切口后30分钟(时间3)和手术后3小时(时间4)。结果:与手术前,手术中或手术后3小时获得的测量参数相比,没有组内或组间差异。结论:从目前的研究来看,我们没有发现任何一种单独的麻醉技术对接受诊断性关节镜手术的患者的止血有影响。
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引用次数: 0
GTPCH is not a rate-limiting factor for hemorrhagic shock-induced hepatic nitric oxide biosynthesis. GTPCH不是出血性休克诱导的肝一氧化氮生物合成的限速因素。
Pub Date : 2002-09-01 DOI: 10.6955/AAS.200209.0109
Ching-Rong Cheng, Chun-Jen Huang, Yen-Ta Lu, Y. Hsu, P. Tsai, N. Su, J. Skimming
BACKGROUNDHemorrhagic shock upregulates inducible nitric oxide (NO) synthase (iNOS) expression and the resultant NO overproduction. Liver is one of the major organs that is responsible for increased NO production after trauma-hemorrhage and resuscitation. Guanosine triphosphate cyclohydrolase I (GTPCH) is the rate-limiting enzyme for the synthesis of tetrahydrobiopterin (BH4), a necessary co-factor for iNOS activity. Very little is known about the effects of hemorrhagic shock on hepatic GTPCH expression.METHODSFifteen male Sprague-Dawley rats were randomly assigned to one of three groups, i.e. a sham instrumented (Sham) group, a sustained hemorrhagic shock (HS) group, and a hemorrhagic shock with resuscitation (HS/RES) group (n = 5 in each group). Controlled hemorrhagic shock was induced and the mean arterial pressure (MAP) was kept between 40-45 mmHg for sixty minutes in both HS and HS/RES groups. Then resuscitation with infusion of shed autologous blood and normal saline was performed in HS/RES group. Microdialysis probes were put in the liver and the right atrium for collection of serial samples. NO concentrations in dialysate samples were measured using chemiluminescence. Hepatic iNOS and GTPCH mRNA concentrations were analyzed using semiquantitative reverse transcription and polymerase chain reaction (RT-PCR).RESULTSHemorrhagic shock induced both the hepatic and circulating NO biosynthesis as well as hepatic iNOS mRNA expression. Resuscitation with shed blood/normal saline normalized this upregulation. However, no difference was found in mean hepatic GTPCH mRNA concentrations between groups in this experiment.CONCLUSIONSWe provide the evidence that hemorrhagic shock-induced NO biosynthesis involves upregulation of iNOS transcription in liver tissue and GTPCH transcription is unaffected by either hemorrhagic shock or resuscitation. Furthermore, microdialysis is an ideal technique for serial sampling and that events can be followed.
背景:出血性休克可上调诱导型一氧化氮合成酶(iNOS)的表达并导致NO过量产生。肝脏是创伤出血和复苏后负责增加一氧化氮产生的主要器官之一。鸟苷三磷酸环水解酶I (GTPCH)是合成四氢生物蝶呤(BH4)的限速酶,BH4是iNOS活性的必要辅助因子。目前对失血性休克对肝脏GTPCH表达的影响知之甚少。方法雄性Sprague-Dawley大鼠15只,随机分为假手术(sham)组、持续性失血性休克(HS)组和失血性休克伴复苏(HS/RES)组(每组5只)。HS组和HS/RES组均诱导控制性失血性休克,平均动脉压(MAP)保持在40-45 mmHg之间60分钟。HS/RES组给予自体血滴注及生理盐水复苏。在肝脏和右心房放置微透析探针,收集系列样品。采用化学发光法测定透析液样品中的NO浓度。采用半定量反转录和聚合酶链反应(RT-PCR)分析肝脏iNOS和GTPCH mRNA浓度。结果出血性休克诱导肝脏和循环NO生物合成及肝脏iNOS mRNA表达。出血复苏/生理盐水使这种上调正常化。但各组肝脏GTPCH mRNA平均浓度无显著差异。结论我们提供的证据表明,失血性休克诱导的NO生物合成与肝组织中iNOS转录的上调有关,GTPCH转录不受失血性休克和复苏的影响。此外,微透析是一种理想的连续采样技术,可以跟踪事件。
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Acta anaesthesiologica Sinica
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