单肺通气时两种通气模式对PetCO2与PaCO2相关性的影响

目的：探讨胸科开胸手术单肺通气定容通气模式下和定压通气模式下PetC02（呼气末二氧化碳分压）与PaCO2（动脉二氧化碳分压）的相关性。方法：选择40例择期左侧开胸手术单肺通气成年患者,ASAI～II级,随机分为A组（n=20）采用VCV（容量控制通气）模式通气、B组（n=20）采用PCV（压力控制通气）模式通气。比较两组各时段的PaCO2和PetCO2的差异及相关性。结果：经统计学分析,除第一时间点,两组同一时间点的PetC02比较及PaCO2比较差异均有统计学意义（P〈O．05）,A组PetC02四个时间点比较及PaCO2四个时间点比较差异均有有统计学意义（P〈0．001）,B组除PetCO2第三与第四个时间点比较差异无统计学意义外,余PetCO2各时间点相比较及PaCO2各时间点相比较差异均有统计学意义（P〈0．05）。单肺通气定压通气模式下PetCO2与PaCO2在各个时间点的相关系数均大于定容通气模式时。无论是定容还是定压通气模式,单肺通气时间越长,其PetCO2与PaCOz的相关系数也越小。结论：1．同双肺通气相比,单肺通气时定压通气模式下PaCO2及PetCO2的改变小于定容通气模式时。2．单肺通气时,定压通气模式下PetCO2与PaCO2的相关性好于定容通气模式时。3．在这两种通气模式下PetCO2与PaCO2的相关性与单肺通气的时间成反比。     

单肺通气时两种通气模式对PetCO_2与PaCO_2相关性的影响

目的:探讨胸科开胸手术单肺通气定容通气模式下和定压通气模式下PetCO2(呼气末二氧化碳分压)与PaCO2(动脉二氧化碳分压)的相关性。方法:选择40例择期左侧开胸手术单肺通气成年患者,ASAⅠ~Ⅱ级,随机分为A组(n=20)采用VCV(容量控制通气)模式通气、B组(n=20)采用PCV(压力控制通气)模式通气。比较两组各时段的PaCO2和PetCO2的差异及相关性。结果:经统计学分析,除第一时间点,两组同一时间点的PetCO2比较及PaCO2比较差异均有统计学意义(P0.05),A组PetCO2四个时间点比较及PaCO2四个时间点比较差异均有有统计学意义(P0.001),B组除PetCO2第三与第四个时间点比较差异无统计学意义外,余PetCO2各时间点相比较及PaCO2各时间点相比较差异均有统计学意义(P0.05)。单肺通气定压通气模式下PetCO2与PaCO2在各个时间点的相关系数均大于定容通气模式时。无论是定容还是定压通气模式,单肺通气时间越长,其PetCO2与PaCO2的相关系数也越小。结论:1.同双肺通气相比,单肺通气时定压通气模式下PaCO2及PetCO2的改变小于定容通气模式时。2.单肺通气时,定压通气模式下PetCO2与PaCO2的相关性好于定容通气模式时。3.在这两种通气模式下PetCO2与PaCO2的相关性与单肺通气的时间成反比。     

容量与压力控制通气模式对胸科手术单肺通气肺内分流及氧合的影响

目的:为观察术前肺功能正常的开胸手术病人在单肺通气(OLV)期间,定压控制通气模式(PCV)和定容控制通气模式(VCV)对气道压力、肺内分流及氧合的影响.方法:选择40例术前肺功能正常进行开胸手术的病人,随机分为A、B两组.A组:单肺通气采用VCV模式30 min后转换为PCV模式.B组:单肺通气采用PCV模式30 min后转换为VCV模式.在麻醉前(TI)、单肺通气前(T2),容量控制通气(压力控制通气)30min(T3)、转换为压力控制通气(容量控制通气)30min(T4)四个时间段测气道压力和采动脉及混合静脉血行血气分析及计算肺内分流.结果:发现;无论VCV还是PCV在单肺通气期间动脉血氧分压(PaO2)无统计学意义(P=0.534),两组间的肺内分流量(Qs/Qt)比较差异无显著性(p>0.05),PCV气道压力比VCV低((P<0.01).结论:肺功能正常的患者在OLV期间,PCV模式与VCV模式比较并不能提高氧合作用,但PCV模式气道压力低,有利于减少气道损伤.     

有创-无创序贯通气在COPDⅡ型呼吸衰竭中的应用临床观察

目的:探索有创-无创序贯通气法对慢性阻塞性肺疾病(COPD)合并Ⅱ型呼吸衰竭的应用疗效.方法:选择COPDⅡ型呼吸衰竭需机械通气的患者77例,随机分为序贯组35例,常规组32例,所有患者均接受气管插管及机械通气,待肺部感染控制(PIC)窗出现后,选择无创呼吸机模式(BiPAP),常规组则保持机械通气至脱机.观察两组的主要指标并记录序贯组拔管时和BiPAP治疗4h后的血气变化.结果:序贯组的有创通气时间为(73.58± 30.17)h、气管插管复插率为5.7％和VAP发生率为2.9％,均显著低于常规组,差异有统计学意义(均P=0.000),两组总机械通气时间以及呼吸重症监护病房(RICU)住院时间的差异近似,无统计学意义(总机械通气时间:P=0.958; RICU住院时间:P=0.654).序贯组在选择BiPAP后,pH、血氧分压(PaO2)、二氧化碳分压(PaCO2)、心率(HR)和平均动脉压(MAP)值与拔管时的差异均近似,差异无统计学意义(均P＞0.05).结论:有创-无创序贯通气可明显缩短机械通气时间,降低气管插管复插率及VAP发生率,结合有效的护理措施能够有效改善COPD合并Ⅱ型呼吸衰竭.     

序贯机械通气联合尼可刹米治疗AECOPD合并Ⅱ型呼吸衰竭的临床观察

目的：观察序贯机械通气联合尼可刹米在慢性阻塞性肺疾病急性加重期（AECOPD）合并Ⅱ型呼吸衰竭中的的临床疗效及安全性。方法：按照随机原则将64例AECOPD合并Ⅱ型呼吸衰竭分成两组,对照组32例给予常规有创机械通气,治疗组患者给予序贯机械通气联合尼可刹米治疗,对两组治疗前、后24 h和48h的pH值、PaO2、PaCO2以及VAP、总机械通气时间、ICU时间,总住院时间,再插管率以及死亡率进行评价。结果：治疗组与对照组相比,pH值改善明显、PaO2明显增长、PaCO2下降显著,有统计学差异（P〈0.05）;治疗组ICU时间,总住院时间,再插管率以及死亡率与对照组相比,下降明显,有统计学差异（P〈0.05）。结论：序贯机械通气联合尼可刹米治疗AECOPD合并Ⅱ型呼吸衰竭的临床疗效确切,值得临床推广。     

机械通气治疗急性呼吸窘迫综合征的肺复张策略研究

目的:探讨机械通气治疗急性呼吸窘迫综合征(Acute respiratory distress syndrome,ARDS)的肺复张策略的作用。方法:选择2012年1月~2012年12月我院收治的采用机械通气并进行肺复张治疗的ARDS患者94例,根据肺复张方法不同,将所有患者分为对照组和实验组,并比较两组患者的不同时点的氧合指数、肺顺应性及两组出现的并发症。结果:对照组肺复张成功率为72.34%,实验组肺复张成功率为95.75%,X2=38.928,P0.05,两组患者肺复张成功率差异具有统计学意义。两组患者氧合指数、肺顺应性和PaCO2在肺复张实施前比较,差异无统计学意义。肺复张策略实施后24h、48h和72h的氧合指数和PaCO2比较,这三个时点的氧合指数和PaCO2差异具有统计学意义。两组患者肺顺应性在肺复张策略实施后1h、2h和6h比较,t分别=4.939,5.391和5.999,P0.05,此三个时点的肺顺应性差异同样具有统计学意义。对照组气压伤发生率为82.98%,实验组气压伤发生率为59.57%,两组患者气压伤发生率差异具有统计学意义。结论:ARDS的患者在机械通气治疗的过程中上采用肺复张策略,不但可以提高肺复张成功率,改善肺部通气效果,且安全性好,适合临床使用。     

HFOV联合PS对治疗新生儿ALI/ARDS的疗效及对肺动态顺应性的影响

摘要 目的：探讨高频振荡通气（HFOV）联合肺表面活性物质（PS）对治疗新生儿急性肺损伤/急性呼吸窘迫综合征（ALI/ARDS）的疗效及对肺动态顺应性的影响。方法：选择2018年1月至2020年12月我院新生儿科收治的160例ALI/ARDS患儿进行研究,按照随机数表法分为观察组和对照组,每组80例。对照组患儿给予常频通气（CMV）模式联合PS治疗,观察组患儿给予HFOV模式联合PS治疗。比较两组患儿一般治疗情况、治疗前后肺动态顺应性、动脉血氧分压（PaO₂）、动脉二氧化氮分压（PaCO₂）、氧合指数（OI）、血清肿瘤坏死因子-α（TNF-α）、白细胞介素（IL）-6、IL-10的变化,以及治疗期间并发症发生情况。结果：观察组胸片恢复正常时间、机械通气时间、氧暴露时间、ICU停留时间、住院时间结果均明显短于对照组（P＜0.05）,两组患儿病死率相比较,无统计学意义（P＞0.05）;治疗后12 h、24 h、48 h时,观察组肺动态顺应性及PaO₂、OI结果明显高于对照组,PaCO₂明显比对照组低,差异有统计学意义（P＜0.05）;治疗后48 h时,观察组血清TNF-α、IL-6水平均明显低于对照组,IL-10明显比对照组高,差异有统计学意义（P＜0.05）;两组治疗期间,呼吸机相关性肺损伤、颅内出血、气漏、呼吸道感染的总发生率比较,无统计学意义（P＞0.05）。结论：HFOV联合PS治疗新生儿ALI/ARDS疗效明显,可有效改善患儿肺动态顺应性,促进血气分析指标恢复,且可降低炎症因子的表达,值得推广应用。     

允许性高碳酸血症对大鼠机械通气相关性肺损伤NF-kB 表达的影响

目的：探讨允许性高碳酸血症对大鼠机械通气相关性肺损伤（VILI）时NF-kB 表达的影响。方法：健康雄性Wistar 大鼠30 只,体重220～280 g,采用随机数字表法,将大鼠随机分3 组（n=10)：对照组（C 组）保留自主呼吸、机械通气肺损伤组（V 组）和 VILI+ 高碳酸血症干预治疗组(H 组)行机械通气4 h。采用吸气相高气道压机械通气模式制备机械通气相关性肺损伤模型。H 组通 过调整吸入的CO2浓度来维持动脉血PaCO2分别为80～100 mmHg。于机械通气15 min 时、机械通气1 h、2 h和4 h 时记录 MAP,采集股动脉血样,进行动脉血气分析,记录PaO2;机械通气结束时,测定支气管肺泡灌洗液(BALF)中总蛋白、TNF-琢和巨噬 细胞炎症蛋白-2（MIP-2）的浓度;取肺组织,测定湿干重比（W/D 比）、细胞间粘附分子（ICAM-1）和NF-kb 蛋白的表达水平,并观 察病理学结果,进行肺损伤评分。测定肺组织丙二醛（MDA）含量及过氧化物歧化酶（SOD）活性。结果：与C 组比较,V 组和H 组 肺损伤评分、W/D 比、ICAM-1表达水平、BALF中总蛋白浓度、TNF-alpha和MIP-2 浓度、MDA 含量和肺组织NF-资B 活性升高,PaO2 降低（P<0.05）;与V 组比较,H 组肺损伤评分、W/D 比、ICAM-1表达水平、BALF 中总蛋白浓度、TNF-alpha和MIP-2 浓度和肺组织 NF-kB 表达降低,SOD活性增强,PaO2升高（P<0.05）。结论：允许性高碳酸血症可下调NF-资B的表达,从而抑制炎症反应减轻大 鼠机械通气相关性肺损伤。     

对比分析间歇正压通气与无创高频振荡通气分别联合微创肺表面活性物质治疗新生儿呼吸窘迫综合征疗效及安全性

摘要 目的：对比经鼻间歇正压通气（NIPPV）与无创高频振荡通气（nHFOV）分别联合微创肺表面活性物质（PS）治疗新生儿呼吸窘迫综合征（RDS）的临床效果及安全性。方法：选择2019年1月至2021年12月我院新生儿科收治的100例RDS患儿作为研究对象,采用随机数字表法分为对照组和观察组,各50例。对照组新生儿采用NIPPV联合微创PS治疗,观察组新生儿采用nHFOV联合微创PS治疗。比较两组患儿治疗相关指标（机械通气时间、氧暴露时间、住院天数）、临床症状（吸气三凹征、进行性呼吸困难、气促）改善时间、血气指标[脉血氧分压（PaO₂）、动脉血二氧化碳分压（PaCO₂）、氧合指数（OI）]、呼吸暂停发生率、通气失败率以及并发症发生率。结果：（1）观察组患儿机械通气时间、氧暴露时间、住院时间均较对照组少（P<0.05）。（2）观察组患儿进行性呼吸困难、吸气三凹征、气促改善时间均显著少于对照组（P<0.05）。（3）观察组患儿治疗72 h时的PaO₂显著高于对照组,PaCO₂和OI显著低于对照组（P<0.05）。（4）观察组呼吸暂停发生率和通气失败率为16.00%和10.00%,与对照组并无显著差异（P＞0.05）。（5）观察组术后并发症总发生率为4.00 %显著低于对照组的26.00 %（P<0.05）。结论：与NIPPV联合无创PS比较,nHFOV联合微创PS更能有效改善NRDS患儿肺通气功能,缩短机械通气时间,减少并发症。     

不同潮气量机械通气对大鼠肺组织HMGB1表达的影响

目的观察不同潮气量机械通气大鼠肺组织高迁移率族蛋白1（HMGB1） mRNA及其蛋白的表达水平,探讨HMGB1在呼吸机相关性肺损伤（VILI）发病中的作用。方法24只雄性Wister大鼠随机分为对照组、小潮气量组和大潮气量组,分别采用原位分子杂交技术和免疫组织化学染色法检测肺组织HMGB1 mRNA及其蛋白的表达水平。结果与对照组和小潮气量组比较,大潮气量组大鼠肺组织HMGB1 mRNA及其蛋白表达水平明显升高（均P〈0.01）,小潮气量组与对照组各项指标比较差异无统计学意义（P〉0.05）。结论大潮气量机械通气可诱导肺组织HMGB1 mRNA及其蛋白高表达;HMGB1分泌增多导致肺组织炎症反应扩大,可能是呼吸机相关性肺损伤（VILI）发生的重要因素之一。     

Ventilation response to CO2 and exercise-induced hypoxaemia in master athletes

Exercise-induced hypoxaemia (EIH) in master athletes may be related to a diminished exercise hyper- pnoea. The aim of this study was to determine whether EIH is associated with a change in the sensitivity of the ventilation response to activation of the central chemoreceptors. The ventilation response to CO₂ was measured in nine elderly untrained men (UT) [mean age 66.3 (SEM 3.1) years] and nine master athletes (MA) [mean age 62.7 (SEM 0.8) years] at rest, during moderate exercise (40% maximal oxygen uptake, V˙O_2max), and during strenuous exercise (70% V˙O_2max) using the rebreathing method. Our results showed that the ventilation response to CO₂ did not differ with endurance training and/or exercise, that the threshold of the CO₂ response (Th) increased with exercise (P < 0.001), that the increase in Th in MA was higher than in UT between rest and moderate exercise [ΔTh_0–40: 8.55 (SEM 1.8) vs 3.06 (SEM 1.72) mmHg, P < 0.05], and that ΔTh_0–40 and Th during moderate exercise were negatively correlated with arterial O₂ saturation during maximal exercise (r = 0.50, P<0.05). We concluded therefore that exercise-induced hypoxaemia in master athletes may not be due to a lower ventilation response to CO₂, but may be partly related to a greater increase in Th during moderate exercise. Accepted: 18 August 1997     

The Effect of Moderate Hypocapnic Ventilation on Nuclear Ca2+-ATPase Activity, Nuclear Ca2+ Flux, and Ca2+/Calmodulin Kinase IV Activity in the Cerebral Cortex of Newborn Piglets

Previous studies have shown that hypocapnia results in fragmentation of nuclear DNA in the cerebral cortex of newborn piglets. We tested the hypothesis that hypocapnia results in decreased ATP and phosphocreatine (PCr) levels and increased nuclear high-affinity Ca++-ATPase activity, intranuclear Ca++ flux, and CaM kinase IV activity in neuronal nuclei of piglets. Three groups of piglets were ventilated as either hypocapnic (a PaCO2 of 20 mm Hg), normocapnic (a PaCO2 of 40 mm Hg), or corrected hypocapnic (ventilated as hypocapnic but with CO2 added to maintain normocapnia) for 1 h. Tissue ATP levels were lower in the hypocapnic than in the normocapnic group. PCr levels were lower and 45Ca++-influx, Ca++-ATPase activity and CaM kinase IV activity were higher in hypocapnic than in normocapnic or corrected hypocapnic piglets. We conclude that hypocapnia alters nuclear membrane Ca++ flux mechanisms and may alter neuronal phosphorylation mechanisms in the cerebral cortex of piglets.     

Inhibition of thymidylate synthase by 2′,2′-difluoro-2′-deoxycytidine (Gemcitabine) and its metabolite 2′,2′-difluoro-2′-deoxyuridine

2′,2′-Difluoro-2′-deoxycytidine (dFdC, gemcitabine) is a cytidine analogue active against several solid tumor types, such as ovarian, pancreatic and non-small cell lung cancer. The compound has a complex mechanism of action. Because of the structural similarity of one metabolite of dFdC, dFdUMP, with the natural substrate for thymidylate synthase (TS) dUMP, we investigated whether dFdC and its deamination product 2′,2′-difluoro-2′-deoxyuridine (dFdU) would inhibit TS. This study was performed using two solid tumor cell lines: the human ovarian carcinoma cell line A2780 and its dFdC-resistant variant AG6000. The specific TS inhibitor Raltitrexed (RTX) was included as a positive control. Using the in situ TS activity assay measuring the intracellular conversion of [5-³H]-2′-deoxyuridine or [5-³H]-2′-deoxycytidine to dTMP and tritiated water, it was observed that dFdC and dFdU inhibited TS. In A2780 cells after a 4 h exposure to 1 μM dFdC tritium release was inhibited by 50% but did not increase after 24 h, Inhibition was also observed following dFdU at 100 μM. No effect was observed in the dFdC-resistant cell line AG6000; in this cell line only RTX had an inhibitory effect on TS activity. In the A2780 cell line RTX inhibited TS in a time dependent manner. In addition, DNA specific compounds such as 2′-C-cyano-2′-deoxy-1-beta-D-arabino-pentafuranosylcytosine and aphidicoline were utilized to exclude DNA inhibition mediated down regulation of the thymidine kinase.Inhibition of the enzyme resulted in a relative increase of mis-incorporation of [5-³H]-2′-deoxyuridine into DNA. In an attempt to elucidate the mechanism of in situ TS inhibition the ternary complex formation and possible inhibition in cellular extracts of A2780 cells, before and after exposure to dFdC, were determined. With the applied methods no proof for formation of a stable complex was found. In simultaneously performed experiments with 5FU such a complex formation could be demonstrated. However, using purified TS it was demonstrated that dFdUMP and not dFdCMP competitively inhibited TS with a Ki of 130 μM, without ternary complex formation. In conclusion, in this paper we reveal a new target of dFdC: thymidylate synthase.     

Ventilation and acid-base balance in awake dogs exposed to heat and CO2

Some awake quiet dogs pant at cool ambient temperature (Ta) and some do not pant even when acutely exposed to heat. The purpose of the study was to determine whether this puzzling variability in respiratory behavior diminished during prolonged heat. The contributions of thermal and CO2 drives to respiratory adaptations were also examined. Five awake dogs acclimated to 20 degrees C were studied before and 2 and 48 h following exposure to 30-31 degrees C. Rectal temperature did not change; the important thermal stimulus, even at 48 h, appeared to be the increase in peripheral temperature. Variability between nonpanting and panting persisted over 48 h. On the average, ventilation (VE) doubled during heat, largely due to increased dead space ventilation. Nonpanting dogs at cool Ta decreased the threshold of the ventilatory response to CO2. A panting dog at cool Ta changed its slope of the ventilatory response from negative to positive. During hypercapnia in acute heat, ventilatory pattern changed so that frequency increased and tidal volume decreased for a given VE. By 48 h of heat, the ventilatory response to CO2 returned to control in only two dogs, but the ventilatory pattern during hypercapnia returned to control in four dogs. Since thermal stimuli remained unchanged at 48 h, adaptations of respiratory control may have been related to progressive adjustments of strong ions and acid-base balance.