不同浓度CO2对肺泡Ⅱ型上皮细胞模型A549细胞活性的影响

目的观察不同浓度的CO2对A549细胞生物学性状的影响,探讨允许性高碳酸血症(PHC)的肺保护机制。方法 A549细胞株,分别采用5%CO2(A组)、10%CO2(B组)、18%CO2(C组)培养。分别于细胞培养24 h、36 h、48 h时,应用噻唑蓝比色法检测各组的细胞活性(吸光度值);采用血气分析仪检测细胞培养液p H值、二氧化碳分压(PCO2)、碳酸氢根(HCO3-);应用流式细胞仪检测细胞周期和细胞凋亡。结果 (1)3组A549细胞吸光度值随培养时间延长而增高(P<0.05),B组各时点吸光度值均高于A组;与A组比较,C组于36 h、48 h的吸光度值降低(P<0.05)。(2)3组p H值随培养时间延长而降低(P<0.05),B、C两组p H值均低于A组相同时点,C组的p H值较B组更低(P<0.05)。3组PCO2值随培养时间延长而升高(P<0.05),B、C两组各时点的PCO2值均高于A组,C组的PCO2值较B组更高(P<0.05)。3组HCO3-值随时间延长而降低(P<0.05),B、C两组各时点HCO3-均高于A组,C组36 h、48 h时的HCO3-较B组更高(P<0.05)。(3)3组G1峰值和凋亡率随培养时间延长而升高(P<0.05);A组与B组比较,各时点的G1峰值和凋亡率均无统计学差异(P>0.05);与A组比较,C组在24 h、36 h G1峰值明显增高,并于干预后36 h、48 h凋亡率增加(P<0.05)。结论 10%CO2不影响A549的增殖,但可增加A549细胞活性;18%CO2抑制A549细胞的增殖并促进其凋亡。     

无创正压机械的通气对慢性阻塞性肺疾病患者膈肌功能影响

目的：探索与评估膈肌功能测定对重度慢性阻塞性肺疾病（COPD）急性加重期患者无创正压机械通气（NPPV）疗效的意义。方法：选择住院的急性加重期COPD患者28例,施行常规治疗＋NPPV。分别记录无创通气前,通气后48小时、终止无创通气前的跨膈压（Pdi）,肺功能、动脉血气,同时综合评估通气前、后的支气管-肺部感染情况。结果：1、无创通气治疗成功组：通气后Pdi,第一秒用力呼气容积（FEV1）．动脉血二氧化碳分压（PaCO2）、动脉血氧分压（PaO2）、pH值分别为（14．04±2．40）cmH2O、（0．70±0.24）L、（48．2±4．2）mmHg．（70．0±6．3）mmHg、（7．37±0．05）,与通气前（（10．98±0．45）cmH20、（0．59±0．11）L、（68．2±10．2）mmHg、（52．5±6．1）mmHg、（7．34±0．06））比较差异均有统计学意义（P均〈0．05）。2、开创通气治疗失败者：2例。1例其Pdi在通气前为8．74cmH2O,通气48小时为9．24cmH2O;另1势9Pdi,通气前为7,56cmH2O,结论：在NPPV治疗过程中,Pdi和EIIFEV1．PaCO2、PaO2、pH值的变化有高度一致性,Pdi的动态变化．可以客观地反映膈肌的功能状态;NPPV有助手改善AECOPD患者的膈肌功能。     

腹膜腔纯氧通气改善肺控制性低通气家兔的低氧血症

目的 对控制低通气造成的低氧血症伴高碳酸血症家兔,用纯氧进行腹膜腔通气,观察其对动脉血气的影响.方法 16只家兔经气管切开并插入气管导管,连接呼吸机.调整呼吸机参数,同时使用肌肉松弛剂抑制自主呼吸,造成低通气,致使兔PaO2降低和PaCO2:升高,制备低氧血症伴高碳酸血症家兔模型,然后用纯氧进行腹膜腔内通气,检测腹膜腔内通气开始后0.5、1、1.5及2 h动脉血气.结果 经纯氧腹膜腔内通气后,PaO2由通气前的(52.50±3.46)mm Hg分别显著升至腹膜腔通气后30 min的(76.46±7.79)mm Hg、1 h的(79.62±9.53)mm Hg、1.5 h的(78.54±7.18)mm Hg、2 h的(81.1±8.3)mm Hg(P均<0.05),通气各时点之间差异无统计学意义(P> 0.05).而PaCO2变化不显著(P>0.05),由(63.84±9.09)mm Hg降至腹膜腔通气后0.5 h的(59.84±14.22)mm Hg、1 h的(59.16±15.5)mm Hg、1.5 h的(60.02±7.07)mm Hg、2 h的(61.38±6.56)mm Hg.结论 用纯氧进行腹膜腔内通气能明显改善肺控制性低通气家兔的低氧血症,而对高碳酸血症改善不明显.     

Respiratory changes with seizures in localization‐related epilepsy: Analysis of periictal hypercapnia and airflow patterns

Purpose: The rate of sudden unexpected death in epilepsy (SUDEP) approaches 9 per 1,000 patient‐years in patients with refractory epilepsy. Respiratory causes are implicated in SUDEP. We reported that ictal hypoxemia occurs in one‐third of seizures in localization‐related epilepsy. We now report on respiratory changes in the ictal/postictal period including changes in end‐tidal CO₂ (ETCO₂) that correlate directly with alveolar CO₂, allowing a precise evaluation of seizure‐related respiratory disturbances. Methods: One hundred eighty‐seven seizures were recorded in 33 patients with localization‐related epilepsy, with or without secondarily generalized convulsions, undergoing video‐electroencephalography (EEG) telemetry with recording of respiratory data. Results: The ictal/postictal ETCO₂ increase from baseline was 14 ± 11 mm Hg (11, ?1 to 50) [mean ± standard deviation (SD) (median, range)]. ETCO₂ peak was at or above 50 mm Hg with 35 of 94 seizures, 60 mm Hg with 15, and 70 mm Hg with five seizures. Eleven of the 33 patients had seizures with ETCO₂ elevation above 50 mm Hg. The duration of ictal/postictal ETCO₂ increase above baseline was 424 ± 807 s (154, 4 to 6225). The duration of ictal apnea was 49 ± 46 s (31, 6–222); most ictal apneic events were central. Oxygen desaturation to 60% or less occurred with 10 seizures, including five that did not progress to generalized convulsions. Respiratory rate and amplitude increased postictally. The peak ictal ETCO₂ change and duration of change were not associated with apnea duration or seizure duration. Peak ETCO₂ change was significantly associated with contralateral seizure spread. Conclusions: Severe and prolonged increases in ETCO₂ occur with seizures. Postictally, respiratory effort is not impaired. Ictally triggered ventilation–perfusion inequality from pulmonary shunting or transient neurogenic pulmonary edema may account for these findings.     

Ictal apnea linked to contralateral spread of temporal lobe seizures: Intracranial EEG recordings in refractory temporal lobe epilepsy

Purpose: Respiratory mechanisms are implicated in sudden unexpected death in epilepsy (SUDEP). We previously demonstrated a high incidence of ictal hypoxemia in temporal lobe seizures. We now report on the temporal relationship between ictal apnea and seizure onset and spread in patients undergoing video‐EEG (electroencephalography) telemetry (VET) with intracranial electrodes. Methods: Ten patients with medically refractory temporal lobe epilepsy (TLE) undergoing VET were studied. Data from synchronously recorded digital pulse oximetry (SaO₂), end‐tidal CO₂ (ETCO₂), nasal airflow, abdominal excursions, and electrocardiography were obtained. Results: Sixty‐one seizures were captured. SaO₂ in the ictal/postictal period was available for 52 seizures, apnea onset times for 27 seizures, and ETCO₂ for 16 seizures. Apneas occurred only when seizures spread to the contralateral temporal lobe. The mean delay to apnea onset was significantly shorter after contralateral seizure spread (2.87 s) than after seizure onset (58.4 s); p < 0.001. The mean SaO₂ nadir with partial seizures or partial seizures prior to secondary generalization was 89.4 ± 8.6% (91.5, 69–100). Following generalized convulsions the mean oxygen saturation nadir was 75.8 ± 10.6% (78.5, 58–90). ETCO₂ elevations occurred with each ictal desaturation below 85%. Conclusions: There is a close temporal relationship between spread of seizures to the contralateral hemisphere and the onset of seizure‐associated apnea. Apnea onsets are more tightly linked to time of contralateral spread than to time of seizure onset. Patients with TLE in whom there is evidence of contralateral seizure spread may be at higher risk for ictal‐related respiratory dysfunction than those in whom seizures remain unilateral.     

Differences in tyrosine hydroxylase expression after short-term hypoxia,hypercapnia or hypercapnic hypoxia in rat carotid body

In the carotid body (CB), it has been reported that the expressions of tyrosine hydroxylase (TH) mRNA and TH protein are enhanced by exposure to hypoxia. However, it is not known whether CO₂ affects the expression of TH in the CB. We examined the expression of TH mRNA and the immunoreactivity for TH in the CB of rats exposed to hypoxia (10% O₂), hypercapnia (10% CO₂) and hypercapnic hypoxia (10% O₂ and 10% CO₂) for 2–24 h. The expression of TH mRNA in the CB was markedly enhanced in rats exposed to hypoxia for 4 h (6.6-fold), 6 h (6.0-fold) and 8 h (7.8-fold), and in rats exposed to hypercapnic hypoxia for 12 h (4.8-fold). The most intense TH immunoreactivity was observed in the CB from rats exposed to hypoxia for 12 and 24 h and to hypercapnic hypoxia for 24 h. The expressions of TH mRNA and the immunoreactivity for TH were not altered in the CB of rats exposed to hypercapnia. It is suggested that CO₂ does not affect TH expression in the CB, and that it inhibits hypoxia-enhanced TH expression.     

慢性缺氧和二氧化碳潴留大鼠脑阴离子转运蛋白的研究

目的：观测慢性缺氧和二氧化碳潴留大鼠脑桥组织中脑阴离子转运蛋白（ＡＥ３）ｍＲＮＡ的变化。方法：采用密闭舱内灌注混合气体的方法，分别复制慢性缺氧，慢性缺氧伴二氧化碳潴留及慢性呼吸性酸中毒大鼠模型，以地高辛标记的（ＡＥ３）ｃＤＮＡ探针，应用点杂交技术，对各实验组及对照组大鼠脑桥组织中ＡＥ３ｍＲＮＡ的相对含量进行测定。结果：（１）慢性缺氧组ＡＥ３ｍＲＮＡ的相对含量明显地低于对照组（Ｐ〈０．０５），慢性缺     

Impact of periictal interventions on respiratory dysfunction,postictal EEG suppression,and postictal immobility

Purpose: Sudden unexpected death in epilepsy (SUDEP) is the leading cause of epilepsy‐related mortality. Seizure‐related respiratory dysfunction (RD), the duration of postictal generalized electroencephalography (EEG) suppression (PGES), and duration of postictal immobility (PI) may be important in the pathophysiology of SUDEP. Periictal interventions may reduce the risk of SUDEP. Methods: We assessed the impact of periictal nursing interventions on RD, PGES, and PI duration in patients with localization‐related epilepsy and secondarily generalized convulsions (GCs) recorded during video‐EEG telemetry in the epilepsy monitoring unit. Video‐EEG data were retrospectively reviewed. Interventions including administration of supplemental oxygen, oropharyngeal suction, and patient repositioning were evaluated. Interventions were performed based on nursing clinical judgment at the bedside and were not randomized. The two‐sided Wilcoxon rank‐sum test was used to compare GCs with and those without intervention. Robust simple linear regression was used to assess the association between timing of intervention and duration of hypoxemia (SaO₂ < 90%), PGES, and PI using data from only the first GC for each patient. Key Findings: Data from 39 patients with 105 GCs were analyzed. PGES >2 s occurred following 31 GCs in 16 patients. There were 21 GCs with no intervention (NOINT) and 84 GC with interventions (INT). In the INT group, the duration of hypoxemia was shorter (p = 0.0014) when intervention occurred before hypoxemia onset (mean duration 53.1 s) than when intervention was delayed (mean duration 132.42 s). Linear regression indicated that in GCs with nursing interventions, earlier intervention was associated with shorter duration of hypoxemia (p < 0.0001) and shorter duration of PGES (p = 0.0012). Seizure duration (p < 0.0001) and convulsion duration (p = 0.0457) were shorter with earlier intervention. PI duration was longer for GCs with PGES than GCs without PGES (p < 0.0001). The mean delay to first active nonrespiratory movement following GCs with PGES was 251.96 s and for GC without PGES was 66.06 s. The duration of PI was positively associated with lower SaO₂ nadir (p = 0.003) and longer duration of oxygen desaturation (p = 0.0026). There was no association between PI duration and seizure duration (p = 0.773), between PI duration and PGES duration (p = 0.758), or between PI duration and the timing of first intervention relative to seizure onset (p = 0.823). PGES did not occur in the NOINT group. The mean duration of desaturation was longer (110.9 vs. 49.9 s) (p < 0.0001), mean SaO₂ nadir was lower (72.8% vs. 79.7%) (p = 0.0086), and mean end‐tidal CO₂ was higher (58.6 vs. 50.3 mmHg) (p = 0.0359) in the INT group compared with the NOINT group. The duration of the seizure or of the convulsive component was not significantly different between the INT and NOINT groups. Significance: Early periictal nursing intervention was associated with reduced duration of RD and reduced duration of PGES. These findings suggest the possibility that such interventions may be effective in reducing the risk of SUDEP in the outpatient setting. Validation of these preliminary data with a prospective study is needed before definitive conclusions can be reached regarding the efficacy of periictal interventions in reducing the risk of SUDEP.     

Noninvasive ventilation: experience at a community teaching hospital

Objective: To describe our hospital's experience with noninvasive positive pressure ventilation (bilevel positive airway pressure; BiPAP) for patients with respiratory failure (RF). Design: Retrospective, observational study. Setting: A 300-bed community teaching hospital. Methods: Medical records were analyzed for physiologic and outcome variables for all patients who received BiPAP for RF between January 1994 and December 1996. Results: Eighty patients with a mean (± S. E.) age of 71.5 ± 1.3 years and APACHE II score of 17.2 ± 0.6 received BiPAP for RF during the study period. Thirty-one patients received BiPAP for hypoxemic RF, 25 for acute hypercapnic RF, 9 for chronic hypercapnic RF, 10 for post-extubation RF and 5 could not be categorized. BiPAP success was defined as no need for invasive ventilation. BiPAP was successful in 47 of 75 cases that could be classified; all BiPAP successes lived whereas 18 of 28 BiPAP failures died. In the overall cohort, BiPAP success was associated with a lower ICU length of stay (5.8 ± 0.9 versus 10.6 ± 1.4 days, p < 0.01). The duration of BiPAP dependency in successful cases was 35.3 ± 6.7 h. BiPAP was successful in 20 of 25 patients with acute hypercapnic RF and in 15 of 31 patients with hypoxemic RF. The risk of BiPAP failure was significantly greater (risk ratio = 2.6, 95 %CI = 1.1–6.1) for patients with hypoxemic than for those with hypercapnic RF. BiPAP success was marked by increased PaO₂/FIO₂ in patients with hypoxemic RF and by increased pH and reduced PCO₂ in patients with hypercapnic RF. BiPAP use was also successful in 8 of 10 patients who developed RF within 48 h of endotracheal extubation. Conclusions: BiPAP is highly effective in selected patients with RF during routine use in a community teaching hospital. The success rate is higher amongst patients presenting with hypercapnic than amongst those with hypoxemic RF and BiPAP failure is associated with an increased likelihood of in-hospital mortality. BiPAP may also be used successfully to temporize patients who develop RF in the period following endotracheal extubation. The duration of BiPAP dependency (35 h in this study) was shorter than in previous trials, and, though this is speculative, may have been minimized by our performing a trial of unassisted breathing each day. Received: 12 November 1998 Final revision received: 15 February 1999 Accepted: 3 March 1999     

Maturation of respiratory control in the behaving mammal

Whereas in vitro techniques have contributed greatly to our understanding of detailed neuronal mechanisms of respiratory control, the integrated function of respiratory behavior requires studying conscious, unsedated subjects. Noninvasive approaches, meticulous chronic instrumentation for the recording of multiple respiratory indices, and correlations with brain studies performed after physiological manipulations in vivo can all be employed to get to some understanding of the maturation of respiratory control in the mammal. This article is a selective and critical overview of recent literature on methodologies that can be used in behaving subjects, the relationship of respiration to sleep-wake states, respiratory patterns during normoxia, and on respiratory responsiveness to hypercarbia and hypoxia, all emphasizing processes during development. It is hoped that this review will encourage new investigators interested in the regulation of breathing to resort to experimental approaches that will reveal the mysteries of respiratory behavior in the integrated organism.