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1.
The purpose of this study was to explore new insights in non-linearity, hysteresis and ventilation heterogeneity of asthmatic human lungs using four-dimensional computed tomography (4D-CT) image data acquired during tidal breathing. Volumetric image data were acquired for 5 non-severe and one severe asthmatic volunteers. Besides 4D-CT image data, function residual capacity and total lung capacity image data during breath-hold were acquired for comparison with dynamic scans. Quantitative results were compared with the previously reported analysis of five healthy human lungs. Using an image registration technique, local variables such as regional ventilation and anisotropic deformation index (ADI) were estimated. Regional ventilation characteristics of non-severe asthmatic subjects were similar to those of healthy subjects, but different from the severe asthmatic subject. Lobar airflow fractions were also well correlated between static and dynamic scans (R2 > 0.84). However, local ventilation heterogeneity significantly increased during tidal breathing in both healthy and asthmatic subjects relative to that of breath-hold perhaps because of airway resistance present only in dynamic breathing. ADI was used to quantify non-linearity and hysteresis of lung motion during tidal breathing. Non-linearity was greater on inhalation than exhalation among all subjects. However, exhalation non-linearity among asthmatic subjects was greater than healthy subjects and the difference diminished during inhalation. An increase of non-linearity during exhalation in asthmatic subjects accounted for lower hysteresis relative to that of healthy ones. Thus, assessment of non-linearity differences between healthy and asthmatic lungs during exhalation may provide quantitative metrics for subject identification and outcome assessment of new interventions.  相似文献   
2.
Summary An extracorporeal circulation of rainbow trout (Oncorhynchus mykiss) was utilized to continuously monitor the rapid and progressive effects of endogenous or exogenous catecholamines on blood respiratory/acid-base status, and to provide in vivo evidence for adrenergic retention of carbon dioxide (CO2) in fish blood (cf. Wood and Perry 1985). Exposure of fish to severe aquatic hypoxia (final P wO2=40–60 torr; reached within 10–20 min) elicited an initial respiratory alkalosis resulting from hypoxia-induced hyperventilation. However, at a critical arterial oxygen tension (P aO2) between 15 and 25 torr, fish became agitated for approximately 5 s and a marked (0.2–0.4 pH unit) but transient arterial blood acidosis ensued. This response is characteristic of abrupt catecholamine mobilization into the circulation and subsequent adrenergic activation of red blood cell (RBC) Na+/H+ exchange (Fievet et al. 1987). Within approximately 1–2 min after the activation of RBC Na+/H+ exchange by endogenous catecholamines, there was a significant rise in arterial PCO2 (P aCO2) whereas arterial PO2 was unaltered; the elevation of P aCO2 could not be explained by changes in gill ventilation. Pre-treatment of fish with the -adrenoceptor antagonist phentolamine did not prevent the apparent catecholamine-mediated increase of P aCO2. Conversely, pre-treatment with the -adrenoceptor antagonist sotalol abolished both the activation of the RBC Na+/H+ antiporter and the associated rise in P aCO2, suggesting a causal relationship between the stimulation of RBC Na+/H+ exchange and the elevation of P aCO2. To more clearly establish that elevation of plasma catecholamine levels during severe hypoxia was indeed responsible for causing the elevation of P aCO2, fish were exposed to moderate hypoxia (final P wO2=60–80 torr) and then injected intraarterially with a bolus of adrenaline to elicit an estimated circulating level of 400 nmol·l-1 immediately after the injection. This protocol activated RBC Na+/H+ exchange as indicated by abrupt changes in arterial pH (pHa). In all fish examined, P aCO2 increased after injection of exogenous adrenaline. The effects on P aO2 were inconsistent, although a reduction in this variable was the most frequent response. Gill ventilation frequency and amplitude were unaffected by exogenous adrenaline. Therefore, it is unlikely that ventilatory changes contributed to the consistently observed rise in P aCO2. Pretreatment of fish with sotalol did not alter the ventilatory response to adrenaline injection but did prevent the stimulation of RBC Na+/H+ exchange and the accompanying increases and decreases in P aCO2 and P aO2, respectively. These results suggest that adrenergic elevation of P aCO2, in addition to the frequently observed reduction of P aO2 are linked to activation of RBC Na+/H+ exchange. The physiological significance and the potential mechanisms underlying the changes in blood respiratory status after addition of endogenous or exogenous catecholamines to the circulation of hypoxic rainbow trout are discussed.Abbreviations P aCO2 arterial carbon dioxide tension - P aO2 arterial oxygen tension - P da dorsal aortic pressure - pHa arterial pH - P wO2 water oxygen tension - RBC red blood cell - V f breathing frequency  相似文献   
3.
Airborne particles and ammonia were monitored in horse stalls managed under four conditions. Two ventilation rates, high (27 air changes per h) and low (5 air changes per h) and two bedding types, paper and straw, were employed. At both ventilation rates, the number of airborne particles generated while the stalls were mucked out was higher with straw than with paper. Particles were more efficiently cleared at the higher ventilation rate in both the straw and paper stalls. Ammonia measurements reflected an accumulation over time. In the stalls with low ventilation, ammonia levels were significantly higher than in those stalls with high ventilation regardless of bedding type. Management decisions and their relationships to respiratory disorders are discussed.  相似文献   
4.
These experiments examined the effect of hypoxia and hyperoxia on ventilation, lactate concentration and electromyographic activity during an incremental exercise test in order to determine if coincident chances in ventilation and electromyographic activity occur during an incremental exercise test, despite an enhancement or reduction of peripheral chemoreceptor activity. In addition, these experiments were completed to determine if electromyographic activity and ventilation are enhanced or reduced in response to the inspiration of oxygen-depleted and oxygen-enriched air, respectively. Seven subjects performed three incremental exercise tests, until volitional exhaustion was achieved, while inspiring air with a fractional concentration of oxygen of either 66%, 21% or 17%. In addition, another single subject completed two tests while inspiring air with a fractional concentration of either 17% or 21%. During the tests, ventilation, mixed expired oxygen and carbon dioxide, arterialized venous blood and the electromyographic activity from the vastus lateralis were sampled. From these values ventilation, electromyographic and lactate thresholds were detected during normoxia, hypoxia and hyperoxia. The results showed that although ventilation and lactate concentration were significantly less during hyperoxia as compared to normoxia or hypoxia, the carbon dioxide production values were not significantly different between the normoxic, hypoxic and hyperoxic conditions. For a particular condition, the time, carbon dioxide production and oxygen consumption values that corresponded to the ventilation and electromyographic thresholds were not significantly different, but the values corresponding to the lactate threshold were significantly less than those for the electromyographic and ventilation thresholds. Comparisons between the three conditions showed that the time, carbon dioxide production and oxyen consumption values corresponding to each of these thresholds were not significantly different. These findings have led us to conclude that the changes in lactate concentration observed during exercise may not be directly related to the fractional concentration of inspired oxygen, and that the peripheral chemoreceptors may not be the sole mediators of the first ventilatory threshold. It is suggested that this threshold may be mediated by an increase in neural activity originating from higher motor centers or the exercising limbs, induced in response to the need to progressively recruit fast twitch muscle fibers as exercise power output is increased and as individual muscle fibers begin to fatigue.  相似文献   
5.
The effect of severe acute hypoxia (fractional concentration of inspired oxygen equalled 0.104) was studied in nine male subjects performing an incremental exercise test. For power outputs over 125 W, all the subjects in a state of hypoxia showed a decrease in oxygen consumption ( O2) relative to exercise intensity compared with normoxia (P < 0.05). This would suggest an increased anaerobic metabolism as an energy source during hypoxic exercise. During submaximal exercise, for a given O2, higher blood lactate concentrations were found in hypoxia than in normoxia (P < 0.05). In consequence, the onset of blood lactate accumulation (OBLA) was shifted to a lower O2 ( O2 1.77 l·min–1 in hypoxia vs 3.10 l·min–1 in normoxia). Lactate concentration increases relative to minute ventilation ( E) responses were significantly higher during hypoxia than in normoxia (P < 0.05). At OBLA, E during hypoxia was 25% lower than in the normoxic test. This study would suggest that in hypoxia subjects are able to use an increased anaerobic metabolism to maintain exercise performance.  相似文献   
6.
1. 1. The ventilatory and pulmonary gas exchange responses during moderate exercise can be appropriately modelled with first-order dynamics.
2. 2. A delay term, reflecting tissue-to-lung transit time, is needed for accurate characterization, however.
3. 3. The O2 uptake time constant ( reflects the enzymatically controlled tissue O2 utilization.
4. 4. is appreciably longer than , consequent to the tissue CO2 capacitance.
5. 5. As typically longer than , transient errors in alveolar and arterial blood gas tensions are predicted: small for PCO2 but much larger for PO2.
6. 6. At work rates above the lactate threshold, a slow and delayed component of V̇O2 induces an additional V̇ component (“excess” V̇O2), leading to more rapid fatigue.
7. 7. The ventilatory compensation for the metabolic acidemia at these work rates is slow, with compensation being poor for rapid-incremental exercise.
8. 8. A justifiable control model of the coupling of ventilation to metabolism must cohere with these demonstrable physiological characteristics.
Keywords: Ventilation; pulmonary gas exchange; excess V̇O2; compensatory hyperpnea; model order  相似文献   
7.
摘要 目的:肺栓塞及下肢深静脉血栓是影响肾病综合征(Nephrotic Syndrome,NS)预后的重要因素,但在其发生率以及治疗方面仍存在争议。本文将通过回顾性的病例研究对NS患者中血栓栓塞事件的发生率、危险因素以及是否需要早期干预等问题进行探讨。方法:收集上海交通大学医学院附属新华医院肾内科2014年1-12月诊断为原发性NS患者,并同时收集患者基本临床信息,血栓检查结果以及NS相关血液及尿液检查结果等在内的临床资料,采用多种统计方法分析血栓发生率及其危险因素,并进一步讨论NS患者的预防性抗凝措施。结果:NS患者下肢静脉血栓或肺栓塞的发生率均为15.4%,两种血栓同时发生的概率为9.6%。NS患者血栓事件的发生率与D-二聚体、血浆白蛋白、病程、病理类型呈明显相关,且具有统计学意义。结论:NS患者血栓栓塞的发生率与D-二聚体、血浆白蛋白、病程、病理类型呈显著相关,膜性肾病患者血栓栓塞发生率最高。如NS患者合并高危因素,建议定期筛查,综合评估后预防性抗凝。  相似文献   
8.
摘要 目的:研究Bi PAP呼吸机无创通气以及氧气驱动雾化吸入联用对慢性阻塞性肺疾病(慢阻肺)合并呼吸衰竭的疗效。方法:选择2016年12月~2018年12月我院的121例慢阻肺合并呼吸衰竭患者,随机分为两组。对照组采用Bi PAP呼吸机无创通气疗法,观察组联合氧气驱动雾化吸入布氨溴索和地奈德混悬液。比较两组的呼吸频率、血气指标和心率;血清肺表面活性相关蛋白D(Pulmonary surfactant related protein,SP-D)以及部活化调节趋化因子(PARC/CCL18)水平、肺功能。结果:观察组的有效率明显高于对照组(P<0.05);治疗后,两组的呼吸频率、血气指标和心率明显改善(P<0.05),且观察组的呼吸频率、血气指标和心率明显优于对照组(P<0.05);治疗后,两组的血清PARC/CCL18 以及SP-D水平均明显降低(P<0.05),且观察组的血清PARC/CCL18 以及SP-D水平明显低于对照组(P<0.05);治疗后,两组的FEV1%、呼吸困难指数以及FEV1/FVC明显改善(P<0.05),且观察组的FEV1%、呼吸困难指数以及FEV1/FVC明显优于对照组(P<0.05)。结论:Bi PAP呼吸机无创通气以及氧气驱动雾化吸入联用能改善慢阻肺合并呼吸衰竭的血气指标、生命体征和肺功能,降低血清 PARC/CCL18 以及SP-D水平。  相似文献   
9.
目的:探讨有创无创序贯通气和有创机械通气对急性呼吸衰竭患者血糖水平及预后的影响。方法:选取我院重症医学科2012年3月至2017年10月收治的急性呼吸衰竭患者81例,按照通气方式不同分为两组,对照组(41例)采用单纯有创机械通气治疗,观察组(40例)采用有创-无创序贯通气治疗。比较两组患者的血糖水平、临床指标、治疗时间和临床转归情况。结果:两组患者治疗后血糖水平均较治疗前显著升高(P0.05),而观察组血糖水平显著低于对照组(P0.05);对照组拔管时和观察组通气3h后患者的动脉血二氧化碳分压(PaCO---_2)、动脉血氧分压(PaO_2)、收缩压(SBP)和心率(HR)对比无显著性差异(P0.05);观察组的通气时间、住院时间与对照组相比均较短(P0.05),撤机成功率高于对照组(P0.05),再插管率、呼吸机相关肺炎(VAP)和死亡率均显著低于对照组(P0.05)。结论:有创无创序贯通气急性呼吸衰竭患者血糖水平较低,治疗时间较短,且再插管率、VAP和死亡率较小,显著改善患者预后。  相似文献   
10.
In anuran amphibians, respiratory rhythm is generated within the central nervous system (CNS) and is modulated by chemo- and mechanoreceptors located in the vascular system and within the CNS. The site for central respiratory rhythmogenesis and the role of various neurotransmitters and neuromodulators is described. Ventilatory air flow is generated by a positive pressure, buccal force pump driven by efferent motor output from cranial nerves. The vagus (cranial nerve X) also controls heart rate and pulmocutaneous arterial resistance that, in turn, affect cardiac shunts within the undivided anuran ventricle; however, little is known about the control of central vagal motor outflow to the heart and pulmocutaneous artery. Anatomical evidence indicates a close proximity of the centers responsible for respiratory rhythmogenesis and the vagal motoneurons involved in cardiovascular regulation. Furthermore, anurans in which phasic feedback from chemo- and mechanoreceptors is prevented by artificial ventilation exhibit cardiorespiratory interactions that appear similar to those of conscious animals. These observations indicate interactions between respiratory and cardiovascular centers within the CNS. Thus, like mammals and other air-breathing vertebrates, the cardio-respiratory interactions in anurans result from both feedback and feed-forward mechanisms.  相似文献   
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