弱呼吸敏感电极研究

应用物理学，化学和工艺等方法，分别处理５种国内外敏感器，以组成相应呼吸敏感电极，结果显示，各种电极的气－电转换性能有明显改善，其中以上海复旦片性能达到弱呼吸敏感电极要求。     

Whole-heart cine MRI using real-time respiratory self-gating.

Two-dimensional (2D) breath-hold cine MRI is used to assess cardiac anatomy and function. However, this technique requires cooperation from the patient, and in some cases the scan planning is complicated. Isotropic nonangulated three-dimensional (3D) cardiac MR can overcome some of these problems because it requires minimal planning and can be reformatted in any plane. However, current methods, even those that use undersampling techniques, involve breath-holding for periods that are too long for many patients. Free-breathing respiratory gating sequences represent a possible solution for realizing 3D cine imaging. A real-time respiratory self-gating technique for whole-heart cine MRI is presented. The technique enables assessment of cardiac anatomy and function with minimum planning or patient cooperation. Nonangulated isotropic 3D data were acquired from five healthy volunteers and then reformatted into 2D clinical views. The respiratory self-gating technique is shown to improve image quality in free-breathing scanning. In addition, ventricular volumetric data obtained using the 3D approach were comparable to those acquired with the conventional multislice 2D approach.     

Physiological consequences of a high work of breathing during heavy exercise in humans

The healthy respiratory system has a remarkable capacity for meeting the metabolic demands placed upon it during strenuous exercise. For example, in order to regulate alveolar partial pressure of oxygen and carbon dioxide during heavy workloads, a 20-fold increase in alveolar ventilation can occur. The high metabolic costs and subsequent increased work of breathing associated with this ventilatory increase can result in a number of limitations to the healthy respiratory system. Two examples of respiratory system limitations that are associated with a high work of breathing are expiratory flow limitation and exercise-induced diaphragmatic fatigue. Expiratory flow limitation can lead to an inability to increase alveolar ventilation () in the face of increasing metabolic demands, resulting in gas exchange impairment and diminished endurance exercise performance. Furthermore, the high ventilatory requirements of endurance athletes and the inherent anatomical differences in females could make these groups more susceptible to expiratory flow limitation. Fatigue of the diaphragm has also been documented after strenuous exercise and may be related to a mechanism which increases sympathetic vasoconstrictor outflow and reduces limb blood flow during prolonged exercise. This competition between the muscles of respiration and locomotion for a limited cardiac output may have dramatic consequences for exercise performance. This brief review summarizes the literature as it pertains to the work of breathing, expiratory flow limitation, and exercise-induced diaphragmatic fatigue in healthy humans.     

Fresh gas flow in the Bain circuit during laparoscopy

Twenty-two women were studied during laparoscopy with abdominal insufflation of carbon dioxide. A bain anaesthetic breathing circuit was used with a fresh gas flow (VFG) of 110 ml.min-1.kg-1, and controlled ventilation was applied with a minute ventilation (VE) of 175 ml.min-1.kg-1. Arterial blood gases were analysed at the end of the operation. Nineteen of the women (86 per cent) were found to have a PaCO2 within the range for normocapnia (i.e., 4.7-5.9 kPa (35-45 mmHg), two were hypocapnic with a PaCO2 of 4.4 and 4.5 kPa (33 and 34 mmHg) respectively and one was found to have a PaCO2 of 6.2 kPa (46.5 mmHg). It was concluded that the carbon dioxide absorbed from the abdomen during laparoscopy demands fresh gas flows that are higher than normally used in the Bain circuit if a PaCO2 within the normal range is to be obtained. A simultaneous increase in VFG and VE of about 45 per cent is sufficient to achieve normocapnia.     

Cardio-respiratory measures following isocapnic voluntary hyperventilation

In some individuals, breathing is greater than at rest following voluntary hyperventilation. Most previous investigations have employed short hyperventilation periods; here we examine the time course of cardio-respiratory measures before, during, and after a 5-min voluntary hyperventilation, maintaining isocapnia throughout. We examined the possible co-involvement of the cardiovascular system; hypothesising that post-hyperventilation hyperpnoea results from an increase in autonomic arousal. In four subjects (two males, two females) of 18 (nine males, nine females) we observed a post-hyperventilation hyperpnoea, characterised by a slow decline of ventilation toward resting levels with a time constant of 109.0 +/- 16.1s. By contrast, heart rate, and systolic and diastolic blood pressure were unchanged from rest during and after voluntary hyperventilation for all subjects. We concluded that males and females were equally likely to exhibit post-hyperventilation hyperpnoea, and suggest that they may be characterised by an increased resting heart rate and the choice of breathing frequency to increase ventilation during the voluntary hyperventilation. We further concluded that post-hyperventilation hyperpnoea is rare, but when present is a strong and lasting phenomenon, and that it is not the result of an increased autonomic arousal.     

Relative motion of lung and chest wall promotes uniform pleural space thickness

The pleural space is modeled in two dimensions as a thin layer of fluid separating a deformable membrane and a rigid surface containing a bump. We computed the steady-state membrane configuration and fluid pressure distribution during relative sliding of the two surfaces. For physiologically relevant values of membrane tension, shear flow-induced pressures near the bump and far-field pressure gradients are similar to those measured in vivo within the pleural space (e.g. Lai-Fook et al.) [J. Appl. Physiol.: Respirat. Environ. Exercise Physiol. 56 (1984) 1633-1639]. Deformation of the membrane over the bump suggests that the pressure field generated by the sliding motion promotes an even layer of fluid in the pleural space, preventing asperities from touching. Results also suggest a possible mechanism for pleural fluid redistribution during breathing, whereby irreversible fluid motion is associated with the deformability of the membrane.     

Elastohydrodynamic separation of pleural surfaces during breathing

To examine effects of lung motion on the separation of pleural surfaces during breathing, we modeled the pleural space in two dimensions as a thin layer of fluid separating a stationary elastic solid and a sliding flat solid surface. The undeformed elastic solid contained a series of bumps, to represent tissue surface features, introducing unevenness in fluid layer thickness. We computed the extent of deformation of the solid as a function of sliding velocity, solid elastic modulus, and bump geometry (wavelength and amplitude). For physiological values of the parameters, significant deformation occurs (i.e. bumps are 'flattened') promoting less variation in fluid thickness and decreased fluid shear stress. In addition, deformation is persistent; bumps of sufficient wavelength, once deformed, require a recovery time longer than a typical breath-to-breath interval to return near their undeformed configuration. These results suggest that in the pleural space during normal breathing, separation of pleural surfaces is promoted by the reciprocating sliding of lung and chest wall.     

Effects of tryptophan depletion on central and peripheral chemoreflexes in man

Klein (Arch. Gen. Psychiatry 50, 306-317, 1993) suggests that panic attacks are the result of a defective 'suffocation alarm' threshold that presents with carbon dioxide (CO(2)) hypersensitivity, exaggerated ventilatory response and panic in panic disorder (PD) patients. Serotonergic deficiencies enhance this ventilatory response in PD patients, as per 'suffocation alarm' theory predictions, suggesting that serotonin (5-HT) normalizes the ventilatory response. Other research supports a serotonin system-mediated stimulation of ventilation. Knowledge of 5-HT's role on ventilatory output and its neurophysiological sources impacts on the 'suffocation alarm' theory validity and predictive value. We used tryptophan depletion (TRP-) in concert with a modified Read rebreathing test to determine the effect of deficient serotonergic modulation on the central and peripheral chemoreflex threshold and sensitivity of response to CO(2) in 11 healthy men. TRP- did not affect central or peripheral chemoreflex threshold or sensitivity of response to CO(2). However, basal ventilation was significantly elevated during TRP-. In contrast to 'suffocation alarm' theory predictions, decreased 5-HT neurotransmission does not significantly affect the respiratory chemoreflex response to CO(2), impacting on non-chemoreflex drives to breathe. Panic associated respiratory abnormalities may be related to defective 5-HT modulation of non-chemoreflex drives to breathe, unrelated to any respiratory chemoreflex abnormality.     

Sleep related breathing disorders in older men: A search for underlying mechanisms

—The incidence of sleep-related breathing disorders (SRBDs) associated with hemoglobin desaturation was determined by nocturnal polygraphic evaluations in 26 healthy men, aged 55–70 years. Sixteen subjects (62%) had abnormal rates of at least 12 episodes per hour of sleep: 8 had occlusive, and 8 had central apnea or hypopnea. During waking ten of 16 SRBD subjects and only one subject without SRBDs exhibited either an elevated nasopharyngeal airway resistance (n=4) or a reduced ventilatory response to hypercapnia (n=4) and/or hypoxia (n=3). However, these abnormalities were not related to the type or severity of SRBDs, and 6 subjects with SRBDs demonstrated no respiratory defect. We conclude that SRBDs have a very high incidence in older males and are not usually secondary to pulmonary cardiac, neurological, or behavioral disorders. Additionally, we hypothesize that abnormalities in ventilatory control or upper airway resistance contribute to SRBDs, but depression of brain stem reticular formation activity during sleep plays a primary role in these disorders. Factors related to both aging and SRBDs are reviewed. These include reduced chemoreceptor responses, altered steroid hormone metabolism, and use and metabolism of hypnotic drugs and alcohol.     

Significance of the pleura in the breathing mechanism

Translated fromByulleten' Eksperimental'noi Biologii i Meditsiny, No. 1, pp. 20–21, January, 1993