Disease relevance of Blood-Air Barrier

• Cases associated with oligohydramnios showed a characteristic series of changes with narrow airways, retardation of epithelial and interstitial growth, delay in development of blood-air barriers, and low concentrations of phospholipid phosphorus, lecithin phosphorus, total palmitate, and lecithin palmitate [1].

High impact information on Blood-Air Barrier

• Intracapillary granulocrit, air-blood barrier thickness, and arterial pO2 are normal in the septic C5-deficient twins of these animals [2].
• RLX was also found to promote dilation of alveolar blood capillaries and to reduce the thickness of the air-blood barrier [3].
• Fluid from the second and third aliquots showed increased concentrations of albumin and urea in fluids from the patients, suggesting increased plasma leakage through the alveolocapillary membranes [4].
• To assess the permeability of the alveolocapillary membrane, pulmonary clearance of inhaled technetium-99m-labeled diethylenetriamine pentaacetic acid (99mTc-DTPA) measurements were performed at 3 hrs and compared with data from the control group (n = 5) treated with mechanical ventilation only, using the same ventilatory parameters [5].
• BACKGROUND: The passage of carbon monoxide (CO) through the alveolocapillary membrane and into the plasma and intraerythrocytic compartments determines the diffusing capacity of the lung for CO (DLCO) as defined by the Roughton and Forster equation [6].

Biological context of Blood-Air Barrier

• Lung function assessment showed a mildly restrictive pattern with frequent impairment of transfer factor for carbon monoxide (T1,co) and diffusing capacity of the alveolocapillary membrane (Dm), of late-expiratory airflow rates and with a high prevalence of increased airway resistance [7].
• The data illustrate that maternal nicotine exposure during pregnancy and lactation resulted in alveolar fenestrations, blebbing and rupturing of the blood-air barrier [8].

Anatomical context of Blood-Air Barrier

• Experimental evidence suggests that markers indicative of a dysfunction of the air/blood barrier, such as angiotensin-converting enzyme, total protein, and phospholipids engulfed by alveolar macrophages, were most sensitive to probe this type of changes [9].
• A bilayer of cultured human endothelial and bronchial epithelial cells was used as a model for neutrophil migration through the blood-air barrier [10].
• The diameter of the morphological air/blood barrier is about 165...210 nm in thin areas, excluding a 12...20 nm thick layer covering the luminal plasma membrane of the air capillary epithelium [11].

Associations of Blood-Air Barrier with chemical compounds

• This suggested that the augmentation of responses was not mediated by the action of LPS to modulate the air-blood barrier against the entry of antigen via lung [12].
• Hyperoxia had a less marked effect but appeared to retard the final invagination of the plexus, resulting in a thicker air-blood barrier [13].
• In addition, ESI and EELS are shown to distinguish between different tracers in simultaneous applications of La and terbium (Tb) which were used at the different faces of the pulmonary air-blood barrier [14].
• Ruptured blood-air barriers also occur in the nicotine exposed lungs of rats of all age groups [15].
• The physiological respiratory dynamics were successfully simulated and found to enhance significantly the transpulmonary permeation of progesterone and its hydroxy derivatives through bullfrog lung membrane, a model air-blood barrier [16].

Analytical, diagnostic and therapeutic context of Blood-Air Barrier

• Morphometric results demonstrate a significant increase in intracapillary granulocrit and air-blood barrier thickness 24 hours after cecal ligation and puncture in C5-sufficient septic mice [2].

References