Alveolar capillary membrane

The alveolar-capillary membrane is normally very thin, has a huge surface area, and a large blood supply. Drugs given by this route, such as bronchodilators and pulmonary steroids, are rapidly absorbed into the bloodstream. This is also the route for administering the inhalational anaesthetics. DRUG METABOLISM AND EXCRETION... 

All inhaled anaesthetic drugs must be soluble in blood and brain in order to pass across the alveolar-capillary membrane and the blood-brain barrier. The term used to quantify solubility is partition coefficient. For anaesthetic purposes this is defined as the ratio of the concentration of dissolved gas/vapour in the blood to the concentration in the alveoli at... 

Dettmeyer R, Schmidt P, Musshoff F, Dreisvogt C, Madea B. Pulmonary edema in fatal heroin overdose immunohistological investigations with IgE, collagen IV and laminin—no increase of defects of alveolar-capillary membranes. Forensic Sci Int 2000 110(2) 87-96. 

The respiratory tract is divided into the upper and lower tracts. The upper respiratory tract contains the nares, nasal cavity, pharynx, and larynx and the lower tract consists of the trachea, bronchi, bronchioles, alveoli, and alveolar-capillary membrane. 

The diffusing capacity of the lung for carbon monoxide (CO) is a measure of the ability of the alveolar capillary membrane to transfer or conduct gases from the alveoli to the blood. This transport process is entirely a passive one brought about by diffusion. As described previously in Section 2.2, the barriers for diffusion consist of surfactant, alveolar epithelium, interstitital fluid, capillary endothelium, plasma, and the red blood cell membrane. 

Narcotic-induced pulmonary edema. Pulmonary edema is a common sequel to narcotic overdose (morphine, heroin, methadone, and propoxyphene) and is associated with a significant mortality rate. The exact mechanism has not been delineated, but two reasonable hypotheses have been suggested. First, narcotic-induced pulmonary edema may be a form of neurogenic pulmonary edema because both syndromes have complications of cerebral edema and hypothalamic dysfunction (Jaffe, 1970). Second, narcotics are known to release histamine, which may alter alveolar capillary membrane permeability (Brashear et al, 1974). Early treatment with narcotic antagonists produces immediate reversal of respiratory depression and miosis, while the pulmonary edema resolves more slowly. 

Gas moves by convection into the peripheral airways (airways of < 2-mm diameter) and then by diffusion to the alveolar-capillary membranes. Consequently, there is a much slower dilution of gas at this level. Therefore, toxic inhalants reaching this level may have a more profound effect due to greater relative duration of exposure. 

General supportive measures are likely to be effective in therapy of intoxication. Artificial ventilation could be lifesaving in the case of neurotoxins such as the botulinum toxins and saxitoxin. Oxygen therapy, with or without artificial ventilation, may be beneficial for intoxication with toxins such as ricin that directly damage the alveolar-capillary membrane of the lung. Vasoactive drugs and volume expanders could be used to treat the shocklike state that accompanies some intoxications (eg, with staphylococcal enterotoxin B). These measures could be used in conjunction with more specific therapies. 

Ricin is a large, moderately toxic, protein dichain toxin from the bean of the castor plant, Ricinis communis. It can be produced easily in relatively large quantities. Ricin was developed as a biological weapon by the United States and its allies during World War II. Although ricin is toxic by several routes, when inhaled as a respirable aerosol, it causes severe necrosis of the airways and increased permeability of the alveolar-capillary membrane. The inhalational route... 

The helium is inert and insoluble in lung tissue and blood, and equilibrates quickly in unobstructed patients, indicating the dilution level of the test gas. Acetylene, on the other hand, is soluble in blood and is used to determine the blood flow through the pulmonary capillaries. Carbon monoxide is bound very tightly to hemoglobin and is used to obtain diffusing capacity at a constant pressure gradient across the alveolar-capillary membrane. 

The pathogenesis of pulmonary fibrosis is presumably related to initial loss of alveolar type I epithelial cells and endothelial cells. However, the dysregulated repair of pulmonary fibrosis is followed by persistence of inflammation. This is followed by proliferation of type II cells, recruitment and proliferation of endothelial cells and fibroblasts, and deposition of extracellular matrix leading to end-stage alveolar and interstitial fibrosis. These events involve the complex and dynamic interplay between diverse immune effector cells and cellular constituents of the alveolar-capillary membrane and interstitium of the lung. Interaction of these diverse cell populations and the cytokines that they produce culminate in chronic inflammation, angiogenesis, fibroproliferation, and deposition of extracellular matrix. 

Peimeabilityi The epithelial and endothelial cell membranes and the presence of mucus arxl surfactant affect the permeability of the alveolar-capillary membrane to gases and toxicants. If the toxicant does not initially damage the alveolar-capillary membrane, it is usually absorbed and transported via the blood to other locations. 

The appearance of batwing infiltrates indicates the commencement of pulmonary oedema secondary to damage to the alveolar-capillary membrane. Pulmonary oedema develops later without cardiovascular changes of re-distribution or cardiomegaly (Fig. 8.5). 

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