Pulmonary oxygen toxicity: possible role of ammonia in desorbing lung surfactant.
A porous membrane has been synthesized from a fine-weave cotton fabric carboxylated to simulate the fixed negative charges in the alveolar wall. When this membrane is treated with pulmonary surfactant in physiological concentrations, especially DPL, it loses its fluid permeability and can support a pressure of physiological saline of over 272 torr without bursting through. When the saline is replaced by isotonic ammonium chloride solution, the average penetration pressure is reduced to 187 torr. This is discussed in relation to the known production of ammonia upon hyperbaric exposure (1) and the competition of the resulting positive ammonium ions for the negative sites on the alveolar wall previously occupied by the positive quaternary ammonium ions of the effectively cationic lung surfactant. Successful replacement must then promote edema formation. This is put forward as a possible mechanism for the indirect (blood-borne) effect of oxygen upon the lung. It offers possible explanations for the potentiation of pulmonary oxygen poisoning by higher partial pressures or higher molecular weights of the inert gases present and the finding that increased permeability of epithelium precedes edema formation (18).
D000643:Ammonium Chloride / Q000633:toxicity*; D002266:Carboxymethylcellulose Sodium; D003368:Gossypium; D008567:Membranes, Artificial; D008747:Methylcellulose / Q000031:analogs & derivatives; D008954:Models, Biological; D010100:Oxygen / Q000633:toxicity; D010539:Permeability; D011654:Pulmonary Edema / Q000139:chemically induced; D011663:Pulmonary Surfactants / Q000037:antagonists & inhibitors*
D008567:Membranes, Artificial; D011663:Pulmonary Surfactants; D000643:Ammonium Chloride; D008747:Methylcellulose; D002266:Carboxymethylcellulose Sodium; D010100:Oxygen