Anesthesiology
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Surface membrane dihydropyridine receptor Ca2+ channels may play a role in the response of malignant hyperthermia-susceptible skeletal muscle to volatile anesthetics. ⋯ Volatile anesthetics inhibit the binding of PN200-110 to skeletal muscle membranes by decreasing the number of functionally active dihydropyridine receptor proteins. This inhibition is similar for membranes isolated from both normal and malignant hyperthermia-susceptible muscle, thus providing no evidence for a halothane-induced functional defect in this protein in malignant hyperthermia-susceptible muscle. However, the results of this study also indicate that the mechanism by which volatile anesthetics decrease surface membrane Ca2+ currents in skeletal muscle is by reducing the number of functional dihydropyridine receptor Ca2+ channels.
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Although the bronchial circulation has traditionally been thought to provide adequate blood flow for the lung when the pulmonary artery is obstructed, recent studies have demonstrated that pulmonary artery occlusion results in lung injury. We hypothesized that after pulmonary artery occlusion, aerobic lung metabolic function is altered. We studied the changes in the concentration of adenine nucleotides as markers of injury in the intact rabbit lung after pulmonary artery occlusion in the presence and absence of pneumothorax. ⋯ After pulmonary artery occlusion or lung collapse, adenine nucleotides are preserved if ventilation is continued. The increased permeability of rabbit lungs after 24 h of left pulmonary artery occlusion alone cannot be explained on the basis of depletion of high-energy phosphates. In the absence of ventilation due to lung collapse, pulmonary artery occlusion results in decreased adenosine triphosphate concentrations, demonstrating that the residual circulations (bronchial and pulmonary venous flow) are inadequate to support normal lung aerobic metabolism.
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Biography Historical Article
James Moore (1762-1860). An 18th-century advocate of mitigation of pain during surgery.