Prescribing repertoires of doctors new to general practice.
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Biomedical subjects
Publications and source records attributed to G Austin.
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Acute cerebral edema was created in dogs by the intracarotid injection of sodium lauryl sulfate, a method that produces no structural or vascular disruption in the brain. Cerebrospinal fluid (CSF) pressure elevations were measured through subdural balloons, and ranged from 300 to 1500 mm H2O. The nature of the cerebral edema produced was studied with intravital Trypan blue, electrocorticography, and visual observation of cerebral circulation, and by postmortem histological sections and determinations of brain water content. Two dissimilar diuretic agents were studied: the osmotic diuretic, mannitol; and the renal diuretic, ethacrynic acid. As expected, mannitol reduced CSF pressure effectively, with no significant rebound overshoot. Ethacrynic acid, despite favorable reports, proved to have only a slight effect on CSF pressure but did prove to be a potent diuretic. Unexpectedly, the two agents were found to act synergistically. When both agents were administered, significantly greater reductions in pressure were obtained and pressure reductions were maintained for longer periods.
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ACh-induced depolarization (D response) in D cells markedly decreases as the external Na(+) is reduced. However, when Na(+) is completely replaced with Mg(++), the D response remains unchanged. When Na(+) is replaced with Tris(hydroxymethyl)aminomethane, the D response completely disappears, except for a slight decrease in membrane resistance. ACh-induced hyperpolarization (H response) in H cells is markedly depressed as the external Cl(-) is reduced. Frequently, the reversal of the H response; i.e., depolarization, is observed during perfusion with Cl(-)-free media. In cells which show both D and H responses superimposed, it was possible to separate these responses from each other by perfusing the cells with either Na(+)-free or Cl(-)-free Ringer's solution. High [K(+)](0) often caused a marked hyperpolarization in either D or H cells. This is due to the primary effect of high [K(+)](0) on the presynaptic inhibitory fibers. The removal of this inhibitory afferent interference by applying Nembutal readily disclosed the predicted K(+) depolarization. In perfusates containing normal [Na(+)](0), the effects of Ca(++) and Mg(++) on the activities of postsynaptic membrane were minimal, supporting the current theory that the effects of these ions on the synaptic transmission are mainly presynaptic. The possible mechanism of the hyperpolarization produced by simultaneous perfusion with both high [K(+)](0) and ACh in certain H cells is explained quantitatively under the assumption that ACh induces exclusively an increase in Cl(-) permeability of the H membrane.
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