Kaupp, HA and Lazarus, RE and Wetzel, N and Starzl, TE
(1960)
The role of cerebral edema in ischemic cerebral neuropathy after cardiac arrest in dogs and monkeys and its treatment with hypertonic urea.
Surgery, 48 (2).
404 - 410.
ISSN 0039-6060
Abstract
1. 1. The value of hypertonic urea in forestalling the neurologic sequellae after cardiac arrest has been assessed in dogs and monkeys. Simulated cardiac arrest was produced with an inflow-outflow occlusion technique in which the blood supply to the heart was maintained during the period of complete cerebral ischemia. 2. 2. A number of factors increase the duration of cardiac arrest which can be tolerated without gross neurologic sequellae. These include the presence of an effective circulatory state before and after the arrest, the administration of 100 per cent oxygen before and after the test period, the use of an efficient respirator, and avoidance of premature efforts to promote spontaneous respirations postoperatively. 3. 3. Under optimum conditions almost all dogs and monkeys will recover completely after 12 minutes of simulated cardiac arrest. With longer occlusions, death and serious neurologic morbidity occur. 4. 4. Monkeys and dogs were subjected to simulated cardiac arrest for 14 minutes. Hypertonic urea did not materially decrease either the mortality rate or neurologic morbidity in either species, as compared to the recovery rate in controls, despite the fact that the urea-treated animals had demonstrably less brain swelling. 5. 5. From this it is concluded that cerebral edema is an overemphasized factor in the post-cardiac arrest syndrome, and that the principal deterrent to recovery is anoxic injury to the neurons which is not beneficially influenced by reduction of brain volume. © 1960.
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