Anoxemia secondary to polycythemia and polycythemia secondary to anoxemia.
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Groups of 4 Wistar rat littermates of matched sex and weight received the following daily treatment between the ages of 2 and 11 days: handling (untreated controls, UC), succinylcholine paralysis and ventilation with 100% O2 (respirator control, RC), electroconvulsive seizures (ECS) and ECS while paralyzed and ventilated with O2 (respirator seizures, RS). Analysis of heart blood O2 content showed that mechanical ventilation with 100% O2 effectively prevented the anoxemia observed during convulsive seizures. In the ECS and RS groups, several behavioral milestones (e.g. swimming) matured later than they did in either control group (UC, RC). No difference was observed between the two groups of seizure-treated rats. At the age of 30 days, both ECS and RS groups had smaller brains with a reduced DNA, RNA, protein and cholesterol content in both forebrain and hindbrain, suggesting that seizures curtailed the number of brain cells. The lack of any difference between the two seizure groups suggests that at least part of the adverse effects of experimental neonatal seizures on brain and behaviour are independent of anoxemia.
The author advances the concept that anoxemia, either in its general or restricted form, or both, is probably responsible for a considerable portion of "degenerative diseases," whose etiologic delineation has not yet been traced. It is necessary, he believes, to enlarge greatly the comprehension of the disordered circulatory states to include oxygen want and thereby account for a number of conditions hitherto considered to be of unknown cause. More than this, he finds in oxygen want an explanation of the mechanism of a number of individual lesions or details of lesions otherwise not well understood. The author believes it is very likely that an understanding of cerebral anoxia in its ultimate ramifications will open still wider doors to the understanding of certain clinical syndromes the cause of which remains obscure.
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