Abstract

Brain compression of precisely defined degree and duration was produced by means of expansion of a supratentorial epidural balloon in anaesthetized and mechanically ventilated dogs. After deflation of the balloon there was a rebound of the intracranial pressure (ICP) to values in the range 30-89 mm Hg when critical thresholds of time and compression had been exceeded during the period of compression. A time versus cerebral perfusion pressure (CPP) graph indicated a CPP threshold of about 50 mm Hg and time threshold of about 6 min. Within these limits the critical CPP varied as a function of time. The ICP rebound had an approximately exponential time course with an initial rapid rise levelling off towards a final plateau in about 30 min. The final value was dependent on the time of compression but independent of the CPP. A transtentorial pressure gradient was induced during the compression phase and reestablished after the decompression when a rebound of ICP developed. Hydrostatic compression by means of infusion of fluid into the subarachnoid space was followed by a rebound of ICP in only 2/21 of the experiments in spite of time and CPP parameters which crossed the critical thresholds defined in the balloon compression experiments. These results support the hypothesis that the rebound phenomenon is related to an ischaemic mechanism. The difference in incidence of rebound in balloon compression and hydrostatic compression can probably be accounted for by a greater depth of ischaemia in the former case because of a direct compressive effect on the vascular bed by the balloon.

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