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Vascular responses to acute intracranial hypertension
  1. S. S. Hayreh1,
  2. J. Edwards
  1. Department of Experimental Ophthalmology, Institute of Ophthalmology, University of London


    In 27 rhesus monkeys the cerebrospinal fluid pressure (CSFP) was raised by injections into the cisterna magna to about 40 to 50 mm Hg in steps of 5 mm Hg every five minutes. During the initial phase of the rise of the CSFP to about 15 mm Hg normal animals showed a significant fall in the systolic arterial blood pressure. With a further elevation of the CSFP the BP rose till the CSFP reached 30 to 40 mm Hg. If the CSFP were raised higher than that, a large number of the animals showed a significant fall in the BP. In animals which were shocked before the CSFP was raised there was no drop in the systolic BP during the initial phase. This study indicates that vascular decompensation occurs in the majority of animals when the CSFP goes higher than 30 to 40 mm Hg; there is a significant rise in the pulse rate, superior sagittal sinus pressure (SSP), and internal jugular vein pressure (JVP). The JVP was related to the SSP, indicating that the JVP most probably reflected the pressure changes in the intracranial venous sinuses. Four animals suddenly collapsed at the highest CSFP. In the remaining 23 animals, on a sudden lowering of the CSFP to zero from the highest level, 13 monkeys died in less than half an hour and four in about an hour, while six animals stood this elevation of the CSFP well, with a good recovery. This indicates that, once the vascular decompensation has set in, the prognosis is generally poor even after lowering the CSFP to normal. The drop of the CSFP to zero produced no significant change in the pulse rate but a significant fall in the BP. The SSP rose when its pre-lowering level was less than 7·5 mm Hg and fell when the level was at or above 7·5 mm Hg level. The JVP showed a significant correlation with the variations in the SSP. The fundus examination at the end of the experiment revealed no abnormality.

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    • 1 Present address: Department of Ophthalmology, University of Edinburgh, Chalmers Street, Edinburgh, EH3 9HA. This study was carried out during the tenure of a Beit Memorial Research Fellowship to SSH.