Abstract
Using parietal cranial windows and multichannel videoangiometry, pial vessel responses were studied in cats during stepwise elevation of superior sagittal sinus pressure (Psss) to a level of 50 mmHg or reduction of CSF-pressure (PCSF). PCSF was monitored via a needle in the great cistern, known from previous studies to be identical to supratentorial CSF-pressure. During elevation of PSSS, large and small pial veins dilated by 14 +/- 6.1% from resting diameter. Small arteries remained unresponsive until they were dilated by 9 +/- 2.1% at the level of PSSS 50 mmHg. Large arteries dilated by 18 +/- 5.5% at the level of PSSS 50 mmHg. PSSS was always approximately twice as high as PCSF during increase of PSSS. During reduction of PCSF to -5 mmHg, pial veins also dilated, by 7.4 +/- 1% on the average. This observation suggests that normal PCSF is a result of mainly venous vascular pressure, and that the level of normal venous pressure is not dictated by PCSF but by the function and architecture of the cerebral vasculature. Since the rapid reduction of cerebral perfusion pressure CPP by elevation of venous pressure does not induce autoregulatory adjustment according to the level of CPP, but to the level of arterial transmural pressure, it is concluded, that the basic mechanism underlying autoregulation of CBF is myogenic.
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