Kato Y, Mokry M, Pucher R, Auer L M
Department of Neurosurgery, University of Graz, Austria.
Acta Neurochir (Wien). 1991;109(1-2):52-6. doi: 10.1007/BF01405698.
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.
利用顶骨颅骨视窗和多通道视频血管造影术,在猫身上研究了上矢状窦压力(Psss)逐步升高至50 mmHg或脑脊液压力(PCSF)降低期间软脑膜血管的反应。通过在大脑大池中的一根针监测PCSF,根据先前的研究可知,该压力与幕上脑脊液压力相同。在PSSS升高期间,大小软脑膜静脉从静息直径扩张了14±6.1%。小动脉直到在PSSS为50 mmHg时扩张了9±2.1%之前都没有反应。大动脉在PSSS为50 mmHg时扩张了18±5.5%。在PSSS升高期间,PSSS总是大约是PCSF的两倍。在将PCSF降低至-5 mmHg期间,软脑膜静脉也扩张了,平均扩张了7.4±1%。这一观察结果表明,正常的PCSF主要是静脉血管压力的结果,并且正常静脉压力水平不是由PCSF决定的,而是由脑血管的功能和结构决定的。由于通过升高静脉压力快速降低脑灌注压CPP不会根据CPP水平诱导自动调节调整,而是根据动脉跨壁压力水平进行调整,因此得出结论,脑血流量自动调节的基本机制是肌源性的。