Portnoy H D, Chopp M, Branch C, Shannon M B
J Neurosurg. 1982 May;56(5):666-78. doi: 10.3171/jns.1982.56.5.0666.
Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.
在13只犬身上进行了系统动脉（SAPW）、脑脊液（CSFPW）和矢状窦（SSPW）脉搏波的系统分析，实验条件包括高碳酸血症（5%二氧化碳）、颅内正常压力（吸入100%氧气）和颅内高压（吸入100%氧气加脑室内输注）。测定了每个波形的功率振幅和相位谱，并计算了脑脊液（CSF）压力与系统动脉压力之间以及矢状窦压力与CSF压力之间的功率振幅和相位传递函数。研究表明，当脑静脉与矢状窦之间的阻抗最小时，CSFPW和SSPW几乎相同，这表明CSF脉冲源自脑静脉床。在吸入100%氧气期间，SAPW穿过毛细血管前阻力血管进入脑静脉脉冲（由CSFPW表示）的传输是非线性的，而穿过外侧陷窝进入矢状窦的传输是线性的。在颅内高压期间，穿过毛细血管前阻力血管的波传输是线性的，而穿过外侧陷窝的传输是非线性的。在高碳酸血症期间，穿过毛细血管前阻力血管和外侧陷窝的波传输是线性的。当波传输是非线性时，较低谐波尤其是基频的传输也会受到抑制，并且相位传递函数更正向，表明存在惯性效应或脉冲加速度降低。从毛细血管前阻力血管的非线性传输转变为线性传输是血管运动张力丧失的证据，并伴有CSFPW的变圆。提出了一个包含上述数据并基于可塌陷管中的血流和血管运动张力变化的血管模型，以解释脑血管床中脉动血流的控制和脉搏波形变化。该模型有助于阐明颅内压、脑血流量和脑自动调节之间的紧密相互关系。
