Nakamura K, Osborn J W, Cowley A W
Department of Physiology, Medical College of Wisconsin, Milwaukee 53226.
Hypertension. 1987 Dec;10(6):635-41. doi: 10.1161/01.hyp.10.6.635.
Acute relationships between cerebrospinal fluid hydrostatic pressure and arterial pressure were quantified in conscious rats. The rats were catheterized with a left femoral artery catheter, and a double set of catheters was implanted into the third cerebral ventricle. In three groups of rats, artificial cerebrospinal fluid with various sodium concentrations (142, 152, and 162 mM) was infused into the third ventricle for 3 hours at 1.0 microliter/min. Mean arterial pressure (MAP) and third ventricular pressure were monitored simultaneously, and both increased progressively over the 3-hour infusion period; the rate of rise was significantly greater with infusion of the hypertonic solution. There were no significant differences between the rat groups infused with low, normal, or high artificial cerebrospinal fluid sodium in either the slope or the intercept of the regression equation relating cerebrospinal fluid pressure and MAP: a 1 cm H2O rise of cerebrospinal fluid pressure was always associated with nearly a 1 mm Hg rise in MAP. In other rats, changes in both cerebrospinal fluid pressure and MAP were shown to be highly dependent on the rate of ventricular infusion. We conclude that elevations of systemic arterial pressure are associated with only small elevations of cerebrospinal fluid pressure and that physiological changes of cerebrospinal sodium (+/- 10 mM) influence arterial pressure by altering intravascular hydrostatic pressure rather than sodium or osmosensitive receptors in the cerebral ventricles.
在清醒大鼠中对脑脊液静水压与动脉压之间的急性关系进行了量化。给大鼠插入左股动脉导管,并将两组导管植入第三脑室。在三组大鼠中,以1.0微升/分钟的速度将不同钠浓度(142、152和162 mM)的人工脑脊液注入第三脑室3小时。同时监测平均动脉压(MAP)和第三脑室压力,在3小时的输注期间两者均逐渐升高;输注高渗溶液时升高速率明显更大。在将脑脊液压力与MAP相关联的回归方程的斜率或截距方面,输注低、正常或高钠人工脑脊液的大鼠组之间没有显著差异:脑脊液压力升高1 cm H2O总是伴随着MAP升高近1 mm Hg。在其他大鼠中,脑脊液压力和MAP的变化都高度依赖于脑室输注速率。我们得出结论,全身动脉压升高仅与脑脊液压力的小幅升高有关,并且脑脊液钠(±10 mM)的生理变化通过改变血管内静水压而非脑室中的钠或渗透压感受器来影响动脉压。