Buñag R D, Riley E
Hypertension. 1979 Sep-Oct;1(5):498-507. doi: 10.1161/01.hyp.1.5.498.
Daily electrical stimulation of the posterior hypotalamus for 12 weeks in awake rats caused persistent cardioacceleration but barely increased systolic pressure. Subsequent postmortem examination showed extensive fibrosis at sites of electrode implantation in both stimulated and unstimulated rats. Because Folkow and Rubinstein had succeeded in elevating blood pressure progressively by stimulating the "hypothalamic defence area," chronic stimulation was repeated following their stereotaxic coordinates. Systolic pressure rose but the elevation was significant only on Weeks 8 and 10. To maintain behavioral effects during chronic stimulation, current strengths had to be increased periodically, and stimulated rats gained weight more rapidly than unstimulated controls. Both these findings indicated that electrical stimulation had damaged the brain, but since local fibrosis made histologic verification difficult, additional experiments were done to determine if functional deficits could be detected. Upon further hypothalamic stimulation, electrical thresholds were higher and pressor and sympathetic nerve responses were smaller in rats that had been stimulated chronically than in those that had not. Although our results do not disprove the hypothesis that centrally-induced sympathetic hyperactivity initiates hypertension, they show that blood pressure cannot be elevated by hypothalamic stimulation alone when the brain has been injured.
对清醒大鼠的下丘脑后部进行为期12周的每日电刺激，导致持续性心动过速，但收缩压几乎没有升高。随后的尸检显示，在接受刺激和未接受刺激的大鼠中，电极植入部位均出现广泛纤维化。由于福尔科夫和鲁宾斯坦通过刺激“下丘脑防御区”成功地逐步升高了血压，因此按照他们的立体定位坐标重复进行慢性刺激。收缩压升高，但仅在第8周和第10周时升高显著。为了在慢性刺激期间维持行为效应，必须定期增加电流强度，并且接受刺激的大鼠比未接受刺激的对照大鼠体重增加得更快。这两个发现均表明电刺激已损伤大脑，但由于局部纤维化使得组织学验证困难，因此进行了额外的实验以确定是否能检测到功能缺陷。进一步刺激下丘脑时，与未接受慢性刺激的大鼠相比，接受慢性刺激的大鼠的电阈值更高，升压和交感神经反应更小。虽然我们的结果并未否定中枢性交感神经过度活跃引发高血压这一假说，但它们表明，当大脑受到损伤时，仅通过下丘脑刺激无法升高血压。
