Werber A H, Fink G D
Am J Physiol. 1981 May;240(5):H685-90. doi: 10.1152/ajpheart.1981.240.5.H685.
These experiments were performed to determine the role of fluid volume contraction in the compensatory cardiovascular response to an abrupt neurogenically mediated increase in systemic arterial blood pressure. Acute neurogenic hypertension was produced by selective aortic baroreceptor deafferentation (ABD) in the rat. Salt and water balance, fluid compartment volumes, and arterial pressure were measured before and for 5 days after the induction of hypertension by ABD. In rats with ABD, arterial pressure was increased approximately 30 mmHg 1 day after deafferentation and declined 15-20 mmHg over the next 4 days. Plasma volume and extracellular fluid volume were decreased 5 days after ABD. Urine output did not increase after ABD, and the fluid volume contraction was instead the result of a significant decrease in water intake. Sham-operated rats did not exhibit significant changes in any of these parameters. Sodium balance decreased slightly in both sham-operated and ABD rats postsurgery. These results confirm that fluid volume contraction is a prominent compensatory response to an abrupt rise in arterial pressure, but suggest that this compensation is not necessarily mediated through alterations in renal salt and water excretion.
进行这些实验是为了确定在对神经源性介导的系统性动脉血压突然升高的代偿性心血管反应中,血容量收缩所起的作用。通过对大鼠进行选择性主动脉压力感受器去传入(ABD)来产生急性神经源性高血压。在通过ABD诱导高血压之前和之后的5天内,测量盐和水平衡、体液腔室容积以及动脉血压。在接受ABD的大鼠中,去传入后1天动脉血压升高约30 mmHg,并在接下来的4天内下降15 - 20 mmHg。ABD后5天,血浆容积和细胞外液容积减少。ABD后尿量未增加,血容量收缩反而归因于水摄入量的显著减少。假手术大鼠在这些参数中均未表现出显著变化。术后,假手术大鼠和接受ABD的大鼠钠平衡均略有下降。这些结果证实血容量收缩是对动脉血压突然升高的一种突出的代偿反应,但表明这种代偿不一定通过肾盐和水排泄的改变来介导。