Nagashima K
Department of Physiology, Kyoto Prefectural University of Medicine, Japan.
Jpn J Physiol. 1995;45(3):381-95. doi: 10.2170/jjphysiol.45.381.
To assess the effects of alpha-adrenergic activation on hemorrhage-induced shifts of K+, Na+ and fluid between the intravascular and extravascular spaces, we continuously measured changes in plasma concentrations of K+ and Na+ (delta[K+]p, delta[Na+]p) and blood volume (delta BV) over 60 min after hemorrhage in nephrectomized rats. Hemorrhage was conducted over 5 min at the level of 0.5, 1.0 and 1.5% of body weight (H0.5, H1.0, H1.5), and the result was compared with hemorrhage of 1.0% body weight after administration of alpha 1-adrenoreceptor antagonist prazosin (0.2 mg/kg, H1.0P). delta[K+]p increased significantly (p < 0.05) after hemorrhage, and the peak value was proportional to the level of hemorrhage (0.18 +/- 0.08, 0.62 +/- 0.22 and 1.64 +/- 0.19 meq/l in H0.5, H1.0 and H1.5, respectively). delta[Na+]p decreased significantly (p < 0.05) after hemorrhage, and the decrease was sustained until the end of the experiment (-0.8 +/- 0.6, -1.0 +/- 0.5 and -2.2 +/- 0.5 meq/l in H0.5, H1.0 and H1.5, respectively). In H1.0P, the increase in delta[K+]p (0.25 +/- 0.09 meq/l at the peak) and the decrease in delta[Na+]p (-0.2 +/- 0.1 meq/l at the bottom) were suppressed significantly (p < 0.05) compared to H1.0. Although delta BV was greater in H1.0P than H1.0, plasma K+ content was not different between the groups. In H1.0, the calculated concentrations of K+ and Na+ in the fluid which shifted into the intravascular space ([K+]sf, [Na+]sf) in the first 30 min after hemorrhage were higher in [K+]sf (6.25 +/- 0.70 meq/l) and lower in [Na+]sf (128.0 +/- 3.2 meq/l) than the pre-hemorrhage plasma level. With regard to H1.0P, [K+]sf and [Na+]sf were not different from the pre-hemorrhage level of plasma. These results suggest that alpha-adrenergic activation after hemorrhage induces K+ movement into plasma to increase [K+]p, which might be related to the fluid shift from the intracellular to the extracellular space.
为评估α-肾上腺素能激活对出血诱导的血管内和血管外间隙之间钾离子、钠离子及液体转移的影响，我们在肾切除大鼠出血后60分钟内持续测量了血浆中钾离子和钠离子浓度的变化（Δ[K⁺]p、Δ[Na⁺]p）以及血容量（ΔBV）。分别以体重的0.5%、1.0%和1.5%的水平进行5分钟的出血操作（H0.5、H1.0、H1.5），并将结果与给予α1-肾上腺素能受体拮抗剂哌唑嗪（0.2mg/kg）后体重1.0%的出血情况（H1.0P）进行比较。出血后Δ[K⁺]p显著升高（p<0.05），且峰值与出血水平成正比（H0.5、H1.0和H1.5组中分别为0.18±0.08、0.62±0.22和1.64±0.19meq/l）。出血后Δ[Na⁺]p显著降低（p<0.05），且该降低持续至实验结束（H0.5、H1.0和H1.5组中分别为-0.8±0.6、-1.0±0.5和-2.2±0.5meq/l）。在H1.0P组中，与H1.0组相比，Δ[K⁺]p的升高（峰值时为0.25±0.09meq/l）和Δ[Na⁺]p的降低（谷底时为-0.2±0.1meq/l）均受到显著抑制（p<0.05）。尽管H1.0P组的ΔBV大于H1.0组，但两组间血浆钾含量并无差异。在H1.0组中，出血后最初30分钟内转移至血管内间隙的液体中钾离子和钠离子的计算浓度（[K⁺]sf、[Na⁺]sf），[K⁺]sf（6.25±0.70meq/l）高于出血前血浆水平，而[Na⁺]sf（128.0±3.2meq/l）低于出血前血浆水平。对于H1.0P组，[K⁺]sf和[Na⁺]sf与出血前血浆水平无差异。这些结果表明，出血后α-肾上腺素能激活诱导钾离子向血浆中移动以增加[K⁺]p，这可能与液体从细胞内转移至细胞外间隙有关。
