Imai Y, Abe K, Otsuka Y, Sato M, Haruyama T, Ito T, Omata K, Yoshinaga K, Sekino H
Jpn Circ J. 1981 Mar;45(3):303-14. doi: 10.1253/jcj.45.303.
We studied the regulatory mechanism of blood pressure in uremic patients (UP) treated with long-term hemodialysis. The cardiac index (CI) was higher in UP than in normal control (NC). Total peripheral resistance (TPR) in hypertensive (U-Hyper) and normotensive (U-Normo) uremic patients was almost the same as that in NC but TPR in hypotensive uremic patients (U-Hypo) was lower than in NC. High CI in U-Hyper and low TPR in U-Hypo seem to be the causes of their blood pressure abnormalities. All patients had severe anemia. There was a significant positive correlation between hematocrit (Ht) and TPR in UP as well as in NC. The regression line of correlation between Ht (x axis) and TPR (y axis) in UP was shifted to the left from that of NC, suggesting TPR was higher even in U-Hypo than in NC. There was a significant negative correlation between Ht and CI in UP as well as in NC. The regression line of correlation between Ht (x axis) and CI (y axis) in UP was shifted to the left from that in NC, suggesting that CI was lower even in U-Hyper than that in NC. Therefore, higher TPR relative to Ht in U-Hyper and lower CI relative to Ht in U-Hypo may actually be principal causes of their blood pressure abnormalities. Circulating plasma volume and extracellular fluid volume were significantly higher in UP even after hemodialysis but there was no significant difference among subgroups of uremia. Plasma renin activity (PRA) was higher in UP than in NC. However, PRA in U-Hypo was significantly lower than that in U-Hyper or U-Normo. PRA in UP, even in U-Hypo, was inappropriately high relative to sodium/volume status. There was a significant positive correlation between TPR and PRA in UP. Therefore, higher TPR in UP relative to Ht than NC might be a result of elevated PRA. The level of blood pressure in UP seems to be regulated mainly by renin-angiotensin system. All patients were dialysed under the same condition. Heart rate and TPR increased after dialysis in U-Hyper and U-Hypo. However, no change occurred in these parameters throughout dialysis in U-Hypo. The responsiveness of renin secretion upon dialysis was lower in U-Hypo than in other two groups. Therefore, autonomic dysfunction may partly contribute to the development and maintenance of chronic hypotension in U-Hypo.
我们研究了长期接受血液透析治疗的尿毒症患者（UP）的血压调节机制。与正常对照组（NC）相比，UP的心脏指数（CI）更高。高血压尿毒症患者（U-Hyper）和血压正常的尿毒症患者（U-Normo）的总外周阻力（TPR）与NC几乎相同，但低血压尿毒症患者（U-Hypo）的TPR低于NC。U-Hyper的高CI和U-Hypo的低TPR似乎是其血压异常的原因。所有患者均患有严重贫血。UP以及NC的血细胞比容（Ht）与TPR之间存在显著正相关。UP中Ht（x轴）与TPR（y轴）的相关回归线相对于NC向左偏移，这表明即使在U-Hypo中TPR也高于NC。UP以及NC的Ht与CI之间存在显著负相关。UP中Ht（x轴）与CI（y轴）的相关回归线相对于NC向左偏移，这表明即使在U-Hyper中CI也低于NC。因此，U-Hyper中相对于Ht较高的TPR以及U-Hypo中相对于Ht较低的CI可能实际上是其血压异常的主要原因。即使在血液透析后，UP的循环血浆量和细胞外液量仍显著高于正常水平，但尿毒症各亚组之间无显著差异。UP的血浆肾素活性（PRA）高于NC。然而，U-Hypo的PRA显著低于U-Hyper或U-Normo。即使在U-Hypo中，UP的PRA相对于钠/容量状态也过高。UP中TPR与PRA之间存在显著正相关。因此，UP中相对于Ht比NC更高的TPR可能是PRA升高的结果。UP的血压水平似乎主要由肾素-血管紧张素系统调节。所有患者均在相同条件下进行透析。U-Hyper和U-Hypo在透析后心率和TPR升高。然而，U-Hypo在整个透析过程中这些参数无变化。U-Hypo中透析时肾素分泌的反应性低于其他两组。因此，自主神经功能障碍可能部分导致U-Hypo中慢性低血压的发生和维持。
