ENHANCED CARDIOVASCULAR PRESSOR REACTIVITY TO NOREPINEPHRINE IN MILD RENAL PARENCHYMAL DISEASE

ENHANCED CARDIOVASCULAR PRESSOR REACTIVITY TO NOREPINEPHRINE IN MILD RENAL PARENCHYMAL DISEASE
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DOI:
10.1038/ki.1982.169
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发表时间:
1982-01-01
影响因子:
19.6
通讯作者:
REUBI, FC
REUBI, FC
中科院分区:
医学1区
文献类型:
--
作者:
BERETTAPICCOLI, C;WEIDMANN, P;REUBI, FC

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在20名患有轻度实质性肾病的患者中评估了与内源性血浆NE或肾素水平相关的对输注的去甲肾上腺素(NE)或血管紧张素II(AII)的心血管升压反应性(血浆肌酐2.20 ± 0.01)。0.58 mg/dl,±. SEM [平均值的标准误差])和20名性别和年龄大致匹配的正常受试者。两组在平均体重、心率、血容量、血浆电解质、可交换钠或尿钠、血浆醛固酮、肾上腺素和肾素水平或AII阈值或升压剂量方面无显著差异。基础(包括输注前)血浆NE水平、在NE输注期间测量的血浆NE与相应的NE输注速率之间的关系、以及NE的总血浆清除率(5.0 ± 0.01)。0.8与5.5 .+-相比。0.5 L/min)也没有显著差异。肾脏疾病患者的NE输注阈值或升压剂量显著降低(94 ± 0.01)。11对134 +-。14 ng/kg/min和21 . ±. 3对40 +-。7ng/kg/min; P < 0.05)。经协方差分析,与基础血浆NE水平相关的个体升压剂量在患者与正常人之间的分布有显著差异(P < 0.01)。血浆NE的动力学在早期肾脏疾病中明显基本不变。这些患者在血浆NE水平正常的情况下往往对NE产生过度的升压反应。这种紊乱可能有利于高血压的发展。
The cardiovascular pressor responsiveness to infused norepinephrine (NE) or angiotensin II (AII) as related to endogenous plasma NE or renin levels was assessed in 20 patients with mild parenchymal kidney disease (plasma creatinine 2.20 .+-. 0.58 mg/dl, .+-. SEM [standard error of the mean]) and in 20 normal subjects approximately matched for sex and age. The 2 groups did not differ significantly in mean body weight, heart rate, blood volume, plasma electrolytes, exchangeable or urinary Na, plasma aldosterone, epinephrine and renin levels, or AII threshold or pressor doses. Basal (including pre-infusion) plasma NE levels, the relationship between plasma NE measured during NE infusion and the corresponding NE infusion rate, as well as the total plasma clearance of NE (5.0 .+-. 0.8 vs. 5.5 .+-. 0.5 l/min) also did not differ significantly between the 2 groups. The threshold or pressor doses of infused NE decreased significantly in the patients with kidney disease (94 .+-. 11 vs. 134 .+-. 14 ng/kg per min and 21 .+-. 3 vs. 40 .+-. 7 ng/kg per min; P < 0.05). Based on analysis of covariance, the individual pressor doses as related to basal plasma NE levels were distributed differently (P < 0.01) between the patients and normal subjects. The kinetics of plasma NE are apparently unaltered largely in early stage kidney disease. Such patients tend to develop an exaggerated pressor responsiveness to NE in the presence of normal plasma NE levels. This disturbance may favor the development of hypertension.