ADRENERGIC REGULATION OF BLOOD-PRESSURE IN CHRONIC RENAL-FAILURE
ADRENERGIC REGULATION OF BLOOD-PRESSURE IN CHRONIC RENAL-FAILURE
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DOI：
10.1172/jci108387
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发表时间：
1976-01-01
影响因子：
15.9
通讯作者：
STONE, RA
中科院分区：
文献类型：
--
作者：
LILLEY, JJ;GOLDEN, J;STONE, RA
以往的研究表明，血液透析期间明显的低血压可能是交感神经系统活动异常引起的。为了进一步评估这些现象，血浆多巴胺。研究了2组患者的-羟化酶（d . β . h）、冷压试验（建议的出诊交感神经系统活动指标）和亚硝基戊酯吸入（整个压力受体反射弧指标）：[I组]，在不到10%的透析期间平均动脉压降至70 mm Hg以下的患者；[II组]（血液透析低血压），90%以上的透析患者平均动脉压降至70 mm Hg以下。各组在血浆肾素活性、肾素对超滤反应、年龄、透析时间、神经传导速度、血浆蛋白浓度、红细胞压积、透析体重变化、静息心率、性别、种族、血压和冷压试验的心率反应、125i -白蛋白血浆容量等方面相似。血液透析低血压患者在透析前后仰卧位平均动脉压均高于非血液透析低血压患者（I组）。血液透析低血压（II组）患者透析前后血浆d . β . h活性均显著高于I组。吸入亚硝酸盐戊酯，表示为delta的变化。R-R（脉搏变化）间期/平均动脉压下降，在血液透析低血压患者较少。血液透析低血压可由压力感受器、心肺感受器或内脏传入神经的病变引起。血液透析性低血压患者的平均动脉压升高可能是神经源性的，这可以通过血浆中d . β . h的活性反映出来，并且与实验动物压力感受器脱神经递质后的高血压相似。
Previous investigations suggested that significant hypotension during hemodialysis may result from abnormalities of sympathetic nervous system activity. To further evaluate these phenomena, plasma dopamine .beta.-hydroxylase (D.beta.H) and cold pressor test (proposed indexes of efferent sympathetic nervous system activity) and amyl nitrite inhalation (an index of the entire baroreceptor reflex arc) were studied in 2 groups of patients: [group I], patients exhibiting a mean arterial pressure decrease to less than 70 mm Hg during less than 10% of dialyses; [group II] (hemodialysis hypotension), patients with a mean arterial pressure decrease to less than 70 mm Hg during more than 90% of dialyses. The groups were similar with respect to plasma renin activity, renin response to ultrafiltration, age, duration of dialysis, nerve conduction velocity, plasma protein concentration, hematocrit, dialysis weight change, resting heart rate, sex, race, blood pressure and hear rate response to cold pressor test, and 125I-albumin plasma volume. Supine mean arterial pressure was higher in patients with hemodialysis hypotension than in patients without hemodialysis hypotension (group I) both before and after dialysis. Plasma D.beta.H activity was significantly higher in patients with hemodialysis hypotension (group II) than in group I both before and after dialysis. Amyl nitrite inhalation, expressed as change in .DELTA.R-R (pulse change) interval/mean arterial pressure decrease, was less in hemodialysis hypotension patients. Hemodialysis hypotension may result from a lesion in the baroreceptors, cardiopulmonary receptors, or visceral afferent nerves. Elevated mean arterial pressure in patients with hemodialysis hypotension may be neurogenic in origin, as reflected by plasma D.beta.H activity, and appears similar to the hypertension that follows baroreceptor deafferentation of experimental animals.