Christensen N J
J Clin Invest. 1972 Apr;51(4):779-87. doi: 10.1172/JCI106872.
Employing a precise and sensitive double-isotope derivative technique, plasma catecholamine concentration (PCA) was measured in four groups of subjects: (a) long-term diabetics with neuropathy, (b) long-term diabetics without neuropathy, (c) hypophysectomized long-term diabetics with neuropathy, and (d) nondiabetic control subjects. Blood samples were obtained from subjects in the supine and in the standing position. In nondiabetic control subjects, PCA (mainly noradrenaline) increased from 0.26 ng/ml in the supine positon to 0.69 and 0.72 ng/ml 5 and 10 min after assuming the standing position. By plotting this increase in PCA on the y axis in a coordinate system vs. increase in pulse rate, PCA was divided into two components: one of these depended on the rise in pulse rate on standing (called CAH) and the other corresponded to the intercept on the y axis where rise in pulse rate equals zero (CAP).Long-term diabetics with neuropathy showed a significant reduction in PCA in both the supine and the standing position. Further analysis demonstrated that CAP was considerably reduced whereas CAH was normal. Long-term diabetics without neuropahty showed normal PCA values.Surprisingly, hypophysectomized diabetics with neuropathy exhibited mean PCA values in both the supine and the standing position which were similar to those found in the nondiabetic subjects and considerably elevated compared with the findings in the nonoperated, long-term diabetics with neuropathy. Further analysis in terms of CAP and CAH demonstrated, however, that CAP was just as abnormally reduced in the hypophysectomized as it was in the nonoperated patients whereas CAH was considerably increased. In contrast to the findings in the nonoperated diabetics with neuropathy, the hypophysectomized diabetic patients with neuropathy demonstrated a negative correlation between rise in PCA and blood pressure on standing indicating that the increase in PCA was at least partially a compensatory phenomenon in the interest of the maintenance of a normal level of blood pressure. An increased sympathetic tone (vasoconstriction) is believed to be at least partially responsible for the increased capillary resistance and decreased capillary permeability occuring after hypophysectomy.
采用精确且灵敏的双同位素衍生技术，对四组受试者的血浆儿茶酚胺浓度（PCA）进行了测量：（a）患有神经病变的长期糖尿病患者；（b）无神经病变的长期糖尿病患者；（c）垂体切除的患有神经病变的长期糖尿病患者；（d）非糖尿病对照受试者。在受试者仰卧位和站立位时采集血样。在非糖尿病对照受试者中，PCA（主要是去甲肾上腺素）从仰卧位时的0.26 ng/ml增加到站立位5分钟和10分钟后的0.69 ng/ml和0.72 ng/ml。通过在坐标系中以PCA的这种增加为纵轴，与脉搏率的增加相对应来绘制，PCA被分为两个部分：其中之一取决于站立时脉搏率的升高（称为CAH），另一个对应于脉搏率升高为零时纵轴上的截距（CAP）。患有神经病变的长期糖尿病患者在仰卧位和站立位时PCA均显著降低。进一步分析表明，CAP显著降低而CAH正常。无神经病变的长期糖尿病患者PCA值正常。令人惊讶的是，垂体切除的患有神经病变的糖尿病患者在仰卧位和站立位时的平均PCA值与非糖尿病受试者相似，并且与未手术的患有神经病变的长期糖尿病患者相比显著升高。然而，根据CAP和CAH进行的进一步分析表明，垂体切除患者的CAP与未手术患者一样异常降低，而CAH则显著增加。与未手术的患有神经病变的糖尿病患者的结果相反，垂体切除的患有神经病变的糖尿病患者在站立时PCA的升高与血压呈负相关，这表明PCA的增加至少部分是为维持正常血压水平的一种代偿现象。交感神经张力增加（血管收缩）被认为至少部分是垂体切除后毛细血管阻力增加和毛细血管通透性降低的原因。
