糖尿病自主神经病变的血压调节。

J Hilsted
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摘要

在患有自主神经病变的糖尿病患者中,站立、运动和肾上腺素输注的血压反应存在缺陷。在这些患者中,运动和站立时血压反应的循环机制得到了很好的表征:在这两种实验情况下,阻力血管收缩不足已被证明。血管收缩缺陷的大小足以解释当前的低血压。此外,自主神经病变患者在运动时心输出量低,这一发现可能导致这些患者出现运动性低血压。在低血糖期间,自主神经病变患者的血压调节似乎完好无损。这可能是由于在这些实验中释放了大量的儿茶酚胺。在肾上腺素输注期间,自主神经病变患者血压显著下降,可能是由于过度的肌肉血管舒张。目前还不清楚为什么低血糖时血压调节完好无损,而在儿茶酚胺浓度相似的情况下,肾上腺素输注时血压调节严重受损。
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Blood pressure regulation in diabetic autonomic neuropathy.

Defective blood pressure responses to standing, exercise and epinephrine infusions have been demonstrated in diabetic patients with autonomic neuropathy. The circulatory mechanisms underlying blood pressure responses to exercise and standing up in these patients are well characterized: In both experimental situations insufficient contraction of resistance vessels has been demonstrated. The vasoconstrictor defects demonstrated are of a magnitude sufficient to account for the prevailing hypotension. Furthermore, during exercise cardiac output is low in patients with autonomic neuropathy, a finding which may contribute to exercise hypotension in these patients. During hypoglycemia, blood pressure regulation seems intact in patients with autonomic neuropathy. This is probably due to release of substantial amounts of catecholamines during these experiments. During epinephrine infusions a substantial blood pressure fall ensues in patients with autonomic neuropathy, probably due to excessive muscular vasodilation. It is unresolved why blood pressure regulation is intact during hypoglycemia and severely impaired--at similar catecholamine concentrations--during epinephrine infusions.

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