Laederach-Hofmann K, Weidmann P, Ferrari P
Medical Outpatient, SPPM, University of Berne, Switzerland.
Am J Med. 1999 Jan;106(1):50-8. doi: 10.1016/s0002-9343(98)00367-2.
To investigate whether body sodium content and blood volume contribute to the pathogenesis of orthostatic hypotension in patients with diabetes mellitus.
Exchangeable sodium, plasma and blood volumes, and catecholamine, renin, and aldosterone levels were assessed in 10 patients with Type II diabetes mellitus who had orthostatic hypotension and control groups of 40 diabetic patients without orthostatic hypotension and 40 normal subjects of similar age and sex. In subgroups, clinical tests of autonomic function and cardiovascular reactivity to norepinephrine and angiotensin II infusions were performed.
In diabetic patients with orthostatic hypotension, mean (+/- SD) supine blood pressure was 165/98 +/- 27/12 mm Hg (P <0.05 compared with other groups) and mean upright blood pressure was 90/60 +/- 38/18 mm Hg. Compared with controls, diabetic patients with orthostatic hypotension had a 10% lower blood volume. They also had less exchangeable sodium than patients with diabetes who did not have orthostatic hypotension (P <0.01). Compared with both groups of controls, diabetic patients with orthostatic hypotension had decreased 24-hour urinary norepinephrine excretion and a reduced diastolic blood pressure response to handgrip (P <0.05). Moreover, they displayed reduced products of exchangeable sodium or blood volume and sympathetic function indexes. Cardiovascular pressor reactivity to norepinephrine was enhanced (P <0.01) and beat-to-beat variation decreased (P <0.01) in both groups of diabetic patients. Microvascular complications were more prevalent in the diabetic patients with orthostatic hypotension (90% vs 35%).
Patients who have Type II diabetes mellitus and orthostatic hypotension are hypovolemic and have sympathoadrenal insufficiency; both factors contribute to the pathogenesis of orthostatic hypotension.
研究机体钠含量和血容量是否在糖尿病患者体位性低血压的发病机制中起作用。
对10例患有体位性低血压的II型糖尿病患者、40例无体位性低血压的糖尿病患者对照组以及40例年龄和性别相仿的正常受试者进行可交换钠、血浆和血容量以及儿茶酚胺、肾素和醛固酮水平的评估。在亚组中，进行自主神经功能的临床测试以及对去甲肾上腺素和血管紧张素II输注的心血管反应性测试。
患有体位性低血压的糖尿病患者，仰卧位平均（±标准差）血压为165/98±27/12 mmHg（与其他组相比，P<0.05），直立位平均血压为90/60±38/18 mmHg。与对照组相比，患有体位性低血压的糖尿病患者血容量低10%。他们的可交换钠也比没有体位性低血压的糖尿病患者少（P<0.01）。与两组对照组相比，患有体位性低血压的糖尿病患者24小时尿去甲肾上腺素排泄减少，对手握力的舒张压反应降低（P<0.05）。此外，他们的可交换钠或血容量与交感神经功能指标的乘积降低。两组糖尿病患者对去甲肾上腺素的心血管升压反应增强（P<0.01），逐搏变化减小（P<0.01）。体位性低血压的糖尿病患者微血管并发症更常见（90%对35%）。
患有II型糖尿病和体位性低血压的患者血容量不足且存在交感肾上腺功能不全；这两个因素都在体位性低血压的发病机制中起作用。
