The splanchnic circulation and postural hypotension in diabetic autonomic neuropathy

Postural hypotension results from sympathetic failure to cause superior peripheral vasoconstriction. The importance of the splanchnic circulation was studied by measuring mesenteric artery blood flow with duplex Doppler scanning. Nine normal and 9 Type 1 diabetic controls were compared to 8 Type 1 patients with autonomic neuropathy whose pressure fell 40-113 mmHg (range) on tilting. Measurements were made supine and after vertical tilt, fasting without insulin and after a 550 kcal meal. Superior mesenteric artery diameter decreased on tilting in normal controls but not in diabetic control or neuropathy groups (supine vs tilted: controls. 6.3 +/- 0.9 to 5 +/- 0.9 mm, p = 0.004, diabetic controls: 6.0 +/- 0.6 to 6.0 +/- 1.0 mm, and neuropathy group: 6.4 +/- 0.9 to 5.6 +/- 0.9 mm), but proportional blood flow changes were similar in all subjects (controls: 407 +/- 154 to 255 +/- 67 ml min-1 (-31%, p = 0.03), diabetic controls: 379 +/- 140 to 306 +/- 149 ml min-1 (-8%, p = 0.28), neuropathy group: 639 +/- 371 to 435 +/- 142 ml min-1 (-23%, p = 0.10). Postprandially supine superior mesenteric artery flow increased in all subjects but this did not affect the degree of systolic blood pressure drop on tilting (fasting vs postprandial blood flow: controls: 407 +/- 154 to 775 +/- 400 ml min-1 (p = 0.04), diabetic controls: 379 +/- 140 to 691 +/- 262 ml min-1 (p = 0.01), neuropathy group: 639 +/- 371 to 943 +/- 468 ml min-1 (p < 0.06)). The similarity of superior mesenteric artery responses to tilting in the three groups, and the lack of exacerbation of postural hypotension in the presence of postprandial hyperaemia indicates that control of splanchnic blood flow is less important in the aetiology of diabetic autonomic postural hypotension than previously thought.