OH is relatively common in patients with diabetic neuropathy (10,15,16), although the frequency reflects referral bias. OH was found in 43% of 16 patients (10) and 26% of 73 patients (1). Mulder et al. (17) found OH in 18 of 103 unselected patients with diabetes of whom 43 had polyneuropathy. Veglio et al. (16) reported orthostatic intolerance in 34% of 221 patients with NIDDM patients. In some studies clinical failure is very uncommon. For instance, Young et al. (18) in a study of teenagers, did not find any symptoms of autonomic failure. The prevalence of symptomatic OH is less than 1% in population based studies (19), but if asymptomatic OH is considered the prevalence, might be about 10% (ongoing Rochester diabetic study of PJ Dyck).
The mechanism of diabetic OH is multiplex. There is denervation of postgan-glionic adrenergic nerve fibers that innervate arterioles and venules that occurs as an integral part of diabetic peripheral neuropathy (3). As a result, the adrenergic sympathetic component of the baroreflex arc is defective and arteriolar vasoconstriction fails to occur; and total systemic resistance fails to increment. In the Autonomic laboratory, this is manifested as an exaggerated fall in BP during the Valsalva maneuver with failure of reflex vasoconstriction (loss of late phase II and IV and delayed BP recovery). Reflex changes in heart rate fail to occur because of cardiovagal failure. An important additional mechanism is the consistent and early degeneration of sympathetic pre- and postganglionic fibers supplying the splanchnic mesenteric bed (10,20). The autonomic denervation of the muscle resistance bed is also present, but in humans sustained postural normotension is more dependent on the splanchnic system, whereas innervation of skeletal muscle is important in the regulation of moment to moment adjustments (21). Plasma volume, cardioacceleration, and central blood volume are normal or near-normal in diabetic OH (20). Subcutaneous vasoconstrictor function is impaired (10,20).
Limited information is available on recording of the splanchnic-mesenteric bed in diabetic neuropathy patients. It is possible to measure superior mesenteric artery flow using a duplex scanner (22). Normal subjects undergo a two- to threefold increase in superior mesenteric flow with a meal, and splanchnic capacitance falls with tilt-up.
Patients with neurogenic OH are reported to undergo a normal increase in capacity post-prandially, and hypotension develops because of failure of muscle arteriolar vasoconstriction (23). Some workers have reported similar responses to tilt and a meal in diabetic neuropathy patients when compared with controls and conclude that the splanchnic bed may be less important than was assumed (24). One possible explanation is that there is heterogeneity of responses in patients with diabetic neuropathy (22).
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