Possible mechanisms of impaired endotheliumdependent vasodilation

Although the data are conflicting, overwhelming evidence presently suggests that DM is associated with an impairment of endothelial vasodilation. The mechanism(s) for this impairment is even less well understood. The most likely initial insult is hyperglycemia. Tesfamarian and colleagues took normal rabbit aortic rings and exposed them to high concentrations of glucose (up to 800 mg/dL for 3 hours), resulting in a decrease in endothelium-dependent relaxation, in response to acetylcholine and ADP (52,53). This effect appears to be both concentration and time dependent. As stated earlier, this effect does not appear to be a result of the hyperosmolar effects of glucose because mannitol did not cause any such endothelium-dependent vasodilation (53). Bohlen and Lash (73) demonstrated that hyperglycemia at 300 and 500 mg/dL suppressed the vasodilatory response to acetylcholine but not to nitroprusside. Similarly, Williams and colleagues (68) found that acute hyperglycemia attenuated endothelium-dependent relaxation in forearm resistance vessels in healthy humans (Fig. 4). Akbari and colleagues (74) found that acute hyperglycemia resulted in similar degrees of impairment of endothelium-dependent vasodilation in the micro- and macrocirculation (Fig. 5).

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