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1 J. Recanati Autonomic Dysfunction Center, Rambam Medical Center, Haifa, Israel
* To whom correspondence should be addressed. E-mail: g_jacob{at}rambam.health.gov.il.
Conflicting data exist on the role of nitric oxide (NO) in cerebral blood flow (CBF) autoregulation. Previous studies involving human and animal subjects seem to indicate that NO involvement is limited to the CO2-dependent mechanism (chemoregulation) and not to the pressure dependent autoregulation (mechanoregulation). We tested this hypothesis in patients with impaired endothelial function compared to healthy controls. Blood pressure, heart rate, end-tidal carbon dioxide (CO2), CBF velocities (CBFV), forearm blood flow, and reactive hyperemia were assesed in 16 patients with diabetes mellitus and/or hypertension, and compared to age-sex matched 12 healthy controls. Pressure dependent autoregulation was determined by escalating doses of phenylephrine. CO2-vasoreactivity index was extrapolated from individual slopes of mean CBFV during normocapnia, hyperventilation and CO2 inhalation. Measurements were repeated after sodium nitroprusside infusion. Indices of endothelial function, maximal and area under the curve (AUC) of forearm blood flow changes, were significantly impaired in patients (max flow: 488±75 vs. 297±31 %; p=0.01, AUC 
F: 173±17 vs. 127±11; p=0.03). Patients and controls showed similar changes in cerebrovascular resistance during BP challenges (identical slopes). CO2-vasoreactivity was impaired in patients compared to controls: 1.19±0.1 vs 1.54±0.1 cm/sxmmHg; p=0.04. NO donor (sodium nitroprusside) offsets this disparity. These results suggest that patients with endothelial dysfunction have impaired CO2-vasoreactivity and preserved pressure dependent autoregulation. This supports our hypothesis that NO is involved in CO2-dependent CBF regulation alone. CBF chemoregulation could therefore be a surrogate of local cerebral endothelial function.
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