Stimulus‐specific cerebrovascular dysfunction in humans with metabolic syndrome

Abstract

Metabolic syndrome (MetS) and reduced cerebrovascular reactivity are each associated with increased risk of stroke in humans. Animal models of MetS demonstrate reduced cerebral artery dilation, but cerebrovascular function in humans with MetS remains untested. We tested the hypothesis MetS humans would have reduced cerebrovascular reactivity to hypoxia and hypercapnia. Blood pressure (BP), arterial oxygen saturation (SpO2), expired carbon dioxide (PETCO2), and middle cerebral artery blood velocity (CBV, transcranial Doppler ultrasound) were measured in MetS adults (n=9, 37 ± 3 yr) and healthy controls (n=10, 32 ± 2 yr). Cerebral conductance index (CVCI = CBV / BP) was calculated to normalize CBV for higher BP in MetS adults. Cerebral vasodilation (ΔCVCI) to hypoxia (SpO2 = 90% and 80%) and hypercapnia (+10 mmHg PETCO2) were assessed. MetS adults exhibited markedly lower ΔCVCI to 90% SpO2 (1 ± 2 vs 6 ± 2 cm s−1 mmHg−1, p<0.05) and 80% SpO2 (5 ± 2 vs 15 ± 3 cm s−1 mmHg−1, p<0.05). In contrast, MetS adults displayed preserved cerebrovascular reactivity to hypercapnia (ΔCVCI = 18 ± 2 vs 20 ± 2 cm s−1 mmHg−1). We conclude younger MetS adults exhibit markedly reduced stimulus‐specific cerebrovascular reactivity during hypoxia. Poor hypoxia‐mediated cerebral dilation may contribute to the increased risk and severity of cerebrovascular disease in MetS humans. Support: NIH HL091397 & AHA 11PRE7390038