Atherosclerosis and Lipoproteins |
From The Hypertension Unit, Heart Institute (InCor), University of São Paulo Medical School, Brazil.
Address correspondence to José Augusto S. Barreto-Filho, MD, Hypertension Unit, Heart InstituteInCorHCFMUSP, Av.Dr.Eneas de Carvalho Aguiar, 44, 05403-000 São Paulo, Brazil. E-mail jose.barreto{at}incor.usp.br
Objective During hypoxia, active substances released by the endothelium play a key role in the cardiovascular and respiratory responses elicited to optimize oxygen delivery. As hypercholesterolemia is a major cause of endothelial dysfunction, it may interfere with these responses.
Methods and Results We studied cardiovascular and ventilatory responses to acute systemic hypoxia in 14 patients with hypercholesterolemia (HC) and 13 control (CO) subjects. Oxygen saturation decreased similarly in both groups. Diastolic blood pressure increased only in the HC group (P=0.0002) and, despite systolic blood pressure increases both in the HC group, 140±4 (95% confidence interval [CI],131 to 149 mm Hg) to 154±4 mm Hg (95% CI,145 to 164 mm Hg), and in the CO group, 133±3 (95% CI,126 to 140 mm Hg) to 140±4 mm Hg (95% CI,132 to 148 mm Hg), the HC group showed an enhanced pressor response (P=0.03, group comparison). Both groups had increased forearm blood flow, but the decrease in forearm vascular resistance in the CO group, 40±5 (95% CI, 30 to 51 UR) to 31±4 UR (95% CI,23 to 39 UR) (P=0.0001) was not seen in the HC group, 29±3 (95% CI, 22 to 37 UR) to 26±3 UR (95% CI, 20 to 33 UR), (P=0.03, group comparison).
Conclusions Hypercholesterolemic patients demonstrate a hyperreactive pressor response and absence of forearm vasodilation during acute systemic hypoxia.
Key Words: lipids endothelium hypoxia blood flow blood pressure
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