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1 Charles A. Dana Institute and Harvard-Thorndike Laboratory of Beth Israel Deaconess Medical Center, 2 Beth Israel Deaconess Sleep Disorders Center, 3 Department of Medicine, Beth Israel Deaconess Medical Center, and 4 Department of Medicine, Harvard Medical School, Boston, Massachusetts 02215
The mechanisms by which obstructive apneas
produce intermittent surges in arterial pressure remain poorly defined.
To determine whether termination of obstructive apneas produce
peripheral vasoconstriction, we assessed forearm blood flow during and
after obstructive events in sleeping patients experiencing spontaneous
upper airway obstructions. In all subjects, heart rate was monitored
with an electrocardiogram and blood pressure was monitored continuously
with digital plethysmography. In 10 patients (protocol 1),
we used forearm plethysmography to assess forearm blood flow, from
which we calculated forearm vascular resistance by performing venous
occlusions during and after obstructive episodes. In an additional four
subjects, we used simultaneous Doppler and B-mode images of the
brachial artery to measure blood velocity and arterial diameter, from
which we calculated brachial flow continuously during spontaneous
apneas (protocol 2). In protocol 1, forearm
vascular resistance increased 71% after apnea termination (29.3 ± 15.4 to 49.8 ± 26.5 resistance units, P < 0.05) with all patients showing an increase in resistance. In
protocol 2, brachial resistance increased at apnea
termination in all subjects (219.8 ± 22.2 to 358.3 ± 46.1 mmHg · l
1 · min; P = 0.01). We conclude that termination of obstructive apneas is associated
with peripheral vasoconstriction.
forearm blood flow; vasoconstriction; upper airway obstructions
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