The mechanisms by which obstructive apneas produce intermittent surges in a
rterial pressure remain poorly defined. To determine whether termination of
obstructive apneas produce peripheral vasoconstriction, we assessed forear
m blood flow during and after obstructive events in sleeping patients exper
iencing spontaneous upper airway obstructions. In all subjects, heart rate
was monitored with an electrocardiogram and blood pressure was monitored co
ntinuously with digital plethysmography. In 10 patients (protocol 1), we us
ed forearm plethysmography to assess forearm blood flow, from which we calc
ulated forearm vascular resistance by performing venous occlusions during a
nd after obstructive episodes. In an additional four subjects, we used simu
ltaneous Doppler and B-mode images of the brachial artery to measure blood
velocity and arterial diameter, from which we calculated brachial flow cont
inuously during spontaneous apneas (protocol 2). In protocol 1, forearm vas
cular 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 increas
e in resistance. In protocol 2, brachial resistance increased at apnea term
ination in all subjects (219.8 +/- 22.2 to 358.3 +/- 46.1 mmHg . l(-1) . mi
n; P = 0.01). We conclude that termination of obstructive apneas is associa
ted with peripheral vasoconstriction.