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Section of Cardiology, Department of Medicine, The Milton S. Hershey Medical Center, Pennsylvania State University College of Medicine, Hershey, Pennsylvania 17033
In humans,
hypoxia leads to increased sympathetic neural outflow to skeletal
muscle. However, blood flow increases in the forearm. The mechanism of
hypoxia-induced vasodilation is unknown. To test whether
hypoxia-induced vasodilation is cholinergically mediated or is due to
local release of adenosine, normal subjects were studied before and
during acute hypoxia (inspired O2
10.5%; ~20 min). In experiment I,
aminophylline (50-200
µg · min
1 · 100 ml forearm tissue1) was
infused into the brachial artery to block adenosine receptors (n = 9). In
experiment II, cholinergic
vasodilation was blocked by atropine (0.4 mg over 4 min) infused into
the brachial artery (n = 8). The
responses of forearm blood flow (plethysmography) and forearm vascular
resistance to hypoxia in the infused and opposite (control) forearms
were compared. During hypoxia (arterial O2 saturation 77 ± 2%),
minute ventilation and heart rate increased while arterial pressure
remained unchanged; forearm blood flow rose by 35 ± 6%
in the control forearm but only by 5 ± 8% in the aminophylline-treated forearm (P < 0.02). Accordingly, forearm vascular resistance decreased by 29 ± 5% in the control forearm but only by 9 ± 6% in the
aminophylline-treated forearm (P < 0.02). Atropine did not attenuate forearm vasodilation during hypoxia. These data suggest that adenosine contributes to hypoxia-induced vasodilation, whereas cholinergic vasodilation does not play a role.
cholinergic vasodilation; aminophylline
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