Lack of sympathetic vasoconstriction in hypoxemic humans at rest.

A three-part experiment was designed to show whether hypoxemia alters splanchnic vasomotor responses to other stresses by vasodilating splanchnic organs, preventing norepinephrine (NE)-induced vasoconstriction, or altering total sympathetic nervous activity (SNA) assessed by plasma levels of NE and epinephrine (Epi). Splanchnic blood flow (SBF) was measured by plasma clearance and hepatic extraction of indocyanine green (constant infusion). Part I: two degrees of hypoxemia [fractional concn of inspired O2 (FIO2) = 10.4 and 7.6%, arterial PO2 (PaO2) = 34.8 and 27 Torr] caused a small splanchnic vasodilation; resistance fell 16 and 26%, respectively, in five men; and SBF rose from 1.78 to 2.04 (10.4% O2) and to 2.02 1 X min-1 (7.6% O2). Plasma NE was unaffected by hypoxemia and by a fall in mean arterial pressure from 82 to 63 Torr at FIO2 = 7.6%. Part II: NE infused intravenously to raise pressure by 20 Torr in five subjects breathing air and 10.3% O2 caused splanchnic vasoconstriction irrespective of PaO2. Part III: in six subjects, two levels of hypoxemia (FIO2 = 10.4 and 7.7%) did not increase NE levels in five men, and Epi increased in two men only at FIO2 = 7.7%. We conclude that hypoxemia caused only a small splanchnic vasodilation not mediated by Epi, did not prevent transient NE-induced vasoconstriction, and either did not significantly increase SNA or prejunctionally inhibited NE release. Severe hypoxemia abolished the rise in NE and heart rate in response to falling pressure.