The contribution sf carbon monoxide (CO) to the acute cardiovascular e
ffects of smoking is not clear, Using a double-blind, randomized, vehi
cle-controlled study design, we examined the sympathetic and vascular
responses to modest increases in carboxyhemoglobin in 10 healthy human
s. We measured muscle sympathetic nerve activity (microneurography), f
orearm blood flow (plethysmography): heart rate, blood pressure, and m
inute ventilation at baseline and during 60 minutes of CO inhalation (
1000 ppm during the first 30 minutes and 100 ppm during the last 30 mi
nutes). The same measurements were made in a vehicle session (room air
inhalation) on a separate clay. During the first 30 minutes: of CO in
halation, carboxyhemoglobin levels increased progressively from 0.2+/-
0.1% ta 8.3+/-0.5% arid were maintained at about this level for a furt
her 30 minutes. Forearm vascular resistance did not change with CO but
increased slightly with vehicle; the effects of CO on muscle sympathe
tic nerve activity, forearm blood flow, blood pressure, heart rate, an
d minute ventilation were not significantly different from the effects
of vehicle. Modest increases in carboxyhemoglobin levels equivalent t
o those resulting from cigarette smoking are unlikely to contribute to
the acute sympathetic and hemodynamic effects of smoking in healthy h
umans.