We hypothesized that the decrease in single-breath diffusing capacity
of CO (DL(CO)) as observed in patients with Raynaud's phenomenon (P. J
. Fahey et al. Am. J. Med. 76: 263-269, 1984) may be present in normal
subjects. Therefore, we examined 31 healthy subjects in two different
laboratories. Two series of experiments were performed. In the first
series DL(CO) was measured in 22 volunteers before (twice) and 5, 10,
and 30 min after a cold presser test (CPT), which consisted of immersi
ng both hands in a 12 degrees C water bath for 2 min. In the second se
ries right heart catheterization was performed in nine healthy seated
subjects. Cardiac output, mean pulmonary arterial pressure, heart rate
, and pulmonary wedge pressure were measured before, during, and 10, 2
0, and 30 min after the CPT. In every volunteer the CPT induced a decr
ease in DL(CO) that was still present 30 min after the test. In the ni
ne catheterized subjects DL(CO) increased above control values during
the CPT and then decreased below control values for 30 min. The CPT ha
d no effect on cardiac output, heart rate, or pulmonary wedge pressure
. In contrast, pulmonary arterial pressure and pulmonary vascular resi
stance increased during the CPT and then became lower than the control
values for at least 30 min. In summary, the CPT induced a biphasic ev
olution of DL(CO) in normal subjects, being increased during the CPT a
nd decreased after it. Our data are best explained by the West model o
f the lung. Our data suggest that the pulmonary Raynaud's phenomenon i
s not specific to patients with primary Raynaud's phenomenon. The decr
ease in DL(CO) after a CPT is not due to a vasospasm but rather to a v
asodilatation of the pulmonary artery.