It is known that pulmonary microcirculation theology is partly affecte
d by plasma levels of lipoproteins, but only a few data are available
for humans. Therefore, in a sample of 30 normal volunteers and 90 pati
ents with various types of primary hyperlipoproteinaemia, the plasma l
evels of total cholesterol (Chol), low density cholesterol (LDL), the
high density cholesterol(HDL), triglyceride (Tg) and fibrinogen (Fib)
were measured in conjunction with determinations of plasma viscosity (
PV) and the pulmonary capillary red cell volume (RCV(c)). RCV(c) was e
stimated from measurements of the vascular component of the single-bre
ath-diffusing lung capacity for carbon monoxide, using our own modific
ation of the Roughton-Forster's method. By stepwise regression analysi
s, the variation in RCV, was almost completely accounted for (r(2) = 0
.87) by variations in PV, Chol, Tg and the anthropometric confounding
factors. The proposed explanations for increased pulmonary capillary r
ed cell mass (up to 151% of the predicted value) in hyperlipidaemic pa
tients included the hypothesis of increased pulmonary microhaematocrit
, which agrees with the observed in-vitro lipoprotein-dependent increa
se in erythrocyte aggregability.