Limited information is available for humans on whether blood viscosity
affects total peripheral resistance and, hence, blood pressure. Our s
tudy was aimed at assessing the effects of acute changes in blood visc
osity on both clinic and 24-hour ambulatory blood pressure (BP) values
. In 22 normotensive and hypertensive patients with polycythemia, clin
ic and 24-hour ambulatory BPs were measured before and 7 to 10 days af
ter isovolumic hemodilution; this was performed through the withdrawal
of 400 to 700 mL of blood, with concomitant infusion of an equivalent
volume of saline-albumin solution. Hematocrit, plasma renin activity,
plasma endothelin-1, right atrial diameter (echocardiography), and bl
ood viscosity were measured under both conditions. Plasma renin activi
ty and right atrial diameter were used as indirect markers of blood vo
lume changes. Plasma endothelin-1 was used to obtain information on a
vasomotor substance possibly stimulated by our intervention, which cou
ld counteract vasomotor effects. Isovolumic hemodilution reduced hemat
ocrit from 0.53+/-0.05 to 0.49+/-0.05 (P<.01). Plasma renin activity,
plasma endothelin-1 and right atrial diameter were unchanged. Clinic b
lood pressure was reduced by hemodilution (systolic, 144.3+/-5.4 to 13
6.0+/-3.9 mm Hg[mean+/-SEM]; diastolic, 87.0+/-2.8 to 82.1+/-2.6 mm Hg
, P<.05 for both) and a reduction was observed also for 24-hour averag
e ABP (systolic, 133.6+/-2.9 to 129.5+/-2.7 mm Hg; diastolic, 80.0+/-2
.0 to 77.3+/-1.7 mm Hg, P<.05 for both). The reduction was consistent
in hypertensive patients (n=12), whereas in nomotensive patients (n=10
) it nas small and not significant. Both clinic and 24-hour average he
art rates were unaffected by the hemodilution. Thus, in polycythemia,
reduction in blood viscosity without changing blood volume causes a si
gnificant fall in both clinic and 24-hour ambulatory BPs; this is part
icularly true when, as can often happen, blood pressure is elevated. T
his emphasizes the importance this variable may have in the determinat
ion of blood pressure and the potential therapeutic value of its corre
ction when altered.