Transient pleural effusions occurred in rats receiving continuous intraveno
us infusion of norepinephrine (NE, 0.1 mg/kg/h). We hypothesized that these
pleural effusions result from a NE-induced increase in right ventricular s
ystolic pressure (RVSP) and total peripheral resistance (TPR). NE was admin
istered over time intervals between 20 min and 72 h. It induced an immediat
e doubling in RVSP whereas LVSP remained at the control level. TPR increase
d with a delay of 6 h. At this time, pleural effusions occurred in NE-treat
ed animals, reached their maximum after 8h and disappeared after 24 h of NE
stimulation. Combining NE with the alpha -blocker prazosin normalized TPR
and prevented pleural effusions. Therefore, we interpret the pleural effusi
on as a consequence of pulmonary venous congestion, mainly caused by an inc
reased TPR. LV hypertrophy which developed after 24 h of NE stimulation is
considered to compensate for the hemodynamic disturbance due to the NE-indu
ced elevation in TPR. This is reflected in the disappearance of pleural eff
usion.