Hypertension, Vol 6, 262-266, Copyright © 1984 by American Heart Association
D Susic, AK Mandal and D Kentera
This study describes the effect of a chronic decrease in hematocrit on
blood pressure, cardiac output (CO), total peripheral resistance (TPR), and
plasma volume in spontaneously hypertensive rats (SHR), and all but plasma
volume in normotensive Wistar rats (NWR). Hematocrit was decreased by
treatment with either heparin, vitamin K inhibitor ( pelentan ), or by
repeated blood letting (BL). The results show that in SHR, a decrease in
hematocrit, regardless of how produced, was associated with a significant
decrease (p less than 0.01) in blood pressure. Prevention of
heparin-induced decrease in hematocrit by repeated transfusions of red
blood cells abolished the blood-pressure- lowering effect of heparin. By
using combined data on hematocrit and systolic blood pressure in all five
SHR groups, a significantly positive correlation and linear regression
between hematocrit and blood pressure were obtained. When compared to
control untreated SHR, heparin- or pelentan -treated SHR showed a
significant (p less than 0.001) decrease in TPR and a significant increase
in CO, while in SHR BL, no difference in TPR or CO was found. Plasma or
blood volume did not differ among the groups. In NWR, heparin treatment
resulted in significantly decreased hematocrit, decreased TPR, and
increased CO compared to control normotensive rats. However, blood pressure
did not change. Results confirming the authors' previous study and those of
other investigators indicate a direct association between hematocrit and
systemic hypertension. Lowering the hematocrit can effectively lower an
elevated blood pressure. Moreover, the data suggest that heparin or
pelentan induces a vasodilator effect that cannot be attributed to a
decrease in hematocrit alone.
ARTICLES
Hemodynamic effects of chronic alteration in hematocrit in spontaneously hypertensive rats
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