Hemodynamic effects of chronic alteration in hematocrit in spontaneously hypertensive rats.

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Abstract
This study describes the effect of a chronic decrease in hematocrit [Hct] 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). Hct was decreased by treatment with either heparin, vitamin K inhibitor (pelentan) or by repeated Hct blood letting (BL). In SHR, a decrease in Hct, regardless of how produced, evidently was associated with a significant decrease (P < 0.01) in blood pressure. Prevention of heparin-induced decrease in Hct by repeated transfusions of red blood cells abolished the blood-pressure-lowering effect of heparin. By using combined data on Hct and systolic blood pressure in all 5-SHR groups, a significantly positive correlation and linear regression between Hct and blood pressure were obtained. When compared to control untreated SHR, heparin- or pelentan-treated SHR showed a significant (P < 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 Hct, decreased TPR and increased CO compared to control normotensive rats. However, blood pressure did not change. Results confirming previous studies and those of other investigators indicate a direct association between Hct and systemic hypertension. Lowering the Hct can effectively lower an elevated blood pressure. Heparin or pelentan evidently induces a vasodilator effect that cannot be attributed to a decrease in Hct alone.