Effects of Defibrination on Hemorheology, Cerebral Blood Flow Velocity, and CO 2 Reactivity During Hypocapnia in Normal Subjects

Abstract

Background and Purpose Plasma fibrinogen is reported to be an independent risk factor for stroke and cardiovascular diseases. The effects of defibrination on hemorheology, middle cerebral artery (MCA) blood flow velocity, and CO 2 reactivity during hypocapnia were evaluated in normal subjects. Methods Twenty-five healthy subjects (mean age, 31.8±5.7 years) were included in the study. Measurements were done at rest and repeated 24 hours after administration of 10 batroxobin units. Plasma fibrinogen, plasma viscosity, and whole blood viscosity were measured as hemorheological factors. MCA blood flow velocity was measured with a transcranial Doppler flowmeter. Blood flow velocity was corrected to 40 mm Hg of end-tidal CO 2 partial pressure (P etco 2 ), and expressed as CV 40 . CO 2 reactivity was measured as percent change in mean blood flow velocity per millimeter of mercury P etco 2 . Results Plasma fibrinogen (from 7.04 to 2.29 μmol/L; P <.001), whole blood viscosity, and plasma viscosity decreased after administration of batroxobin. Mean MCA blood flow velocity at rest, CV 40 , and CO 2 reactivity during hypocapnia increased significantly (from 67.4 to 73.6 cm/s, from 71.7 to 77.7 cm/s, and from 2.9%/mm Hg to 3.2%/mm Hg, respectively; P <.01) after defibrination. Mean arterial blood pressure and P etco 2 at rest were constant before and 24 hours after administration of batroxobin. There was a significant positive correlation between CV 40 and CO 2 reactivity ( r =.623, P <.0001). Conclusions The increase in MCA blood flow velocity was associated with improved CO 2 reactivity and reduced blood viscosity after defibrination. The data may suggest that defibrination increases cerebral blood flow by reducing blood viscosity.