Role of the Hematocrit in a Rabbit Model of Arterial Thrombosis and Bleeding

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Abstract
Background: A decrease in hematocrit lengthens bleeding time. The authors studied the role of hematocrit variations in an experimental model of arterial thrombosis and bleeding. Methods: The Folts model was used in 24 rabbits. After anesthesia was induced and common monitors were positioned, the right common carotid artery was exposed and a 60% stenosis was induced. A compression injury of the artery was then produced, which triggered a series of cyclic episodes of thrombosis and clot lysis (cyclic flow reductions [CFRs]). After counting the number of CFRs that occurred in 20 min (CFR1), the animals were assigned randomly to one of three groups (n = 8 in each group): control, hemodilution with rabbit homologous platelet-rich plasma, and hemodilution with gelatin solution and then reinfusion of the shed blood. The effect of hemodilution with replacement by platelet-rich plasma or by colloid was observed by recording the number of CFRs during another 20-min period (CFR2). A third period of observation (CFR3) followed shed blood reinfusion in the gelatin solution group. Ear immersion bleeding time was recorded after each CFR period. Results: In the two experimental groups, the decrease in hematocrit (from 36 +/- 3% to 23 +/- 2% and from 38 +/- 3% to 23 +/- 2%, respectively; mean +/- SD) abolished CFRs (from a median of 4 to 0 and 7 to 0, respectively) and significantly lengthened bleeding time (from 76 +/- 24 s to 114 +/- 36 s and from 84 +/- 37 s to 127 +/- 29 s, respectively). Blood reinfusion in the group that received the gelatin solution caused CFR to reappear (CFR3 = 4). Conclusions: Decreases in hematocrit reduced the cyclic arterial thrombosis rate and increased the bleeding time in the rabbits in this study. Hematocrit normalization caused thrombosis to reappear.

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