Sustained
high blood pressure causes functional changes in both vascular endothelial cells and platelets. Therefore, we hypothesized that in vivo platelet
thrombus formation would be increased in the cremaster muscle microvessels of rats during genetic
hypertension. Experiments were carried out on spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY) at 12 weeks of age.
Fluorescein isothiocyanate tagged to
bovine serum albumin (
FITC-BSA) was injected intraarterially and 450 to 490 nm light was used to activate the
FITC-BSA and induce a
thrombus within the vasculature. In vivo television microscopy was used to quantitate
thrombus formation and microvascular diameter changes. The time of platelet
thrombus initiation and subsequent time of
thrombus growth were studied at wall shear rates of approximately 2000 sec(-1) and 270 sec(-1) in third-order arterioles and venules, respectively. In SHR, times for platelet
thrombus initiation and vessel occlusion were significantly less in both arterioles and venules, whereas time for platelet
thrombus growth following initiation was significantly prolonged. Greater shear rates in arterioles compared to venules decreased platelet adhesion and subsequently decreased the rate of
thrombus formation in both WKY and SHR groups. However, the ratio of WKY to SHR platelet
thrombus growth (platelet aggregation) time remained similar (0.83 +/- 0.06 in arterioles and 0.79 +/- 0.06 in venules). These results indicate that there is increased
thrombus formation during
hypertension and that the platelet adhesion processes may be of greater importance than platelet aggregation in producing this increase.