Dabigatran prevents α-thrombin-induced loss of microvessel basal
lamina matrix proteins in vivo. In a balanced
factorial design, employing 32 animals, stereotaxic striatal
injection of 40 mU α-thrombin significantly decreased microvessel
basal lamina collagen IV (α1-chain), laminin (β1-chain), and
perlecan immunoreactivity (black bars) compared to placebo in
subjects fed placebo-containing chow, while dabigatran ingestion
prevented this decrease (white bars). Upper graph. Collagen IV. A
GLM analysis of subsequent microvessel collagen IV (α1-chain)
immunoreactivity with main effects α-thrombin and dabigatran, found
a significant α-thrombin effect (p = 0.001), a
borderline significant dabigatran effect
(p = 0.063), and a large α-thrombin × dabigatran
interaction (p = 0.001), owing to the significantly
lower level of collagen IV immunoreactivity (placebo chow–α-thrombin
group). Middle graph. Laminin. Similarly, for the laminin β1-chain a
significant α-thrombin effect (p = 0.019), a
non-significant dabigatran effect (p = 0.125), and
a significant α-thrombin × dabigatran interaction
(p = 0.036) were found, owing to the
significantly lower level of laminin immunoreactivity (placebo
chow–α-thrombin group). Lower graph. Perlecan.Continued.For
microvessel perlecan immunoreactivity significant main effects for
α-thrombin (p = 0.002) and for dabigatran
(p = 0.008) and a significant
α-thrombin × dabigatran interaction (p = 0.005)
were found. The significant interaction owes to the significantly
decreased perlecan immunoreactivity in the placebo chow–α-thrombin
group relative to the other groups (Bonferroni, α = 0.05).