Effects of l-arginine on cerebral blood flow, microvascular permeability, number of perfused capillaries, and brain water content in the traumatized mouse brain.
Research output: Contribution to journal › Article
It is has been suggested that decreased production of the vasodilatory and anti-aggregative substance NO (nitric oxide) may result in lower cerebral blood flow (CBF) in injured areas of the traumatized brain. The NO-precursor L-arginine has been shown to counteract CBF decreases early after trauma, but microcirculatory and more long-term effects on CBF of L-arginine have not been investigated. In an attempt to analyze effects Of L-arginine on the microcirculation in the traumatized brain, the present study was designed to evaluate the effects Of L-arginine compared to vehicle (0.9% saline) following a standardized controlled cortical-impact brain trauma in mice. Cerebral blood flow (autoradiography [C-14]-iodoantipyrine), number of perfused capillaries (FITC-dextran fluorescence technique), brain water content (wet vs. dry weight) and the blood to brain transfer constant K-i for [Cr-51]-EDTA were analyzed in the injured and the contralateral cortex. Cortical blood flow in the injured cortex was 0.43 +/- 0.3 mL/g/min and 0.8 +/- 0.3 mL/g/min 3 h after trauma in the vehicle and L-arginine groups, respectively (p < 0.05), and no treatment effect was seen 24 h after trauma. The number of perfused capillaries decreased following trauma and was unaffected by L-arginine. Ki increased following trauma and was unaffected by L-arginine. Brain water content was lower in the L-arginine group than in the vehicle group 3 h after trauma and there was no difference between the groups 24 h after trauma. We conclude that L-arginine reduces brain edema formation and improves cortical blood flow in the early phase after a brain trauma, whereas no circulatory effects can be seen after prolonged treatment.