Testing of cerebral endothelium function with L-arginine after stroke

Endothelium-dependent vasodilatation could be impaired during hypoperfusion. L-arginine (L-A), a precursor of nitric oxide, is able to elicit endothelium-dependent vasodilatation. To determine cerebral vascular endothelial function in the early stages after ischemic stroke, we studied cerebrovascular reactivity to L-A with transcranial Doppler (TCD).

The study group consisted of 15 patients with the middle cerebral artery syndrome, aged 57.6+/-9.8 years. They were investigated on days 7 to 10 after ischemic stroke. The control group consisted of 15 healthy volunteers, aged 58+/-10.7 years. All subjects received an intravenous infusion of L-A over 20 min at a rate of 1.5 g/min. The mean arterial velocity (vm) was measured in both middle cerebral arteries by using a bitemporal monitoring system (Multi-Dop X4, DWL). At the same time, the mean arterial pressure (MAP) and heart rate (HR) were measured by Finapres and ECG. The end-tidal CO2 (Et-Co2) was monitored by capnograph. The Vm over 5-min intervals at rest and during the infusion of L-A was determined by using the DWL TCD8 software.

The Vm significantly increased in both hemispheres of both groups (p=0.00). Vm differences between rest and L-A stimulation were lower in the ischemic hemispheres compared to the healthy ones (p=0.00), but did not differ between the ischemic hemispheres and hemispheres of the healthy group (p>0.05). MAP, HR and Et-Co2 did not change during the infusion (p>0.05).

Cerebrovascular reactivity to L-A is impaired in patients with recent stroke. The amino acid could thus be useful in testing endothelium function both in healthy persons and in stroke patients since endothelium dysfunction seems to be an important factor in reperfusion injury.