In a study, an experimental apoplectic stroke was provoked in experimental animals. The blood supply and the electrical activity was registered to a peripheral area of the damage. As the blood vessels were closed, the blood supply to the area was drastically reduced, and the EEG impulses ceased to appear.
Concurrently with infusing the amino acid L-arginine, the blood supply to the area was again increased. When the blood supply reached a critical limit of 30 - 35% of the initial value, it was possible to measure the normal electrical activity of the brain returning.
By inhibiting the formation of nitric oxide (NO) and by using another technique, the researchers were able to demonstrate that the positive effect of L-arginine was attributable to its formation of NO.
For this reason, the maintenance of the blood supply to a damaged area by means of NO is important. NO has many functions in case of an apoplectic stroke.
As a result of the reduced blood supply to the damaged area, glutamate is released and a large influx of calcium into the cells occurs. In this way, larger amounts of NO is produced inside the cells. The process is self-increasing and as a consequence of this, large amounts of free radicals are produced.
The reason why L-arginine is capable of improving the blood supply to the brain and its electrical activity is believed to depend upon the large amount of NO in the brain cells consuming a large part of the existing arginine. As the arginine is consumed in this way, there will not be enough L-arginine in order for the endothelial cells to produce sufficient amounts of NO.
By administering an intravenous L-arginine drip, it would probably be possible to improve the early and very important first aid treatment of apoplectic strokes as early as in the ambulance.