Secondary growth of a cortical necrosis: effect of NOS inhibition by aminoguanidine post insult.

Background: A cortical tissue necrosis from a focal freezing injury expands to 140% of its initial volume within 24 hrs in rats. Previous studies of our laboratory have shown that administration of the NOS inhibitor aminoguanidine (AG) prior to trauma attenuates this process of secondary brain damage. Objective of the present study was to analyse whether this agent is also protective when treatment commences after the insult.

Nitric oxide in the penumbra of a focal cortical necrosis in rats.

After a focal cortical freezing lesion in rats, nitric oxide (NO) end products were studied with microdialysis in the extracellular space of the penumbra throughout the whole period of secondary expansion of the cortical necrosis (i.e. 24 h).

Measurement of absolute values of hemoglobin oxygenation in the brain of small rodents by near infrared reflection spectrophotometry.

Reflection near infrared spectroscopy (reNIRS) has been proposed as a novel technique for the measurement of absolute values of total hemoglobin (tHb), oxygenated hemoglobin (oxHb), hemoglobin saturation (SO2), and cytochrome aa3 oxidation status (oxCyt aa3) in living tissue. In this study, we evaluated reNIRS during physiological cerebral blood flow conditions in rats (n=6) and during the induction of global cerebral ischemia in gerbils (n=6). ReNIRS parameters were assessed over the exposed cerebral cortex and compared to regional cerebral blood flow (rCBF) data obtained by laser Doppler flowmetry.

Attenuation of secondary lesion growth in the brain after trauma by selective inhibition of the inducible NO-synthase.

In previous studies we have demonstrate that aminoguanidine pretreatment attenuates the secondary necrosis growth after focal brain trauma. Purpose of the present investigation was to elucidate the therapeutic potential of this iNOS-inhibitor when administered post lesion. Sprague-Dawley rats were subjected to a highly standardized cortical freezing lesion and administered with aminoguanidine (100 mg/kg i.

Interstitial lactate in the peritraumatic penumbra of rat brain.

A traumatic brain tissue necrosis is expanding to approximately 150% within 24 h after lesion. This process is accompanied by marked reduction of the perifocal cerebral blood flow likely to activate anaerobic glycolysis from a reduced O2-supply leading to an accumulation of lactic acid. The current study was carried out to assess the interstitial levels of lactic acid as a potential factor of secondary brain damage.