Spatiotemporal pattern of neuroinflammation after impact-acceleration closed head injury in the rat.

Inflammatory processes have been implicated in the pathogenesis of traumatic brain damage. We analyzed the spatiotemporal expression pattern of the proinflammatory key molecules: interleukin-1beta, interleukin-6, tumor necrosis factor-alpha, and inducible nitric oxide synthase in a rat closed head injury (CHI) paradigm. 51 rats were used for RT-PCR analysis after CHI, and 18 for immunocytochemistry.

Continuous measurement of intracranial pressure in awake rats after experimental closed head injury.

The present study validates a method for continuous measurement of intracranial pressure (ICP) in freely moving rats after experimental induction of impact-acceleration injury. Rats subjected to either mild or moderate trauma were individually placed in a Bas-Ratturn system, equipped with a sensor that synchronously turns the cage in response to the locomotor activity of the animal. In this way correct probe positioning is permanently assured and damage due to coiling is avoided.

Ultrasound agents may open the blood-brain barrier in rats and aggravate pathologic consequences of experimental head trauma.

Unilateral intracarotid injection of contrast agents may considerably destabilize the blood-brain barrier in rats. This leads to vasogenic edema in the ipsilateral hemisphere. Mortality and extravasation increased significantly when administration of these ultrasound contrast agents was followed by mild traumatic brain injury.

Cerebral blood flow assessment with indocyanine green bolus transit detection by near-infrared spectroscopy in the rat.

In this study we evaluated the feasibility of measuring cerebral blood flow in rats by monitoring the transit of an indocyanine green bolus through the brain with multiwavelength near-infrared spectroscopy. Different volumes of a 1 mg/ml indocyanine green solution (5, 15, 25, 50 microl) were injected intravenously in the search for an optimal dose. Clear transit curves were obtained with all doses and a blood flow index could easily be determined.

Nitric oxide does not inhibit cerebral cytochrome oxidase in vivo or in the reactive hyperemic phase after brief anoxia in the adult rat.

In this study, near-infrared spectroscopy was applied to examine whether cytochrome oxidase in the rat brain is inhibited by nitric oxide in vivo. During normoxia, intravenous N(G)-nitro-L-arginine methyl ester (L-NAME) administration significantly decreased the cerebral saturation of hemoglobin with oxygen but did not alter the cytochrome oxidase redox state. Anoxia significantly reduced the cytochrome oxidase.