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PubMed1983

Effects of naloxone on systemic and cerebral responses to experimental concussive brain injury in cats.

This study examined the effects of bolus injections of naloxone hydrochloride, a specific narcotic antagonist, on systemic cardiovascular function, intracranial and cerebral perfusion pressures, blood gas status, and cortical encephalograms (EEG's) in 38 cats after two different grades of experimental brain injury. Naloxone had no prolonged effects on uninjured control animals. However, as compared to a saline-injected control group, naloxone significantly reversed the hypotension and reduction in pulse pressure seen after higher grades of injury. These changes persisted for at least 60 minutes after injection and were accompanied by increased intracranial and perfusion pressures. More severely injured hypotensive cats injected with naloxone also had higher values of arterial pO2 and pH, lower pCO2, as well as higher EEG amplitudes. In less severely injured normotensive cats, naloxone produced greater effects on cardiovascular variables and intracranial pressure when injected 15 minutes rather than 45 minutes after injury. These data suggest that endogenous opiates may contribute to some instances of hypotension seen after concussive brain injury. Levels of endogenous opiates may also increase transiently even with lesser degrees of injury not associated with hypotension. The possible clinical application of narcotic antagonists to the treatment of head injury is discussed.

Animals↗
PubMed1995

Lactate accumulation following concussive brain injury: the role of ionic fluxes induced by excitatory amino acids.

During the first few minutes following traumatic brain injury, cells are exposed to an indiscriminate release of glutamate from nerve terminals resulting in a massive ionic flux (e.g., K+ efflux) via stimulation of excitatory amino acid (EAA)-coupled ion channels. The present study was undertaken to elucidate the causal relationship between these ionic shifts and lactate accumulation in the injured brain, by examining the effects of ouabain (an inhibitor of Na+/K+-ATPase), Ba2+ (an inhibitor or non-energy-dependent glial K+ uptake) and kynurenic acid (KYN; a broad-spectrum EAA antagonist) on lactate accumulation. Two microdialysis probes were placed bilaterally in the rat parietal cortex. One was perfused with a test drug (1.0 mM ouabain, 2.0 mM Ba2+ or 10 mM KYN) and the other with Ringer's solution (control) for 30 min prior to injury. Following a 2.2-2.7 atm fluid-percussion injury, lactate levels in the dialysate increased (up to 116.6% above baseline) for the first 16 min and returned to baseline levels within 20 min after injury. This lactate accumulation was attenuated by preinjury administration of ouabain and KYN and was prolonged by Ba2+ administration. These findings indicate that lactate accumulations following concussive brain injury is a result of increased glycolysis which supports ion-pumping mechanisms, thereby, restoring the ionic balance which was disrupted by stimulation of EAA-coupled ion channels.

Animals↗
PubMed1981

Cyclooxygenase products of arachidonic acid metabolism in cat cerebral cortex after experimental concussive brain injury.

Previous studies have suggested that following experimental fluid percussion brain injury, increased prostaglandin (PG) synthesis, with its concomitant production of oxygen free radicals, causes functional and morphological abnormalities of the cerebral arterioles. The purpose of this study was to chemically determine if PGs are altered following this injury. To facilitate interpretation of neurochemical measurements the cats were ventilated, blood pressure was measured, and a cranial window, for microscopic observation of pial arteriolar diameter was inserted. PG levels were determined in quick-frozen cortical tissue removed from control and 3 groups of injured cats at 1.5, 8,0, and 60 min after injury. Analysis of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha was performed by HPLC and GC/MS. The control levels of PGE2, PGF2 alpha, and 6-keto-PGF1 alpha were 216 +/- 44, 210 +/- 48, and 48 +/- 12 ng/g wet weight, respectively. Following injury, produced by a 22 ms increase in intracranial pressure, the pial arterioles dilated irreversibly and a transient hypertensive response occurred, thereby producing hyperemia. During the maximum hyperemic response, the total PGs were 75% of control. At 8 min after injury, when blood pressure returned to control level, the PGs were 158% of control and PGs fell to 111% of control at 60 min. These experiments supported our previous studies implicating increased PG synthesis in te genesis of the physiologic and morphologic sequelae of experimental concussive brain injury.

Animals↗
PubMedDate not supplied

[Epidemiology, diagnosis and prognosis in the clinical syndrome of brain concussion].

The paper is a continuation of the preliminary communication in Neurologia i Neurochirurgia Polska No 3/1995. The study in 1993-1995 included a group of 50 patients who had clinical symptom complex of brain concussion. After preliminary neurological assessment within 3 days in all cases brain CT and cerebral perfusion determination (SPECT M-PAO) were obtained. Focal reduction of blood flow was demonstrated in 47 cases, mostly in the temporal area (78%). In 30 cases EEG was done finding in 18 disturbances of cerebral electric activity. In 9 cases neuropsychological examination was done. After 3 months control study of cerebral perfusion was done in 28 cases and in 27 flow changes were found to persist. Another follow-up examination in 6 cases after a year demonstrated in all of them focal disturbances of cerebral blood flow associated with symptoms of postconcussion syndrome.

Adult↗