Changes of nitric oxide and its relationship with clinical features intracranial pressure and outcome in acute head injury

Abstract

To investigate the content and dynamics of nitric oxide (-NO) in the cerebrospinal fluid (CSF) of patients with acute head injury and to clarify the relationship of NO with clinical features and intracranial pressure (ICP) as well as outcomes, 38 adults with acute head injury were studied. Glasgow Coma Scale (GCS) obtained at admission and Glasgow Outcome Scale (GOS) 3 months after injury was assessed.ICP was surveyed via intraventricular catheter and lumbar puncture and CSF samples were obtained simultaneously. NO was determined with Griess reagents. Results showed that NO peak content in the head injury group was significantly higher than that of the control group. During dynamic research, no peak content of mildly injured cases and severely injured ones appeared in different time windows respectively. The peak value of NO was distinctly higher in the severe group than in the mild group. NO peak value of the raised ICP group was remarkably higher than that of the normal ICP group. The peak value of NO was considerately higher in the poor outcome group than in the good outcome group. When the content of NO was, over 6. 5 μmol/L., the rate of poor outcome was increased. There existed a correlation between NO and GCS, ICP and GOS. It is concluded that the content of NO was increased in patients with acute head injury and the changes of NO had different time windows in severely injured patients and mildly injured ones. The more sever the injury, the higher the NO content; and the more serious the secondary brain injury and brain edema, the worse the outcomes. When NO is combined with GCS, GOS and ICP, it increases the accuracy of judgement to the degree of head injury and outcome.

Keywords

nitric oxide / Glasgow coma scale / intracranial pressure / Glasgow outcome scale / head injury

References

[1] SharmaA C, MisraM, PratR, et al.. A differential response of diffuse brain injury on the concentrations of endothelium and nitric oxide in the plasma and brain region in rats. Neurol Res, 1998, 20: 632-632

[2] KumuraE, KosakaH, ShigaT, et al.. Elevation of plasma nitric oxide end products during focal cerebral ischemia and reperfusion in the rat. J Cereb Blood Flow Metab, 1994, 14: 487-487

[3] MesengeC, VerrecchiaC, AllixM, et al.. Reduction of the neurological deficit mice with traumatic brain injury by nitric oxide synthase inhibitors. J Neurotrauma, 1996, 13: 209-209

[4] IadecolaC, ZhangF, XuX. Inhibition of inducible nitric oxide synthase ameliorates cerebral ischemia damage. Am J Physiol, 1995, 268: R286-R286

[5] HewettS J, MuirJ K, LobnerD, et al.. Potentiation of oxygen-glucose deprivation-induced neuronal death after induction of iNOS. Stroke, 1996, 27: 1586-1586

[6] FaraciF M, BrianJ E. Nitric oxide and the cerebral circulation. Stroke, 1994, 25: 692-692

[7] AlagarsamyS, De WittD S, JohnsonK M. Effects of moderate, central fluid percussion traumatic brain injury on nitric oxide synthase activity in rats. J Neurotrauma, 1998, 15: 627-627

[8] RaoA M, DoganA, HatcherJ F, et al.. Fluorometric assay of nitric and nitrate in brain tissue after traumatic brain injury and cerebral ischemia. Brain Res, 1998, 793: 265-265

[9] GoldingE M, SteenbergM L, CherianL, et al.. Endothelial-mediated dilations following severe controlled cortical impact injury in the rat middle cerebral artery. J Neurotrauma, 1998, 15: 635-635

[10] CobbsC S, FenoyA, BredtD S, et al.. Expression of nitric oxide synthase in the cerebral microvasculature after traumatic brain injury in the rat. Brain Res, 1997, 751: 336-336

[11] MesengeC, Charriaut-MarlangueC, VerrecchiaC, et al.. Reduction of tyrosine nitration after N-nitro-L-arginine methylester treatment of mice with traumatic brain injury. Eur J Pharmacol, 1998, 353: 53-53

[12] 1997,20:67

[13] SakamotoK I, FujisawaH, KoizumiH, et al.. Effects of hypothermia on nitric oxide synthesis following contusion trauma in the rat. J Trauma, 1997, 14: 349-349