Substance P is Associated with the Development of Brain Edema and Functional Deficits after Traumatic Brain Injury

[1]  T. Mcintosh,et al.  The duality of the inflammatory response to traumatic brain injury , 2001, Molecular Neurobiology.

[2]  R. Vink,et al.  The temporal profile of edema formation differs between male and female rats following diffuse traumatic brain injury. , 2006, Acta neurochirurgica. Supplement.

[3]  Taeun Chang,et al.  The pathobiology of moderate diffuse traumatic brain injury as identified using a new experimental model of injury in rats , 2004, Neurobiology of Disease.

[4]  C. Bennett,et al.  Neurogenic inflammation is associated with development of edema and functional deficits following traumatic brain injury in rats , 2004, Neuropeptides.

[5]  R. Vink,et al.  Interaction between anesthesia, gender, and functional outcome task following diffuse traumatic brain injury in rats. , 2003, Journal of neurotrauma.

[6]  B. Roth,et al.  Novel Diketopiperazine Enhances Motor and Cognitive Recovery after Traumatic Brain Injury in Rats and Shows Neuroprotection In Vitro and In Vivo , 2003, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[7]  R. Vink,et al.  Magnesium attenuates persistent functional deficits following diffuse traumatic brain injury in rats , 2003, Neuroscience Letters.

[8]  R. Hamm.  Neurobehavioral assessment of outcome following traumatic brain injury in rats: an evaluation of selected measures. , 2001, Journal of neurotrauma.

[9]  M. Küçük,et al.  Magnesium sulfate attenuates increased blood-brain barrier permeability during insulin-induced hypoglycemia in rats. , 2001, Canadian journal of physiology and pharmacology.

[10]  C. Culmsee,et al.  Adaptive Plasticity in Tachykinin and Tachykinin Receptor Expression after Focal Cerebral Ischemia Is Differentially Linked to GABAergic and Glutamatergic Cerebrocortical Circuits and Cerebrovenular Endothelium , 2001, The Journal of Neuroscience.

[11]  James J. Pekar,et al.  Diffusion and High Resolution MRI of Traumatic Brain Injury in Rats: Time Course and Correlation with Histology , 2000, Experimental Neurology.

[12]  S. McMahon,et al.  Abnormal substance P release from the spinal cord following injury to primary sensory neurons , 2000, The European journal of neuroscience.

[13]  A. Marmarou,et al.  The permissive nature of blood brain barrier (BBB) opening in edema formation following traumatic brain injury. , 2000, Acta neurochirurgica. Supplement.

[14]  A. Aeron-Thomas,et al.  ESTIMATING GLOBAL ROAD FATALITIES , 2000 .

[15]  M S Kramer,et al.  Discovery of the antidepressant and anti-emetic efficacy of substance P receptor (NK1) antagonists. , 1999, Trends in pharmacological sciences.

[16]  A. Saria,et al.  The tachykinin NK1 receptor in the brain: pharmacology and putative functions. , 1999, European journal of pharmacology.

[17]  R G Hill,et al.  Distinct mechanism for antidepressant activity by blockade of central substance P receptors. , 1998, Science.

[18]  M. Morganti-Kossmann,et al.  The role of the complement system in traumatic brain injury , 1998, Brain Research Reviews.

[19]  P. Moore,et al.  Neurogenic oedema and vasodilatation: effect of a selective neuronal NO inhibitor , 1998, NeuroReport.

[20]  T. Mcintosh,et al.  Time course of cerebral edema after traumatic brain injury in rats: effects of riluzole and mannitol. , 1997, Journal of neurotrauma.

[21]  G. Levi,et al.  Functional characterization of substance P receptors on cultured human spinal cord astrocytes: Synergism of substance P with cytokines in inducing interleukin‐6 and prostaglandin E2 production , 1997, Glia.

[22]  G. Cheng,et al.  Neurokinin‐1 receptor antagonist SR140333: a novel type of drug to treat cerebral ischemia , 1997, Neuroreport.

[23]  R. Vink,et al.  Magnesium sulphate improves neurologic outcome following severe closed head injury in rats , 1997, Neuroscience Letters.

[24]  T. Phillips,et al.  Magnesium-deficiency-enhanced post-ischemic myocardial injury is reduced by substance P receptor blockade. , 1997, Journal of molecular and cellular cardiology.

[25]  T A Gennarelli,et al.  Neuropathological sequelae of traumatic brain injury: relationship to neurochemical and biomechanical mechanisms. , 1996, Laboratory investigation; a journal of technical methods and pathology.

[26]  R. Lin.  Reactive astrocytes express substance-P immunoreactivity in the adult forebrain after injury , 1995, Neuroreport.

[27]  S. Brain,et al.  An investigation into the mechanism of capsaicin‐induced oedema in rabbit skin , 1995, British journal of pharmacology.

[28]  Alan I. Faden,et al.  Diffusion‐Weighted Imaging Differentiates Ischemic Tissue From Traumatized Tissue , 1994, Stroke.

[29]  A. Marmarou,et al.  A new model of diffuse brain injury in rats. Part I: Pathophysiology and biomechanics. , 1994, Journal of neurosurgery.

[30]  A. Marmarou,et al.  A new model of diffuse brain injury in rats. Part II: Morphological characterization. , 1994, Journal of neurosurgery.

[31]  C. Pothoulakis,et al.  CP-96,345, a substance P antagonist, inhibits rat intestinal responses to Clostridium difficile toxin A but not cholera toxin. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[32]  R. Reed,et al.  Neurogenic inflammation in rat trachea is accompanied by increased negativity of interstitial fluid pressure. , 1993, Circulation research.

[33]  Y. Olsson,et al.  Met-Enkephalin-Arg6-Phe7 in spinal cord and brain following traumatic injury to the spinal cord: Influence of p-chlorophenylalanine. An experimental study in the rat using radioimmunoassay technique , 1993, Neuropharmacology.

[34]  T. Phillips,et al.  Pathobiology of magnesium deficiency: a cytokine/neurogenic inflammation hypothesis. , 1992, The American journal of physiology.

[35]  P. Hedqvist,et al.  Nerve-induced tachykinin-mediated vasodilation in skeletal muscle is dependent on nitric oxide formation. , 1991, European journal of pharmacology.

[36]  G. Wilkin,et al.  Eicosanoid synthesis by spinal cord astrocytes is evoked by substance P; possible implications for nociception and pain. , 1991, Advances in prostaglandin, thromboxane, and leukotriene research.

[37]  T. Yaksh,et al.  Intrathecal somatostatin, somatostatin analogs, substance P analog and dynorphin A cause comparable neurotoxicity in rats , 1990, Neuroscience.

[38]  P. K. Dey,et al.  Alteration of substance P after trauma to the spinal cord: An experimental study in the rat , 1990, Neuroscience.

[39]  J. Palmblad,et al.  Substance P activates and modulates neutrophil oxidative metabolism and aggregation. , 1989, The Journal of rheumatology.

[40]  R. Sarabia,et al.  Posttraumatic cerebral hemispheric swelling. Analysis of 55 cases studied with computerized tomography. , 1988, Journal of neurosurgery.

[41]  R. Sarabia,et al.  Cerebral hemisphere swelling in severe head injury patients. , 1988, Acta neurochirurgica. Supplementum.

[42]  N. Yonehara,et al.  Contribution of substance P to heat-induced edema in rat paw. , 1987, The Journal of pharmacology and experimental therapeutics.

[43]  A. Saria,et al.  Substance P in sensory nerve fibres contributes to the development of oedema in the rat hind paw after thermal injury , 1984, British journal of pharmacology.