Effects of Mild Hypothermia on Nitric Oxide Synthesis Following Contusion Trauma in the Rat

Sakamoto, Kenichi; Fujisawa, Hironori; Koizumi, Hiroyasu; Tsuchida, Eiji; Ito, Hiroki; Sadamitsu, Daikai; Maekawa, Taira

doi:10.1089/neu.1997.14.349

Cited by 65 publications

(27 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…After trauma, a very short-lasting peak of NO concentration as well as a transient rise in constitutive, i.e., eNOS and nNOS activity was described to occur in animals that underwent CCI trauma. [17][18][19][20][21] Within seconds after the insult, both NO concentration and cNOS activity decrease significantly and remain suppressed for up to 7 days. [17][18][19][20]22,23 NOS downregulation is most prominent in the tissue adjacent to the lesion.…”

Section: Discussionmentioning

confidence: 99%

Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

Terpolilli¹,

Kim²,

Thal³

et al. 2012

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood-brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

Terpolilli¹,

Kim²,

Thal³

et al. 2012

J Cereb Blood Flow Metab

View full text Add to dashboard Cite

show abstract

“…A previous study by Kader et al (1994) reported that mild hypothermia inhibited the activation of NOS following focal cerebral ischemia in rats. Sakamoto et al (1997) …”

mentioning

confidence: 99%

Effects of Moderate Hypothermia on Constitutive and Inducible Nitric Oxide Synthase Activities After Traumatic Brain Injury in the Rat

Chatzipanteli

Wada

Busto

et al. 1999

Journal of Neurochemistry

View full text Add to dashboard Cite

Abstract:We investigated the effects of therapeutic hypothermia (30°C) on alterations in constitutive (cNOS) and inducible (iNOS) nitric oxide synthase activities following traumatic brain injury (TSI). Male Sprague-Dawley rats were anesthetized with 0.5% halothane and underwent moderate (1.8-2.2 atm) parasagittal fluid-percussion (F-P) brain injury. In normothermic rats (37°C) the enzymatic activity of cNOS was significantly increased at 5 min within the injured cerebral cortex compared with contralateral values (286.5 t 68.9% of contralateral value; mean ? SEM). This rise in nitric oxide synthase activity was significantly reduced with pretraumatic hypothermia (138.8 t 17% of contralateral value; p < 0.05). At 3 and 7 days after normothermic TBI the enzymatic activity of cNOS was decreased significantly (30 f 8.4 and 28.6 t 20.9% of contralateral value, respectively; p < 0.05). However, immediate posttraumatic hypothermia (3 h at 30°C) preserved cNOS activity at 3 and 7 days (69.5 f 23.3 and 78.6 ? 7.6% of contralateral value, respectively; mean ? SEM; p < 0.05). Posttraumatic hypothermia also significantly reduced iNOS activity at 7 days compared with normothermic rats (0.021 t 0.06 and 0.23 2 0.06 pmol/mg of proteidmin, respectively; p < 0.05). The present results indicate that hypothermia (a) decreases early cNOS activation after TBI, (b) preserves cNOS activity at later periods, and (c) prevents the delayed induction of iNOS. Temperature-dependent alterations in cNOS and iNOS enzymatic activities may participate in the neuroprotective effect of hypothermia in this TBI model. Key Words: Hypothermia-Nitric oxideConstitutive nitric oxide synthase-Inducible nitric oxide synthase-Fluid-percussion brain injury.

show abstract

“…Sakamoto et al [393] used in vivo brain dialysis and CZE analysis of NO 2 − and NO 3 − to study the effects of mild hypothermia on trauma-induced synthesis of NO in the rat parietal cortex after traumatic brain injury. They showed a significant increase in NO end-products in samples from posttraumatic rats.…”

Section: Microdialysis and Push-pull Sampling Hpce Of No Metabolitesmentioning

confidence: 99%

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

Boudko

2007

Journal of Chromatography B

View full text Add to dashboard Cite

This review briefly summarizes recent progress in fundamental understanding and analytical profiling of the L-arginine/nitric oxide (NO) pathway. It focuses on key analytical references of NO actions and on the experimental acquisition of these references in vivo, with capillary electrophoresis (CE) and high-performance capillary electrophoresis (HPCE) comprising one of the most flexible and technologically promising analytical platform for comprehensive high-resolution profiling of NO-related metabolites. Second aim of this review is to express demands and bridge efforts of experimental biologists, medical professionals and chemical analysis-oriented scientists who strive to understand evolution and physiological roles of NO and to develop analytical methods for use in biology and medicine.

show abstract

Effects of Mild Hypothermia on Nitric Oxide Synthesis Following Contusion Trauma in the Rat

Cited by 65 publications

References 24 publications

Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

Effects of Moderate Hypothermia on Constitutive and Inducible Nitric Oxide Synthase Activities After Traumatic Brain Injury in the Rat

Bioanalytical profile of the l-arginine/nitric oxide pathway and its evaluation by capillary electrophoresis

Contact Info

Product

Resources

About