Brain Temperature Alters Hydroxyl Radical Production During Cerebral Ischemia/Reperfusion in Rats

Kil, Hae Keum; Piantadosi, Claude A.

doi:10.4097/kjae.1994.27.9.1035

Cited by 58 publications

(71 citation statements)

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“…Although temperature-dependent neuronal death has been attributed to release of glutamate from synaptic vesicles (Arai et al, 1993), intracel- (Mitani et al, 1991) and production of free radicals (Kil et al, 1996), the present findings suggest that Zn 2 þ translocation from Zn 2 þ -enriched (ZEN) neuronal terminals into postsynaptic neurons is also temperature-dependent. The higher the pre/post-TBI brain temperature, the more vesicular zinc was released at 1 h after TBI, and the more TSQ-positive and eosinophilic neurons were identified 6 h after TBI.…”

Section: Discussionmentioning

confidence: 51%

“…Systemic hypothermia, which inhibits neuronal release of glutamate, prevents or reduces neuronal death after cerebral ischemia (Busto et al, 1987(Busto et al, , 1989Churn et al, 1990;Dietrich et al, 1993;Hu et al, 1995;Kil et al, 1996;Minamisawa et al, 1990a;Rosomoff, 1959;Tanimoto and Okada, 1987), prolonged seizures (Liu et al, 1993;Lundgren et al, 1994) and traumatic brain injury (TBI) (Clifton et al, 1991), especially if initiated before an insult. Conversely, hyperthermia aggravates the neuronal death produced by those conditions (Dietrich, 1992;Dietrich et al, 1996;Lundgren et al, 1994;Minamisawa et al, 1990b).…”

Section: Introductionmentioning

confidence: 99%

“…Many processes related to neuronal injury are temperature-dependent, including the release of glutamate from synaptic vesicles (Arai et al, 1993;Zornow, 1995), intracellular accumulation of Ca 2 þ (Mitani et al, 1991), modulation of calcium/calmodulin-dependent protein kinase (Churn et al, 1990) and production of free radicals (Kil et al, 1996). Any or all of those temperature dependencies could contribute to the influence of temperature on neuronal injury after TBI.…”

Section: Introductionmentioning

confidence: 99%

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Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Suh

Frederickson

Danscher

2006

J Cereb Blood Flow Metab

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Hypothermia reduces excitotoxic neuronal damage after seizures, cerebral ischemia and traumatic brain injury (TBI), while hyperthermia exacerbates damage from these insults. Presynaptic release of ionic zinc (Zn 2 þ ), translocation and accumulation of Zn 2 þ ions in postsynaptic neurons are important mechanisms of excitotoxic neuronal injury. We hypothesized that temperature-dependent modulation of excitotoxicity is mediated in part by temperature-dependent changes in the synaptic release and translocation of Zn 2 þ . In the present studies, we used autometallographic (AMG) and fluorescent imaging of N-(6-methoxy-8-quinolyl)-para-toluenesulfonamide (TSQ) staining to quantify the influence of temperature on translocation of Zn 2 þ into hippocampal neurons in adult rats after weight drop-induced TBI. The central finding was that TBI-induced Zn 2 þ translocation is strongly influenced by brain temperature. Vesicular Zn 2 þ release was detected by AMG staining 1 h after TBI. At 301C, hippocampus showed almost no evidence of vesicular Zn 2 þ release from presynaptic terminals; at 36.51C, the hippocampus showed around 20% to 30% presynaptic vesicular Zn 2 þ release; and at 391C vesicular Zn 2 þ release was significantly greater (40% to 60%) than at 36.51C. At 6 h after TBI, intracellular Zn 2 þ accumulation was detected by the TSQ staining method, which showed that Zn 2 þ translocation also paralleled the vesicular Zn 2 þ release. Neuronal injury, assessed by counting eosinophilic neurons, also paralleled the translocation of Zn 2 þ , being minimal at 301C and maximal at 391C. We conclude that pathological Zn 2 þ translocation in brain after TBI is temperature-dependent and that hypothermic neuronal protection might be mediated in part by reduced Zn 2 þ translocation.

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Section: Discussionmentioning

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Suh

Frederickson

Danscher

2006

J Cereb Blood Flow Metab

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“…As we and others have shown, sustained hyperthermia markedly enhances the neurotoxic damage produced by MDMA (Colado et al, 1998b;Broening et al, 1995) presumably because hyperthermia is conducive to enhancing free radical production (Kil et al, 1996). If L-DOPA produced a sustained hyperthermia in the strain of rats used by Schmidt et al (1990) rather than the more transient e ect we observed, then neurotoxic damage would probably be increased.…”

Section: Discussionmentioning

confidence: 67%

Studies on the role of dopamine in the degeneration of 5‐HT nerve endings in the brain of Dark Agouti rats following 3,4‐methylenedioxymethamphetamine (MDMA or ‘ecstasy’) administration

Colado

O’Shea

Granados

et al. 1999

British J Pharmacology

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1 We investigated whether dopamine plays a role in the neurodegeneration of 5-hydroxytryptamine (5-HT) nerve endings occurring in Dark Agouti rat brain after 3,4-methylenedioxymethamphetamine (MDMA or`ecstasy') administration. 2 Haloperidol (2 mg kg 71 i.p.) injected 5 min prior and 55 min post MDMA (15 mg kg 71 i.p.) abolished the acute MDMA-induced hyperthermia and attenuated the neurotoxic loss of 5-HT 7 days later. When the rectal temperature of MDMA+haloperidol treated rats was kept elevated, this protective e ect was marginal. 3 MDMA (15 mg kg 71 ) increased the dopamine concentration in the dialysate from a striatal microdialysis probe by 800%. L-DOPA (25 mg kg 71 i.p., plus benserazide, 6.25 mg kg 71 i.p.) injected 2 h after MDMA (15 mg kg 71 ) enhanced the increase in dopamine in the dialysate, but subsequent neurodegeneration was unaltered. L-DOPA (25 mg kg 71 ) injected before a sub-toxic dose of MDMA (5 mg kg 71 ) failed to induce neurodegeneration. 4 The MDMA-induced increase in free radical formation in the hippocampus (indicated by increased 2,3-and 2,5-dihydroxybenzoic acid in a microdialysis probe perfused with salicylic acid) was unaltered by L-DOPA. 5 The neuroprotective drug clomethiazole (50 mg kg 71 i.p.) did not in¯uence the MDMA-induced increase in extracellular dopamine. 6 These data suggest that previous observations on the protective e ect of haloperidol and potentiating e ect of L-DOPA on MDMA-induced neurodegeneration may have resulted from e ects on MDMA-induced hyperthermia. 7 The increased extracellular dopamine concentration following MDMA may result from e ects of MDMA on dopamine re-uptake, monoamine oxidase and 5-HT release rather than aǹ amphetamine-like' action on dopamine release, thus explaining why the drug does not induce degeneration of dopamine nerve endings.

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“…Hypothermia does not affect CBF during complete global ischemia (Busto et al, 1987;Jiang et al, 1994;Kil et al, 1996;Sonn et al, 2002;Sugimura et al, 1998); global ischemia reduces CBF to less than 5% of normal (Busto et al, 1987), making it unlikely that hypothermia would have a further significant effect on CBF. However, there are a wide range of findings on CBF after reperfusion in global ischemia: hypothermia increases (Jenkins et al, 2001;Jiang et al, 1994;Karibe et al, 2000), decreases (Huang et al, 1999;Mori et al, 1998), or has no effect on CBF (Baldwin et al, 1991;Hoffman and Thomas, 1996;Horiguchi et al, 2003;Kil et al, 1996;Sonn et al, 2002;Sugimura et al, 1998).…”

Section: Cerebral Blood Flowmentioning

confidence: 99%

General versus Specific Actions of Mild-Moderate Hypothermia in Attenuating Cerebral Ischemic Damage

Zhao

Steinberg

Sapolsky

2007

J Cereb Blood Flow Metab

155

135

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Mild or moderate hypothermia is generally thought to block all changes in signaling events that are detrimental to ischemic brain, including ATP depletion, glutamate release, Ca 2 + mobilization, anoxic depolarization, free radical generation, inflammation, blood-brain barrier permeability, necrotic, and apoptotic pathways. However, the effects and mechanisms of hypothermia are, in fact, variable. We emphasize that, even in the laboratory, hypothermic protection is limited. In certain models of permanent focal ischemia, hypothermia may not protect at all. In cases where hypothermia reduces infarct, some studies have overemphasized its ability to maintain cerebral blood flow and ATP levels, and to prevent anoxic depolarization, glutamate release during ischemia. Instead, hypothermia may protect against ischemia by regulating cascades that occur after reperfusion, including blood-brain barrier permeability and the changes in gene and protein expressions associated with necrotic and apoptotic pathways. Hypothermia not only blocks multiple damaging cascades after stroke, but also selectively upregulates some protective genes. However, most of these mechanisms are addressed in models with intraischemic hypothermia; much less information is available in models with postischemic hypothermia. Moreover, although it has been confirmed that mild hypothermia is clinically feasible for acute focal stroke treatment, no definite beneficial effect has been reported yet. This lack of clinical protection may result from suboptimal criteria for patient entrance into clinical trials. To facilitate clinical translation, future efforts in the laboratory should focus more on the protective mechanisms of postischemic hypothermia, as well as on the effects of sex, age and rewarming during reperfusion on hypothermic protection.

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Brain Temperature Alters Hydroxyl Radical Production During Cerebral Ischemia/Reperfusion in Rats

Cited by 58 publications

References 0 publications

Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Neurotoxic Zinc Translocation into Hippocampal Neurons is Inhibited by Hypothermia and is Aggravated by Hyperthermia after Traumatic Brain Injury in Rats

Studies on the role of dopamine in the degeneration of 5‐HT nerve endings in the brain of Dark Agouti rats following 3,4‐methylenedioxymethamphetamine (MDMA or ‘ecstasy’) administration

General versus Specific Actions of Mild-Moderate Hypothermia in Attenuating Cerebral Ischemic Damage

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