Cerebral oxygenation and metabolism during progressive hyperthermia

Nemoto, E. M.; Frankel, Herman M.

doi:10.1152/ajplegacy.1970.219.6.1784

Cited by 46 publications

(19 citation statements)

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“…One mechanism proposed was a 5–7% increase in metabolic demand for every degree of temperature increase, in tissues with impaired blood flow [10]. However, it has been demonstrated that the cerebroprotective effect of hypothermia is not related to a decrease in metabolic demand [9, 27], or to a modification of the collateral blood flow to the ischemic regions [28].…”

Section: Discussionmentioning

confidence: 99%

“…The mechanism by which the temperature increase aggravates cerebral injury remains unclear. The hypothesis of a 5–7% increase in metabolic demand for every degree of hyperthermia [10]has not been confirmed, and the role of lactic acidosis has been refuted [11]. Recent experimental works suggested that hyperthermia-induced neuronal damage might be mediated by an excitotoxic mechanism [12]: glutamate release was significantly higher in hyperthermic animals during the intraischemic period [13].…”

Section: Introductionmentioning

confidence: 99%

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Aggravation of Acute Ischemic Stroke by Hyperthermia Is Related to an Excitotoxic Mechanism

1999

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Objective: To examine whether hyperthermia aggravates cerebral injury in acute ischemia by an excitotoxic mechanism, we studied the relationship between body temperature on admission and CSF concentrations of neuroexcitatory amino acids in 128 patients with acute ischemic stroke of less than 24 h duration. Methods: Stroke worsening was defined as the percent change between the Canadian Stroke Scale (CSS) at 48 h and the CSS on admission. Infarct volume was measured on days 4–7 on cranial computed tomography. Excitatory amino acids were analyzed using HPLC. Results: Glutamate concentration [median (min.-max.)] was 11 (2–19) µmol/l in hyperthermic patients (body temperature >37.5°C) and 5 (2–22) µmol/l in normothermic patients (p < 0.0001). Glycine concentration in hyperthermic and normothermic patients was 16 (3–21) µmol/l and 9 (3–50) µmol/l, respectively (p < 0.0001). Glutamate was significantly higher in patients with hyperthermia only during the first 12 h after the onset of symptoms. The CSF concentrations of glutamate (r = 0.52; p < 0.0001) and glycine (r = 0.62; p < 0.0001) correlated with body temperature. Body temperature was significantly related to stroke worsening and infarct size, but this effect was dependent on the glutamate effect. Conclusion: Glutamate and glycine release during the acute phase of cerebral ischemia could be responsible for the increased brain damage in hyperthermia.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Aggravation of Acute Ischemic Stroke by Hyperthermia Is Related to an Excitotoxic Mechanism

1999

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“…23 Infections can facilitate electrolytic unbalance, hypoxia, and fever, which could theoretically impair neuronal survival within the ischemic penumbra. 34 Fever may increase the cerebral metabolic demands, 35 change the blood-brain barrier permeability, and promote acidosis and release of excitatory amino acids. 36 Entry of bacteria and lypopolisaccharide into the bloodstream also favors thrombosis through tumor necrosis factor (TNF)-␣ release, 37 activation of the tissue factor-mediated extrinsic pathway of blood coagulation, 38 reduction of thrombomodulin (anticoagulant), and inhibition of the fibrinolytic system.…”

Section: Infection After Acute Stroke: Magnitude Of the Problemmentioning

confidence: 99%

Infection After Acute Ischemic Stroke

Chamorro

Urra²,

Planas³

2007

Stroke

348

161

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Background and Purpose-Infection after experimental focal ischemia may result from brain-induced immunodepression, but it is unsettled whether a similar syndrome occurs in human stroke. Summary of Review-Many patients develop infections shortly after acute stroke regardless of optimal management.Mortality is higher in these patients and the severity of stroke is the strongest determinant of the infectious risk. However, it is controversial whether infections promote neurological worsening or alternatively represent a marker of severe disease. The brain and the immune system are functionally linked through neural and humoral pathways, and decreased immune competence with higher incidence of infections has been demonstrated in several acute neurological conditions. In experimental brain ischemia, infections are associated with the activation of the autonomous nervous system and neuroendocrine pathways, which increase the strength of anti-inflammatory signals. A strong cytokinemediated anti-inflammatory response was recently observed in stroke patients at higher risk of infection, although infection could not demonstrate an independent association with the progression of the symptoms. Conclusions-The appearance of infection in patients with acute stroke obeys in part to immunological mechanisms triggered by acute brain injury. An excessive anti-inflammatory response is a key facilitating factor for the development of infection, and it is likely that this immunological response represents an adaptive mechanism to brain ischemia. Contrarily, it is unclear whether infection contributes independently to poor outcome in human stroke. Overall, a better understanding of the cross-talk between the brain and the immune system might lead to more effective therapies in patients with acute stroke.

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“…[2][3][4][5][6] The period in which hyperthermia is associated with poor outcome may be limited to the first 12 or 24 hours from stroke onset. 6,7 The harmful effects of an early rise in body temperature have been attributed to increased cerebral metabolic demands, 8 changes in the blood-brain barrier permeability, acidosis, and an increased release of excitatory amino acids. 9 In animal models of temporary focal cerebral ischemia, mild intraischemic hyperthermia increased infarct volume, 10 whereas mild hypothermia reduced infarct size.…”

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confidence: 99%

Effect of Paracetamol (Acetaminophen) on Body Temperature in Acute Ischemic Stroke

Dippel

Breda

Gemert

et al. 2001

Stroke

130

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on Behalf of the PAPAS InvestigatorsBackground and Purpose-Body temperature is a strong predictor of outcome in acute stroke. However, it is unknown whether antipyretic treatment leads to early and clinically worthwhile reduction of body temperature in patients with acute stroke, especially when they have no fever. The main purpose of this trial was to study whether early treatment of acute ischemic stroke patients with acetaminophen (paracetamol) reduces body temperature. Methods-Seventy-five patients with acute ischemic stroke confined to the anterior circulation were randomized to treatment with either 500 mg (low dose) or 1000 mg (high dose) acetaminophen or with placebo, administered as suppositories 6 times daily during 5 days. Body temperatures were measured with a rectal electronic thermometer at the start of treatment and after 24 hours and with an infrared tympanic thermometer at 2-hour intervals during the first 24 hours and at 6-hour intervals thereafter. The primary outcome measure was rectal temperature at 24 hours after the start of treatment. Results-Treatment with high-dose acetaminophen resulted in 0.4°C lower body temperatures than placebo treatment at 24 hours (95% CI 0.1°C to 0.7°C). The mean reduction from baseline temperature with high-dose acetaminophen was 0.3°C (95% CI 0°C to 0.6°C) higher than that in placebo-treated patients. Treatment with low-dose acetaminophen did not result in lower body temperatures. After 5 days of treatment, no differences in temperature were found between the placebo and the high-or low-dose acetaminophen groups. Conclusions-Treatment with a daily dose of 6000 mg acetaminophen may result in a small, but potentially beneficial, decrease in body temperature shortly after ischemic stroke, even in normothermic and subfebrile patients. Further studies should determine whether this effect is reproducible and whether early reduction of body temperature leads to improved outcome. (Stroke. 2001;32:1607-1612.)

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Cerebral oxygenation and metabolism during progressive hyperthermia

Cited by 46 publications

References 1 publication

Aggravation of Acute Ischemic Stroke by Hyperthermia Is Related to an Excitotoxic Mechanism

Aggravation of Acute Ischemic Stroke by Hyperthermia Is Related to an Excitotoxic Mechanism

Infection After Acute Ischemic Stroke

Effect of Paracetamol (Acetaminophen) on Body Temperature in Acute Ischemic Stroke

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