Effects of Brain Temperature on Calmodulin and Microtubuleassociated Protein 2 Immunoreactivity in the Gerbil Hippocampus Following Transient Forebrain Ischemia

Eguchi, Yuki; Yamashita, Katsuhiro; Iwamoto, Tetsuaki; Ito, Hiroki

doi:10.1089/neu.1997.14.109

Cited by 25 publications

(11 citation statements)

References 21 publications

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“…These include (i) enhanced release of neurotransmitters [e.g., glutamate, y-aminobutyric etc. (437)]; (ii) exaggerated reactive oxygen species production (167, 235); (iii) more extensive BBB breakdown (128, 129); (iv) increased numbers of potentially damaging ischemic depolarizations in the focal ischemic penumbra (24,88); (v) impaired recovery of energy metabolism and enhanced inhibition of protein kinases (63,98); and (vi) worsening of cytoskeletal proteolysis (136,303).…”

Section: Stroke and Heat Stressmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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This review provides an in-depth update on the impact of heat stress on cerebrovascular functioning. The regulation of cerebral temperature, blood flow, and metabolism are discussed. We further provide an overview of vascular permeability, the neurocognitive changes, and the key clinical implications and pathologies known to confound cerebral functioning during hyperthermia. A reduction in cerebral blood flow (CBF), derived primarily from a respiratory-induced alkalosis, underscores the cerebrovascular changes to hyperthermia. Arterial pressures may also become compromised because of reduced peripheral resistance secondary to skin vasodilatation. Therefore, when hyperthermia is combined with conditions that increase cardiovascular strain, for example, orthostasis or dehydration, the inability to preserve cerebral perfusion pressure further reduces CBF. A reduced cerebral perfusion pressure is in turn the primary mechanism for impaired tolerance to orthostatic challenges. Any reduction in CBF attenuates the brain's convective heat loss, while the hyperthermic-induced increase in metabolic rate increases the cerebral heat gain. This paradoxical uncoupling of CBF to metabolism increases brain temperature, and potentiates a condition whereby cerebral oxygenation may be compromised. With levels of experimentally viable passive hyperthermia (up to 39.5-40.0 °C core temperature), the associated reduction in CBF (∼ 30%) and increase in cerebral metabolic demand (∼ 10%) is likely compensated by increases in cerebral oxygen extraction. However, severe increases in whole-body and brain temperature may increase blood-brain barrier permeability, potentially leading to cerebral vasogenic edema. The cerebrovascular challenges associated with hyperthermia are of paramount importance for populations with compromised thermoregulatory control--for example, spinal cord injury, elderly, and those with preexisting cardiovascular diseases.

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Section: Stroke and Heat Stressmentioning

confidence: 99%

Cerebral Vascular Control and Metabolism in Heat Stress

Bain

Nybo

Ainslie

2015

Comprehensive Physiology

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“…Hypothermia seems to counteract ischemic brain damage by several mechanisms: prevention of the blood-brain barrier disruption that happens soon after ischemic onset that allows edema formation from extravasation [19]; diminishing of oxygen-based free radical production that results from activation of microglia and other cell types [20]; reduction of the excitotoxic-neurotransmitter release that overstimulates neighboring neurons [21, 22]; lowering of metabolic rate and subsequent energy depletion [23], and anti-inflammatory action [24]. Hyperthermia is thought to be an important event accentuating biochemical and inflammatory ischemic mechanisms within the ischemic penumbra, and thus contributing to progression of the infarct brain [18].…”

Section: Control Of Body Temperaturementioning

confidence: 99%

Non-Pharmacological Neuroprotection: Role of Emergency Stroke Management

Leira¹,

Blanco²,

Rodríguez‐Yáñez³

et al. 2006

Cerebrovasc Dis

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Acute stroke should be considered a medical emergency, where actions taken in the first hours are fundamental for achieving recovery of the damaged cerebral tissue and a better prognosis for the patient. Recanalization and neuroprotective treatment has been used with mixed results. The effectiveness observed in the first hours with thrombolytic drug treatment is only applicable to a small percentage of patients, and attempts to widen this treatment window have not yet proved fruitful. Pharmacological neuroprotective treatment has not yet demonstrated the clinical effectiveness observed in experimental models. The concept of neuroprotection in cerebral ischemia also involves a series of mechanisms that take place at the cerebral level following vascular occlusion. In this context, it should be borne in mind that a series of physiological functions usually involved in the cerebral metabolism (control of blood pressure, of temperature, of glycemia and of arterial oxygen saturation) play a key role in modulation of the ischemic process. Changes in the control of these mechanisms may aggravate the process of cerebral damage in the first hours of ischemic stroke. In this work we review the prognostic importance of the main mechanisms that may influence the acute phase of cerebral ischemic stroke, as well as their therapeutic management and control in the clinical situation.

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“…The marked decrease in calmodulin and MAP2 immunoreactivity induced in the vulnerable hippocampal CA1 sector at 48 hours in normothermic animals and the subsequent delayed death of these neurons were both aggravated by mild intraischemic hyperthermia. 41 …”

Section: Cytoskeletal Degradationmentioning

confidence: 99%

Combating Hyperthermia in Acute Stroke

Ginsberg

Busto

1998

Stroke

432

210

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Background-Moderate elevations of brain temperature, when present during or after ischemia or trauma, may markedly worsen the resulting injury. We review these provocative findings, which form the rationale for our recommendation that physicians treating acute cerebral ischemia or traumatic brain injury diligently monitor their patients for incipient fever and take prompt measures to maintain core-body temperature at normothermic levels. Summary of Review-In standardized models of transient forebrain ischemia, intraischemic brain temperature elevations to 39°C enhance and accelerate severe neuropathological alterations in vulnerable brain regions and induce damage to structures not ordinarily affected. Conversely, the blunting of even mild spontaneous postischemic hyperthermia confers neuroprotection. Mild hyperthermia is also deleterious in focal ischemia, particularly in reversible vascular occlusion. The action of otherwise neuroprotective drugs in ischemia may be nullified by mild hyperthermia. Even when delayed by 24 hours after an acute insult, moderate hyperthermia can still worsen the pathological and neurobehavioral outcome. Hyperthermia acts through several mechanisms to worsen cerebral ischemia. These include (1) enhanced release of neurotransmitters; (2) exaggerated oxygen radical production; (3) more extensive blood-brain barrier breakdown; (4) increased numbers of potentially damaging ischemic depolarizations in the focal ischemic penumbra; (5) impaired recovery of energy metabolism and enhanced inhibition of protein kinases; and (6) worsening of cytoskeletal proteolysis. Recent studies demonstrate the feasibility of direct brain temperature monitoring in patients with traumatic and ischemic injury. Moderate to severe brain temperature elevations, exceeding core-body temperature, may occur in the injured brain. Cerebral hyperthermia also occurs during rewarming after hypothermic cardiopulmonary bypass procedures. Several studies have now shown that elevated temperature is associated with poor outcome in patients with acute stroke. Finally, recent clinical trials in severe closed head injury have shown a beneficial effect of moderate therapeutic hypothermia. Conclusions-The acutely ischemic or traumatized brain is inordinately susceptible to the damaging influence of even modest brain temperature elevations. While controlled clinical investigations will be required to establish the therapeutic efficacy and safety of frank hypothermia in patients with acute stroke, the available evidence is sufficiently compelling to justify the recommendation, at this time, that fever be combated assiduously in acute stroke and trauma patients, even if "minor" in degree and even when delayed in onset. We suggest that body temperature be maintained in a safe normothermic range (eg, 36.7°C to 37.0°C [98.0°F to 98.6°F]) for at least the first several days after acute stroke or head injury. (Stroke. 1998;29:529-534.)

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Effects of Brain Temperature on Calmodulin and Microtubuleassociated Protein 2 Immunoreactivity in the Gerbil Hippocampus Following Transient Forebrain Ischemia

Cited by 25 publications

References 21 publications

Cerebral Vascular Control and Metabolism in Heat Stress

Cerebral Vascular Control and Metabolism in Heat Stress

Non-Pharmacological Neuroprotection: Role of Emergency Stroke Management

Combating Hyperthermia in Acute Stroke

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