Transient hyperthermia protects against subsequent forebrain ischemic cell damage in the rat

Chopp, Michael; Chen, H.; Ho, Khang-Loon; Dereski, Mary O.; Brown, Eileen; Hetzel, Fred W.; Welch, K. M. A.

doi:10.1212/wnl.39.10.1396

Cited by 254 publications

(69 citation statements)

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“…Prior heat stress has been shown to protect against injury in a number of biological systems (28)(29)(30). This study confirms that a similar protection against hypoxia and reoxygenation is seen within rabbit right ventricular papillary muscles.…”

Section: Discussionmentioning

confidence: 99%

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Marber¹,

Walker²,

Latchman³

et al. 1994

J. Clin. Invest.

117

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The aims of this study were to examine the effects of whole body heat stress and subsequent stress protein induction on glycolytic metabolism, mitochondrial metabolism, and calcium handling within the heart. The effect of heat stress on glycolytic and mitochondrial pathways was examined by measuring contractile performance in the presence of glucose and pyruvate, respectively. Calcium handling was assessed using force-interval relationships. Right ventricular papillary muscles taken from heat-stressed and control rabbit hearts were superfused with Kreb's solution containing either glucose or pyruvate and rendered hypoxic for 30 min. After reoxygenation, the greatest recovery of contractile function occurred in the heat-stressed muscles with pyruvate as substrate; there was, however, no difference in the force-interval relationship between the groups. The degree of contractile recovery was related to the content of the inducible 70-kD but not the 65-kD, heat stress protein. This study suggests that heat stress enhances the ability of rabbit papillary muscle to use pyruvate, but not glucose, after reoxygenation, and that the differences seen in contractility may be secondary to induction of the 72-kD stress protein.(J. Clin. Invest. 1994. 93:1087-1094

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Section: Discussionmentioning

confidence: 99%

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Marber¹,

Walker²,

Latchman³

et al. 1994

J. Clin. Invest.

117

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show abstract

“…By varying the length of the conditioning ischemic episode, some investigators have tried to correlate hsp70 expression with subsequent neuroprotection (25). Transient hyperthermia also protects against subsequent lethal cellular injury in the brain (3,8 (27). In a recent in vivo study, administration of an antibody against hsp70 reduced neuronal protection in an ischemia tolerance model in the gerbil (40 (32,46,48).…”

Section: Hyperthermiamentioning

confidence: 99%

Stress Proteins as Molecular Markers of Neurotoxicity

Rajdev

Sharp

2000

Toxicol Pathol

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“…The exact mechanism underlying ischemic preconditioning (IPC)-induced tolerance remains unclear, although a number of possible induction pathways have been investigated, including, among others, neuroactive cytokines (Nawashiro et al, 1996;Ohtsuki et al, 1996), activation of glutamate receptors (Best et al, 1996;Pringle et al, 1996), adenosine receptors, the ATP-sensitive potassium channel (K ϩ ATP ) (Heurteaux et al, 1995;Perez-Pinzon et al, 1996Riepe et al, 1997;Blondeau et al, 2000), nitric oxide (Caggiano and Kraig, 1998;Centeno et al, 1999;GonzalezZulueta et al, 2000), oxidative stress (Ohtsuki et al, 1992), hypothermia (Nishio et al, 2000), and hyperthermia (Chopp et al, 1989;Rordorff et al, 1991).…”

Section: Introductionmentioning

confidence: 99%

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

et al. 2003

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Glutamate receptors and calcium have been implicated as triggering factors in the induction of tolerance by ischemic preconditioning (IPC) in the brain. However, little is known about the signal transduction pathway that ensues after the IPC induction pathway. The main goals of the present study were to determine whether NMDA induces preconditioning via a calcium pathway and promotes translocation of the protein kinase C ⑀ (⑀PKC) isozyme and whether this PKC isozyme is key in the IPC signal transduction pathway. We corroborate here that IPC and a sublethal dose of NMDA were neuroprotective, whereas blockade of NMDA receptors during IPC diminished IPC-induced neuroprotection. Calcium chelation blocked the protection afforded by both NMDA and ischemic preconditioning significantly, suggesting a significant role of calcium. Pharmacological preconditioning with the nonselective PKC isozyme activator phorbol myristate acetate could not emulate IPC, but blockade of PKC activation with chelerythrine during IPC blocked its neuroprotection. These results suggested that there might be a dual involvement of PKC isozymes during IPC. This was corroborated when neuroprotection was blocked when we inhibited ⑀PKC during IPC and NMDA preconditioning, and IPC neuroprotection was emulated with the activator of ⑀PKC. The possible correlation between NMDA, Ca 2ϩ , and ⑀PKC was found when we emulated IPC with the diacylglycerol analog oleoylacetyl glycerol, suggesting an indirect pathway by which Ca 2ϩ could activate the calcium-insensitive ⑀PKC isozyme. These results demonstrated that the ⑀PKC isozyme played a key role in both IPC-and NMDA-induced tolerance.

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Transient hyperthermia protects against subsequent forebrain ischemic cell damage in the rat

Cited by 254 publications

References 0 publications

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Myocardial protection after whole body heat stress in the rabbit is dependent on metabolic substrate and is related to the amount of the inducible 70-kD heat stress protein.

Stress Proteins as Molecular Markers of Neurotoxicity

εPKC Is Required for the Induction of Tolerance by Ischemic and NMDA-Mediated Preconditioning in the Organotypic Hippocampal Slice

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