Interleukin-1 receptor antagonist attenuates the heat stroke-induced neuronal damage by reducing the cerebral ischemia in rats

Lin, Mao Tsun; Kao, Ting-Yu; Jin, Ying; Chen, C.F.

doi:10.1016/0361-9230(95)00046-h

Cited by 80 publications

(41 citation statements)

References 8 publications

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“…For example, heatstroke triggers the increase in extracellular glutamate (18), interleukin-1 (IL-1), and tumor necrosis factor (TNF) (32) in brain. A blockade of the NMDA receptors using MK801 (an NMDA-receptor channel blocker) or the IL-1 receptors using a IL-1-receptor antagonist would be beneficial in preventing heatstroke-induced arterial hypotension and cerebral ischemia (8,32). The formation of reactive oxygen species may be triggered by glutamate, IL-1, TNF, or NO.…”

Section: Discussionmentioning

confidence: 99%

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

et al. 2004

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Abstract. The aim of the present study was to ascertain whether aminoguanidine attenuated intracranial hypertension and cerebral ischemic injury in experimental heatstroke. Urethaneanesthetized rats were exposed to heat stress (ambient temperature of 43°C) to induce heatstroke. Control rats were exposed to 24°C. Mean arterial pressure, cerebral perfusion pressure, and cerebral blood flow after the onset of heatstroke were all significantly lower than in control rats. However, colonic temperature, intracranial pressure, heart rate, cerebral inducible nitric oxide synthase (iNOS)-dependent NO, and neuronal damage score were greater after the onset of heatstroke. Aminoguanidine (30 mmol / kg, i.v.; 30 min before the start of heat exposure) pretreatment significantly attenuated the heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia and neuronal damage, and increased iNOS-dependent NO formation in the brain. The extracellular concentrations of ischemic (e.g., glutamate and lactate / pyruvate ratio) and damage (e.g., glycerol) markers in the hypothalamus were also increased after the onset of heatstroke. Aminoguanidine pretreatment significantly attenuated the increase in hypothalamic ischemia and damage markers associated with heatstroke. Delaying onset of aminoguanidine administration (i.e., 0 or 30 min after the start of heat exposure) reduced the preventive efficiency on heatstroke-induced hyperthermia, arterial hypotension, intracranial hypertension, cerebral ischemia, and increased iNOS-dependent NO formation in brain. These results suggest that aminoguanidine protects against heatstroke-induced intracranial hypertension and cerebral ischemic injury by inhibition of cerebral iNOS-dependent NO production.

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Section: Discussionmentioning

confidence: 99%

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

et al. 2004

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“…When examined for neuronal damage in gray matter, only areas other than those invaded by probes were assessed. Our previous results (24,25) have shown that the striatal, hypothalamic, and cortical neurons are susceptible to cerebral ischemia following heatstroke. However, in the present study, only the striatal and cortical regions were chosen for histological examination of neuronal damage.…”

Section: Neuronal Damage Scorementioning

confidence: 91%

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Liu¹,

Chen²,

Cheng³

et al. 2004

J Pharmacol Sci

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Abstract. In this study, we investigated the acute hemodynamic effects of an infusion of the endothelin-1 (ET-1)-A-selective receptor antagonists BQ-610 and BQ-123 in heatstroke rats with circulatory shock and cerebral ischemia. Heatstroke was induced by putting the anesthetized adult Sprague-Dawley rats into an ambient temperature of 42°C. The moment in which the mean arterial pressure dropped irreversibly from the peak for an extent of 25 mmHg was taken as the onset of heatstroke. The interval between initiation of heat exposure and heatstroke onset was found to be about 80 min for rats treated with vehicle solution. When the animals were exposed to 42°C for 80 min, hyperthermia, arterial hypotension, decrement of cardiac output (due to decreased stroke volume and decreased total peripheral resistance), increment of plasma ET-1 and tumor necrosis factor-a , and increment of cerebral ischemia and injury markers were manifested. Prior antagonism of ET-1 A receptors with BQ-610 (0.5 mg / kg, i.v.) or BQ-123 (1 mg / kg, i.v.), but not ET-1B receptors with BQ-788 (0.5 mg / kg, i.v.), 60 min before the initiation of heat exposure, appreciably alleviated hyperthermia, arterial hypotension, decreased cardiac output, increment of tumor necrosis factor-a , and increment of cerebral ischemia (e.g., glutamate and lactate / pyruvate ratio) and injury (e.g., glycerol) markers exhibited during heatstroke. The data indicates that ET-1A receptor antagonism may maintain appropriate levels of mean arterial pressure and cerebral circulation during heatstroke by reducing production of tumor necrosis factor-a .

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“…IL-1␤ is up-regulated after the focal brain ischemia produced by permanent middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats (Arvin et al, 1996). The IL-1 receptor antagonist (IL-1ra) may play a role in attenuating the neuronal damage in stroke (Lin et al, 1995;Wang et al, 1997), while other cytokine blockers can reduce brain edema and infarct size-as well as enhance functional recovery after experimental stroke-further supporting the important role of cytokines in this disease process. TNF-␣ is expressed early in neuronal cells in and around the ischemic tissue and later in macrophages in the infarcted tissue (Wood, 1995), and may mediate some of the toxicity.…”

Section: Strokementioning

confidence: 98%

Involvement of cytokines in normal CNS development and neurological diseases: Recent progress and perspectives

1998

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Cytokines have been recognized to play an important role both in normal development of the brain, when they act as neurotrophic factors, as well as following injury. While both the cytokines and their receptors are synthesized and expressed in the brain normally (albeit at low levels), it has become clear that elevated levels are associated with many neurological disorders. In this review, we have chosen to present the data for only a few of the cytokines, including interleukin-1beta, interleukin-3, interleukin-6, interferon-gamma, transforming growth factor-beta, and tumor necrosis factor-alpha. Data are presented that suggest roles they may play in human disorders, including stroke, multiple sclerosis, Alzheimer's disease, and several psychiatric disorders. The results in human disease are compared with results obtained in a variety of transgenic animal models. The mouse models have very different disorders depending on whether a cytokine is overexpressed either peripherally or in either astrocytes or neurons. The potential significance of this to the understanding of human disease is discussed.

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Interleukin-1 receptor antagonist attenuates the heat stroke-induced neuronal damage by reducing the cerebral ischemia in rats

Cited by 80 publications

References 8 publications

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

Aminoguanidine Protects Against Intracranial Hypertension and Cerebral Ischemic Injury in Experimental Heatstroke

Prior Antagonism of Endothelin-1A Receptors Alleviates Circulatory Shock and Cerebral Ischemia During Rat Heatstroke

Involvement of cytokines in normal CNS development and neurological diseases: Recent progress and perspectives

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