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Whole-body hyperthermia-induced renal atrophy of mice as evinced by obstruction and degeneration of renal tubules caused by acute ischemia.
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Effects of microwave-induced whole-body hyperthermia (WBH) on the mouse kidney were examined histologically for acute and late effects up to 150 days after WBH treatment at 43.5 degrees C (rectal temperature) for 20 min or 42 degrees C for 40 min. As a whole the damage could be divided into two
Hyperthermia and hypermetabolism in focal cerebral ischemia.
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The reliable and reproducible creation of an animal model of focal cerebral ischemia is not easily accomplished. Using a transortibal approach, we showed that occlusion of the posterior cerebral artery (PCA), middle cerebral artery (MCA), and the contralateral anterior cerebral artery (ACA) created
Postoperative fever, bowel ischaemia and cytokine response to abdominal aortic aneurysm repair--a comparison between endovascular and open surgery.
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OBJECTIVE
To study bowel ischaemia in transfemorally placed endoluminal grafting (TPEG) for abdominal aortic aneurysms, and any relation to cytokine response or postoperative fever.
METHODS
Prospective not randomised. University hospital setting.
METHODS
Fourteen cases of conventional surgery and 23
Heme oxygenase-1 (Hsp32) is involved in the protection of small intestine by whole body mild hyperthermia from ischemia/reperfusion injury in rat.
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OBJECTIVE
The aim of the present study was to explore whether heme oxygenase-1 (HO-1) is involved in the hyperthermia-provided protection of the small intestine from ischemia/reperfusion injury in rats.
METHODS
Intestinal damage was induced in male Sprague-Dawley rats by clamping both the superior
Protein synthesis in perfused rat hearts after in vivo hyperthermia and in vitro cold ischemia.
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Isolated and perfused rat hearts can be maintained for up to 2.5 h with minimal synthesis of a stress protein with a relative mass (Mr) of 71 kilodaltons (SP71). Isolated hearts, subjected to 17 h of cold (4 degrees C) ischemia, upon perfusion (37 degrees C) synthesize a large amount of SP71. In the
Failure of preventive effects of 2-deoxy-D-glucose on ischemia-induced gerbil hippocampal neuronal damage by induced hyperthermia.
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Post-ischemic administration of 2-deoxy-D-glucose (2-DG), a glucose antimetabolite, markedly reduces the occurrence of ischemia-induced delayed neuronal death (DND) in the gerbil hippocampus. This means that the reduction of energy dependent metabolism after ischemia prevents ischemia-induced
Effect of whole body hyperthermia on ischemia and reperfusion injury of rat intestine: real-time ATP change studied using (31)P-MRS.
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We studied the effect of hyperthermia pretreatment on subsequent small intestinal ischemia and reperfusion (I/R) injury in the rat. Systemic hyperthermia has been reported to induce heat shock proteins (HSPs) in several organs [1-6]. We examined the expression of HSP72 in the small intestinal mucosa
Postischemic spontaneous hyperthermia is not a major aggravating factor for neuronal damage following repeated brief cerebral ischemia in the gerbil.
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Brief and non-lethal cerebral ischemia produces most severe neuronal damage when such ischemia is induced repeatedly at 1-h intervals. We examined whether spontaneous postischemic hyperthermia is an aggravating factor for the cumulative damage following repeated ischemia in the gerbil. We maintained
Effect of mild hyperthermia on recovery of metabolic function after global cerebral ischemia in cats.
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We investigated the effect of mild whole-body hyperthermia before and after 16 minutes of global cerebral ischemia on metabolic recovery during recirculation in cats using in vivo phosphorus-31 nuclear magnetic resonance spectroscopy. Hyperthermia (temperature 40.6 +/- 0.2 degrees C) was induced
Postischemic hyperthermia increases expression of hsp72 mRNA after brief ischemia in the gerbil.
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Brain temperature during ischemia critically determines insult severity, and temperature changes during recirculation may also affect subsequent injury. We have examined the impact of postischemic temperature on induction of the 70 kDa stress protein, hsp72, after brief ischemia in the gerbil.
Heat shock RNA levels in brain and other tissues after hyperthermia and transient ischemia.
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A number of studies have demonstrated increased synthesis of heat shock proteins in brain following hyperthermia or transient ischemia. In the present experiments we have characterized the time course of heat shock RNA induction in gerbil brain after ischemia, and in several mouse tissues after
Predictive Factors of Fever After Aneurysmal Subarachnoid Hemorrhage and Its Impact on Delayed Cerebral Ischemia and Clinical Outcomes.
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OBJECTIVE
Fever is relatively common and worsens neurologic injury after aneurysmal subarachnoid hemorrhage (SAH). The aim of this study was to display the time course of body temperature, identify predictive factors of fever after SAH, and evaluate its impact on delayed cerebral ischemia (DCI) and
Postischemic hyperthermia induced caspase-3 activation in the newborn rat brain after hypoxia-ischemia and exacerbated the brain damage.
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The effects of postischemic hyperthermia were investigated in the newborn rat brain after hypoxia-ischemia (HI). Seven-day-old rats were subjected to left carotid artery ligation followed by 8% oxygen for 30 min, and divided into a hyperthermia group (rectal temperature at 39 degrees C for 6 h) and
17beta-estradiol pretreatment reduces CA1 sector cell death and the spontaneous hyperthermia that follows forebrain ischemia in the gerbil.
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Pretreatment with 17beta-estradiol attenuates ischemia-induced hippocampal cornu ammonis 1 (CA1) neuronal death. We assessed whether this is mediated through prevention of hyperthermia that normally follows ischemia in gerbils. Male gerbils were given sustained-released 17beta-estradiol pellets or
Increase of galectin-3 expression in microglia by hyperthermia in delayed neuronal death of hippocampal CA1 following transient forebrain ischemia.
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The ischemic damage in the hippocampal CA1 region following transient forebrain ischemia, delayed neuronal death, is a typical apoptotic response, but the underlying mechanisms are not fully understood. We have reported that mild hyperthermia (38 °C) accelerates DNA fragmentation of the gerbil CA1
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