AI Article Synopsis
- The study examined the impact of hyperthermia on newborn rat brains after they experienced hypoxia-ischemia (HI) by subjecting them to low oxygen levels.
- Rats exposed to hyperthermia showed a significant increase in activated caspase-3, a marker of cell apoptosis, compared to those kept at normal temperature.
- The hyperthermia group also suffered greater brain tissue loss over time, indicating that elevated temperatures worsen HI-induced brain injury in immature rats via apoptosis pathways.
Article Abstract
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 a normothermia group. Hyperthermia resulted in an approximately 5-fold increase in activated caspase-3 24 h after HI when compared with the normothermia group, and gross loss of brain tissue was observed only in the hyperthermia group at 7 and 30 days after HI. Our results show that postischemic hyperthermia exacerbates HI injury in immature brains, and that the mechanism is strongly associated with activation of an apoptotic pathway.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1159/000071952 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cerebral Temperature Dysregulation: MR Thermographic Monitoring in a Nonhuman Primate Study of Acute Ischemic Stroke.
AJNR Am J Neuroradiol
April 2017
From the Departments of Radiology and Imaging Sciences (S.D., D.Q., F.T.).
Background And Purpose: Cerebral thermoregulation remains poorly understood. Temperature dysregulation is deeply implicated in the potentiation of cerebrovascular ischemia. We present a multiphasic, MR thermographic study in a nonhuman primate model of MCA infarction, hypothesizing detectable brain temperature disturbances and brain-systemic temperature decoupling.
View Article and Find Full Text PDFAtrial natriuretic peptide property on the ischemic myocardium inducing HSP72.
Asian Cardiovasc Thorac Ann
March 2014
Department of Experimental and Clinical Medicine, Magna Graecia University of Catanzaro, Italy.
Background: The purpose of this study was to investigate the effectiveness of atrial natriuretic peptide on ischemic myocardium through the induction of heat-shock protein 72.
Methods: 30 isolated rabbit hearts perfused on isolated heart apparatus were randomly assigned to receive either warm Krebs-Henseleit solution with 1 µmol L(-1) atrial natriuretic peptide (n = 15) or warm Krebs-Henseleit solution without atrial natriuretic peptide (n = 15) in preischemic, ischemic, and postischemic conditions. In all rabbit hearts, global ischemia was produced by clamping the aortic and atrial inflow lines.
Applying cerebral hypothermia and brain oxygen monitoring in treating severe traumatic brain injury.
World Neurosurg
December 2010
Department of Neurosurgery, China Medical University Hospital, Taichung, Taiwan, Republic of China.
Background: Severe traumatic brain injury (TBI) was to be one of the major health problems encountered in modern medicine and had an incalculable socioeconomic impact. The initial cerebral damage after acute brain injury is often exacerbated by postischemic hyperthermia and worsens the outcome. Hypothermia is one of the current therapies designed to combat this deleterious effect.
View Article and Find Full Text PDFIschemic tolerance: the mechanisms of neuroprotective strategy.
Anat Rec (Hoboken)
December 2009
Department of Medical Biochemistry, Jessenius Faculty of Medicine, Comenius University, Centre of Excellence: Biomembranes, Malá Hora 4, Martin, Slovakia.
The phenomenon of ischemic tolerance perfectly describes this quote "What does not kill you makes you stronger." Ischemic pre- or postconditioning is actually the strongest known procedure to prevent or reverse neurodegeneration. It works specifically in sensitive vulnerable neuronal populations, which are represented by pyramidal neurons in the hippocampal CA1 region.
View Article and Find Full Text PDFDeep brain hyperthermia while rewarming from hypothermic circulatory arrest.
J Card Surg
September 2010
Department of Cardiothoracic Surgery, Pediatric Division, Schneider Children's Medical Center of Israel, Rabin Medical Center, Petach Tikva, Israel.
Background: Neurologic injury is a feared and serious long-term complication of cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA). Postoperative hyperthermia was found to enhance postischemic neurologic injury. The use of core temperature as the reference point through CPB assumes parallel changes in brain temperature.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!