scholarly journals Circulating Catecholamines Modulate Ischemic Brain Damage

1986 ◽  
Vol 6 (5) ◽  
pp. 559-565 ◽  
Author(s):  
Tohru Koide ◽  
Tadeusz W. Wieloch ◽  
Bo K. Siesjö
Keyword(s):  
Blood Pressure ◽  
Brain Damage ◽  
Neuronal Damage ◽  
Ischemic Insult ◽  
Ischemic Brain Damage ◽  
Neuronal Necrosis ◽  
Ischemic Brain ◽  
Bilateral Carotid ◽  
Response To Stress ◽  
Bilateral Carotid Artery

In search of factors influencing the outcome of an ischemic insult, we induced 10 min of forebrain ischemia in rats and assessed neuronal necrosis by quantitative histopathology after 1 week of recovery. Procedures for inducing ischemia included bilateral carotid artery clamping and reduction of blood pressure to 40–50 mm Hg by bleeding. To facilitate rapid lowering of blood pressure, a ganglionic blocker, trimethaphan (TMP), was administered at the onset of ischemia. Omission of the ganglionic blocker proved to markedly ameliorate neuronal damage. Similarly favorable effects were obtained when a mixture of adrenaline and noradrenaline (1 μg kg−1 min−1 each) was infused during the early recirculation period in animals previously given TMP. Infusion of noradrenaline alone also ameliorated the damage, though the efficacy was somewhat less. The results suggest that catecholamines, released as a response to stress, ameliorate ischemic brain damage.

Ischemic neuronal damage after acute subdural hematoma in the rat: effects of pretreatment with a glutamate antagonist

1991 ◽  
Vol 74 (6) ◽  
pp. 944-950 ◽  
Author(s):  
Min-Hsiung Chen ◽  
Ross Bullock ◽  
David I. Graham ◽  
Jimmy D. Miller ◽  
James McCulloch
Keyword(s):  
Brain Damage ◽  
Subdural Hematoma ◽  
Neuronal Damage ◽  
Nmda Receptor Antagonist ◽  
Acute Subdural Hematoma ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Content Type ◽  
Irreversible Brain Damage ◽  
Slow Injection

✓ The ability of a competitive N-methyl-D-aspartate (NMDA) receptor antagonist (D-CPP-ene) to reduce irreversible brain damage has been examined in a rodent model of acute subdural hematoma. Acute subdural hematoma was produced by the slow injection of 400 µl homologous blood into the subdural space overlying the parietal cortex in halothane-anesthetized rats. Brain damage was assessed histologically in sections at multiple coronal planes in animals sacrificed 4 hours after induction of the subdural hematoma. Pretreatment with D-CPP-ene (15 mg/kg) significantly reduced the volume of ischemic brain damage produced by the subdural hematoma from 62 ± 8 cu mm (mean ± standard error of the mean) in vehicle-treated control rats to 29 ± 7 cu mm in drug-treated animals. These data demonstrate the anti-ischemic efficacy of NMDA antagonists in an animal model of intracranial hemorrhage in which intracranial pressure is elevated, and suggest that excitotoxic mechanisms (which are susceptible to antagonism by D-CPP-ene) may play a role in the ischemic brain damage which is observed in patients who die after acute subdural hematoma.

Abstract 225: Treatment with LCZ696, an Orally Active Angiotensin Receptor Neprilysin Inhibitor Prevents Ischemic Brain Damage

Hypertension ◽  
2014 ◽  
Vol 64 (suppl_1) ◽  
Author(s):  
Hui-Yu Bai ◽  
Masaki Mogi ◽  
Hirotomo Nakaoka ◽  
Harumi Kan-no ◽  
Kana Tsukuda ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Damage ◽  
Superoxide Anion ◽  
Angiotensin Ii Receptor ◽  
Superoxide Anion Production ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Neprilysin Inhibitor ◽  
Anion Production ◽  
Orally Active

Objective: Recent accumulating evidence suggests that an orally active angiotensin II receptor-neprilysin inhibitor, LCZ696, was supposed to be superior compared to angiotensin II receptor blocker (ARB), valsartan alone in treating cardiovascular disease. We previously reported that ARBs prevent ischemic brain damage using middle cerebral artery occlusion (MCAO) mouse model. Moreover, natriuretic peptides such as atrial natriuretic peptide (ANP) or brain natriuretic peptide (BNP) increased by neprilysin inhibitor are also reported to protect brain damage. Therefore, we investigate the possible protective effects of valsartan (VAL) compared with LCZ696 (LCZ) (VAL+ neprilysin inhibitor; 1:1) on the prevention of ischemic damage after stroke. Methods: Focal brain ischemia was induced by MCAO with the intraluminal filament technique in 10-week male C57BL/6J mice. Mice were treated with VAL (3 mg/kg) or LCZ (6 mg/kg) orally as powder in gelatin mini-capsules daily for 2 weeks before MCAO. Ischemic area was evaluated by triphenyl tetrazolium chloride staining, cerebral blood flow (CBF) by laser-Doppler flowmetry, oxidative stress by dihydroethidium staining. Results: Telemetry method showed that systolic blood pressure (SBP), diastolic blood pressure (DBP) and heart rate (HR) did not change before and after treatments. Protective effect of LCZ treatment on ischemic brain damage in each brain section seemed to be more marked than that of VAL treatment. The average ischemic area ratio showed a significant reduction in VAL and LCZ groups compared with CON group. CBF in the peripheral region around ischemic core was significantly improved after treatments. Moreover, VAL and LCZ treatments significantly decreased the increase of superoxide anion production in the cortex of ischemic side. However, significant differences of CBF and superoxide anion production were not observed in VAL and LCZ. Conclusions: Both valsartan and LCZ696 treatments exerted preventive effects on ischemic stroke. The preventive effect of LCZ696 seemed more prominent than VAL. LCZ696 could be a novel powerful approach to protect brain after stroke. Further investigation has been performed to clarify the protective effect of LCZ696 on ischemic brain damage.

scholarly journals The Influence of Mild Body and Brain Hypothermia on Ischemic Brain Damage

1990 ◽  
Vol 10 (3) ◽  
pp. 365-374 ◽  
Author(s):  
Hiroaki Minamisawa ◽  
Carl-Henrik Nordström ◽  
Maj-Lis Smith ◽  
Bo K. Siesjö
Keyword(s):  
Body Temperature ◽  
Brain Damage ◽  
The Body ◽  
Reticular Nucleus ◽  
Temperature Sensitive ◽  
Ischemic Brain Damage ◽  
Neuronal Necrosis ◽  
Ischemic Brain ◽  
Selective Neuronal Vulnerability ◽  
The Brain

The influence of brain and body temperature on ischemic brain damage, notably on the density and distribution of selective neuronal vulnerability, was studied in SPF-Wistar rats subjected to 15 min of forebrain ischemia induced by bilateral occlusion of the common carotid arteries combined with arterial hypotension (50 mm Hg) in a room air environment. In one group of animals, the body temperature was maintained at 37°C but no attempt was made to prevent heat losses from the ischemic brain; i.e., the head was not heated during ischemia. Under those conditions the temperature of the caudoputamen and at a subcutaneous site over the skull bone spontaneously fell to ∼32°C. In four other groups, both the rectal and the subcutaneous skull temperatures were maintained at 38, 37, 35, and 33°C during the ischemia. Our results confirm those recently reported when brain temperature was varied during 20 min of ischemia, with body temperature kept constant. Thus, the histopathological outcome of the brain damage, as assessed after 7 days of recovery, was strongly temperature dependent. Whereas ischemia at 37–38°C consistently caused neuronal necrosis in the hippocampus, neocortex, and caudoputamen, spontaneous cooling of the brain during ischemia at a rectal temperature of 37°C significantly reduced the ischemic damage. Intentional lowering of temperature to 35°C markedly reduced and to 33°C virtually prevented neuronal necrosis in some but not all of the regions studied. While damage to the caudoputamen was extremely temperature sensitive, that affecting the CA1 sector of the hippocampus, and particularly the lateral reticular nucleus of the thalamus, was less so. Our results suggest that whatever biochemical events are responsible for selective neuronal vulnerability, they are temperature sensitive; however, since there are differences in sensitivity between different parts of the brain, more than one mechanism may be involved.

scholarly journals The Contribution of Reoxygenation to Ischemic Brain Damage

1991 ◽  
Vol 11 (6) ◽  
pp. 994-1000 ◽  
Author(s):  
James H. Halsey ◽  
Karl A. Conger ◽  
Julio H. Garcia ◽  
Eniko Sarvary
Keyword(s):  
Cerebral Ischemia ◽  
Brain Damage ◽  
Neuronal Damage ◽  
Global Cerebral Ischemia ◽  
Platinum Electrodes ◽  
Halo Formation ◽  
Neuronal Necrosis ◽  
Ischemic Brain ◽  
Postischemic Reperfusion ◽  
Foot Process

This study examined the hypothesis that the level of postischemic reperfusion affects the severity of the resulting neuronal necrosis. In rats, tissue Po2% was monitored as an index of flow (reoxygenation) at four cortical sites by chronically implanted platinum electrodes. Twenty minutes of total global cerebral ischemia was followed by 30 min of reoxygenation. The level of reoxygenation was controlled to maintain the Po2 nearly constant at one or more of the cortical electrodes. Tissue from within 400 μm of each of 19 electrode sites among seven rats was evaluated histologically. There was a positive correlation between reoxygenation level and severity of neuronal damage. Perineuronal lucent halo formation, probably representing astrocyte foot process swelling, was negatively correlated with reoxygenation level. This study demonstrates that ischemic neuronal damage was aggravated by increased reoxygenation but that perineuronal swelling, as evidenced by halo formation, was somewhat ameliorated.

scholarly journals Evaluation of Altered Glutamatergic Activity in a Piglet Model of Hypoxic-Ischemic Brain Damage Using 1H-MRS

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Yuxue Dang ◽  
Xiaoming Wang
Keyword(s):  
Basal Ganglia ◽  
Brain Damage ◽  
Protein Level ◽  
Excitatory Amino Acid ◽  
Oxygen Mixture ◽  
Control Group ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Protein Levels ◽  
Bilateral Carotid

Background and Objective. The excitotoxicity of glutamate (Glu) is a major risk factor for neonatal hypoxic-ischemic brain damage (HIBD). The role of excitatory amino acid transporter 2 (EAAT2) and the α-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid receptor (AMPAR) subunit GluR2 in mediating the Glu excitotoxicity has always been the hotspot. This study was aimed at investigating the early changes of glutamate metabolism in the basal ganglia following hypoxia-ischemia (HI) in a neonatal piglet model using 1H-MRS. Methods. Twenty-five newborn piglets were selected and then randomly assigned to the control group (n=5) and the model group (n=20) subjected to HI. HI was induced by blocking bilateral carotid blood flow under simultaneous inhalation of a 6% oxygen mixture. 1H-MRS data were acquired from the basal ganglia at the following time points after HI: 6, 12, 24, and 72 h. Changes in protein levels of EAAT2 and GluR2 were determined by immunohistochemical analysis. Correlations among metabolite concentrations, metabolite ratios, and the protein levels of EAAT2 and GluR2 were investigated. Results. The Glu level sharply increased after HI, reached a transient low level of depletion that approached the normal level in the control group, and subsequently increased again. Negative correlations were found between concentrations of Glu and EAAT2 protein levels (Rs=−0.662, P<0.001) and between the Glu/creatine (Cr) ratio and EAAT2 protein level (Rs=−0.664, P<0.001). Moreover, changes in GluR2 protein level were significantly and negatively correlated with those in Glu level (the absolute Glu concentration, Rs=−0.797, P<0.001; Glu/Cr, Rs=−0.567, P=0.003). Conclusions. Changes in Glu level measured by 1H-MRS were inversely correlated with those in EAAT2 and GluR2 protein levels following HI, and the results demonstrated that 1H-MRS can reflect the early changes of glutamatergic activity in vivo.

scholarly journals Diurnal blood pressure rhythm predicts ischemic brain damage

2005 ◽  
Vol 18 (5) ◽  
pp. A244-A244
Author(s):  
G SCHWARTZ ◽  
S TURNER ◽  
C JACK ◽  
D KNOPMAN ◽  
K BAILEY ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Brain Damage ◽  
Ischemic Brain Damage ◽  
Ischemic Brain
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