scholarly journals Ischemic Brain Damage in Rats following Cardiac Arrest Using a Long-Term Recovery Model

1985 ◽  
Vol 5 (3) ◽  
pp. 420-431 ◽  
Author(s):  
Photjanee Blomqvist ◽  
Tadeusz Wieloch
Keyword(s):  
Cardiac Arrest ◽  
Morphological Changes ◽  
Brain Structures ◽  
Radioactive Tracer ◽  
Lateral Septum ◽  
Cresyl Violet ◽  
Reticular Nucleus ◽  
Neuronal Necrosis ◽  
Cardiac Resuscitation ◽  
Complete Cerebral Ischemia

A model is described in which transient complete cerebral ischemia is induced in rats by intracardiac injection of potassium chloride. The animals were intubated and mechanically ventilated with a nitrous oxide/oxygen (70:30) mixture. Cardiac arrest was achieved following a brief period of ventricular fibrillation. After 5–6 min, the circulation was restored by cardiopulmonary resuscitation and partial exchange transfusion. Local CBF (LCBF) during ischemia and cardiac resuscitation was studied by injection of [14C]iodoantipyrine into the right auricle at various periods during cardiac arrest, and was subsequently analyzed by autoradiography. No radioactive tracer could be visualized in any brain structure, demonstrating the absence of CBF during the cardiac standstill. LCBF was also studied at 5 min and 6.5 h after cardiac resuscitation. Five minutes of recirculation showed an increase in blood flow in all brain structures studied, ranging between 130 and 400% of control values. After 6.5 h of recirculation, the CBF was decreased in 13 of 24 brain structures by 20–50%, concomitantly with the depressed rate of glucose utilization found in 15 brain structures. The neocortical, hippocampal, and striatal concentrations of labile phosphates, lactate, pyruvate, phosphocreatine, glucose, and glycogen were measured 5 min after cardiac arrest. Extensive energy failure and elevation of lactate levels were observed and were similar to earlier reported values. One week following recovery from the ischemic insult, the animals were perfusion-fixed with formaldehyde. The brains were embedded in paraffin, sub serially sectioned, and stained with cresyl violet/acid fuchsin. Histopathological changes were assessed by light microscopy as the number of acidophilic or pyknotic neurons. Morphological changes were observed in the hilus of the dentate gyrus, the hippocampal CA1 and subicular regions, the dorsal and lateral septum, the olfactory tubercle, the primary olfactory cortex, the entorhinal cortex, the amygdaloid nuclei, and the reticular nucleus of the thalamus. The distribution of the morphological changes suggests a transsynaptic mechanism, causing neuronal necrosis primarily in the limbic brain areas.

scholarly journals Limited but Significant Protective Effect of Hypothermia on Ultra-Early-Type Ischemic Neuronal Injury in the Thalamus

1997 ◽  
Vol 17 (5) ◽  
pp. 543-552 ◽  
Author(s):  
Kensuke Kawai ◽  
Hitoshi Nakayama ◽  
Akira Tamura
Keyword(s):  
Cardiac Arrest ◽  
Protective Effect ◽  
Morphological Changes ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Early Type ◽  
Density Analysis ◽  
Normothermic Group ◽  
Ischemic Neuronal Injury ◽  
Hypothermic Group

We investigated the protective effect of hypothermia on ultra-early-type ischemic injury in the thalamic reticular nucleus of the rat. Cerebral ischemia was produced by 5 min of cardiac arrest followed by resuscitation. Rectal and cranial temperature during and after cardiac arrest was maintained at 37–38°C in the normothermic group and at 32–33°C in the hypothermic group. In the postischemic hypothermic group, temperature was maintained at 32–33°C starting 15 min after normothermic ischemia. Histological damage was evaluated quantitatively. While after 5 min of recirculation there was no difference in morphological changes in terms of neuronal halo formation, intraischemic hypothermia reduced the severity of the degenerative changes represented by vacuolated or dark neurons by 15 min. Postischemic hypothermia failed to show any evidence of protection by 30 min. The protective effect of intraischemic hypothermia remained significant when evaluated at 14 days after ischemia by volumetry of the lesion and neuronal density analysis, whereas postischemic hypothermia had no clear protective effect. These results suggest that the protective effect of intraischemic hypothermia applies to neurons susceptible to ultra-early-type injury, but the effect of postischemic hypothermia is limited because normothermic ischemia results in extensive degeneration in these neurons by 15 min.

scholarly journals MK-801, an Excitatory Amino Acid Antagonist, Does Not Improve Neurologic Outcome following Cardiac Arrest in Cats

1989 ◽  
Vol 9 (6) ◽  
pp. 795-804 ◽  
Author(s):  
Jerry E. Fleischer ◽  
Akio Tateishi ◽  
John C. Drummond ◽  
Mark S. Scheller ◽  
Marjorie R. Grafe ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cerebral Ischemia ◽  
Care Setting ◽  
Excitatory Amino Acid ◽  
Occipital Cortex ◽  
Intensive Care Setting ◽  
Relevant Model ◽  
Mk 801 ◽  
Treatment Groups ◽  
Complete Cerebral Ischemia

The excitatory amino antagonist MK-801 was administered to cats following resuscitation from cardiac arrest to evaluate its effect on neurologic and neuropathology outcome in a clinically relevant model of complete cerebral ischemia. In 29 cats studied, cardiac arrest (ventricular fibrillation) was maintained for 18 min and resuscitation was successfully performed in 21 cats. Four animals underwent a sham arrest. MK-801 or placebo was administered in a blinded, randomized manner. Beginning at 5 min post resuscitation (PR), MK-801 330 μg/kg over 2 min followed by 73 μg/kg/h for 10 h or the same volume of placebo was administered. Resuscitated animals remained paralyzed and sedated in an intensive care setting for 24–30 h PR. Neurologic examinations were performed at 2, 4, and 7 days PR by observers blinded to the treatment groups. Seventeen cats were entered into data analysis (nine MK-801-treated and eight placebo-treated). MK-801-treated animals had a significantly greater neurologic deficit score (NDS) rank (0 = normal, 100 = brain death) 2 days PR (mean rank 12.1 vs. 5.6; p = 0.008). This difference is most likely due to ongoing sedative actions of MK-801. There were no significant differences in NDS rank at 4 (10.3, MK-801 vs. 7.5, placebo) and 7 (9.6, MK-801 vs. 8.3, placebo) days PR. There were no significant differences in frontal cortex, hippocampus, occipital cortex, or cerebellar neuropathology between groups. Sham-arrested cats had normal neurologic and neuropathologic evaluations. In the circumstance of complete cerebral ischemia as employed in the current study, MK-801 had no beneficial effect upon neurologic or neuropathologic outcome.

scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

Seizure susceptibility to electroconvulsions or pentylenetetrazol after complete cerebral ischemia in rats due to cardiac arrest

2015 ◽  
Vol 67 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Monika Dudra-Jastrzębska ◽  
Marzena Ułamek-Kozioł ◽  
Marta Andres-Mach ◽  
Jarogniew J. Łuszczki ◽  
Sławomir Januszewski ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cerebral Ischemia ◽  
Seizure Susceptibility ◽  
Complete Cerebral Ischemia

scholarly journals Neuroprotective Effect of Angelica Gigas Root in a Mouse Model of Ischemic Brain Injury through MAPK Signaling Pathway Regulation

2020 ◽  
Author(s):  
Se-Eun Lee ◽  
Jung-Hoon Kim ◽  
Chiyeon Lim ◽  
Suin Cho
Keyword(s):  
Oral Administration ◽  
Morphological Changes ◽  
Neuroprotective Effect ◽  
Plasma Concentrations ◽  
Neuronal Cell ◽  
Mapk Signaling ◽  
Cresyl Violet ◽  
Potential Candidate ◽  
Angelica Gigas ◽  
Brain Tissues

Abstract Background: The root of Angelica gigas Nakai (Apiaceae) has been traditionally used as an important herbal medicine to treat blood-deficiency-related disorders in Eastern Asian countries, and recently, it has been recognized as a potential candidate for improving cardiovascular diseases. Methods: In this study, the neuroprotective effect of a methanol extract of A. gigas root (RAGE) was investigated in a mouse stroke model induced by a 90 min transient middle cerebral artery occlusion (tMCAO). Infarction volumes and morphological changes in brain tissues were measured using TTC, cresyl violet, and H&E staining. The neuroprotective mechanism of RAGE was elucidated through investigation of protein expression levels using western blotting, IHC, and ELISA assays. The plasma concentrations of decursin, a major compound in RAGE, were measured after oral administration of RAGE to SD rats. Results: The infarction volumes in brain tissues were significantly reduced and the morphological deteriorations in the brain neuron cells were improved in tMCAO mice when pre-treated with RAGE at 1,000 mg/(kg bw·d) for two consecutive days. The neuroprotective mechanism of RAGE was confirmed to attenuate ERK-related MAPK signaling pathways in the ipsilateral hippocampus hemisphere in mice. The concentrations of decursin in rat plasma samples showed peak absorption and elimination in vivo after oral administration of RAGE at 100 mg/rat.Conclusion: Mice administered RAGE before the tMCAO operation had less neuronal cell death than those that were not administered RAGE prior to the operation, and this study provides preclinical evidence for use of A. gigas in ischemic stroke.

Cardiac Arrest and Resuscitation

2015 ◽  
Author(s):  
Charles N. Pozner ◽  
Jennifer L Martindale
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Arrhythmias ◽  
Perfusion Pressure ◽  
Pulseless Electrical Activity ◽  
Coronary Perfusion Pressure ◽  
Spontaneous Circulation ◽  
Coronary Perfusion ◽  
Chest Compressions ◽  
Cardiac Resuscitation ◽  
Neurologic Function

The most effective treatment for cardiac arrest is the administration of high-quality chest compressions and early defibrillation; once spontaneous circulation is restored, post–cardiac arrest care is essential to support full return of neurologic function. This review summarizes the pathophysiology, stabilization and assessment, diagnosis and treatment, and disposition and outcomes of cardiac arrest and resuscitation. Figures show the foundations of cardiac resuscitation, ventricular arrhythmias, coronary perfusion pressure as a function of time, an algorithm for initial treatment of cardiac arrest, sample capnographs, and the electrocardiographic appearance of varying degrees of hyperkalemia. Tables include components of suboptimal cardiac resuscitation and corrective actions, recommended doses of medications commonly used in cardiac resuscitation, causes of pulseless electrical activity/asystolic arrest to consider, immediate post–return of spontaneous circulation checklist, and resuscitation goals during post–cardiac arrest care. This review contains 6 highly rendered figures, 5 tables, and 142 references.

Sign in / Sign up

Export Citation Format

Share Document