Cerebral Blood flow and Its Responsiveness to CO2 after Traumatic and Ischemic Brain Injuries

1988 ◽  
pp. 135-136
Author(s):  
Y. E. Moskalenko ◽  
G. B. Weinstein ◽  
V. E. Parfenov ◽  
M. Bodó ◽  
B. V. Gaidar
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injuries ◽  
Ischemic Brain

scholarly journals New cerebrovascular agent with hypotensive activity

2019 ◽  
Vol 5 (2) ◽  
pp. 71-77
Author(s):  
Galina A. Kim ◽  
Tamara S. Gan’shina ◽  
Elena V. Kurza ◽  
Ilya N. Kurdyumov ◽  
Denis V. Maslennikov ◽  
...  
Keyword(s):  
Blood Flow ◽  
Antihypertensive Agent ◽  
Brain Injuries ◽  
Cerebrovascular Disorders ◽  
Male Rats ◽  
Hypotensive Activity ◽  
Duration Of Action ◽  
Ischemic Brain ◽  
Cerebrovascular Activity ◽  
The Brain

Introduction: In cerebrovascular disorders, special attention is paid to a hypertensive cerebrovascular crisis, which combines a vascular injury of the brain and hypertension. The paper studies the cerebrovascular properties of the calcium channel blocker of S-Amlodipine nicotinate antihypertensive agent. Materials and methods: Tests were performed on 96 nonlinear male rats, measuring local blood flow in the cerebral cortex in 36 awake animals, using a laser Doppler flowmeter. Cerebral circulation was recorded in the animals when modeling ischemic and hemorrhagic brain injuries. Results and discussion: S-Amlodipine nicotinate (0.1 mg/kg i/v) shows a pronounced cerebrovascular activity in the models of ischemic and hemorrhagic injuries of the brain. In terms of the vasodilating effect in ischemic brain injury, the drug is comparable to mexidol, nimodipine, picamilon, but is superior to nimodipine and picamilon in terms of duration of action, and in the model of hemorrhagic stroke, S-Amlodipine nicotinate is superior to nimodipine and is comparable to picamilon and mexidol. The analysis of the mechanism of action of the agent revealed the participation of GABA A-receptors in the implementation of cerebrovascular properties of the agent. Conclusion: Significant cerebrovascular activity of S-Amlodipine nicotinate (0.1 mg/kg i/v) antihypertensive agent was revealed. The presence of GABAergic mechanism on cerebral blood flow in the agent action along with blockade of slow calcium channels ensures its high efficacy in treatment of both ischemic and hemorrhagic brain injuries.

Abstract WP113: Administration of Direct Angiotensin II Type-2 Receptor Agonist, Compound 21, Even After Stroke Prevents Ischemic Brain Damage

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Masaki Mogi ◽  
Li-Juan Min ◽  
Fei Jing ◽  
Kana Tsukuda ◽  
Kousei Ohshima ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Damage ◽  
Receptor Agonist ◽  
Receptor Stimulation ◽  
Ischemic Brain Damage ◽  
Ischemic Brain ◽  
Compound 21 ◽  
Deficient Mice

Objectives: Previous our studies showed that angiotensin II type-2 (AT 2 ) receptor stimulation protects neurons after brain ischemic damage using AT 2 receptor-deficient mice. Recently, Compound 21 (C21) is available to use as a direct AT 2 receptor agonist. We reported that administration of C21 induces vascular dilatation via bradykinin-nitric oxide pathway and maintains cerebral blood flow, resulting in prevention of cognitive impairment. These results inspired us the possibility that administration of C21 could protect ischemic brain damage; therefore, we assessed the effect of C21 on stroke expansion by not only pre-treatment, but also a treatment immediately after stroke. Methods: 10 week-old wild-type male C57BL6 mice were subjected to the middle cerebral artery occlusion (MCAO) by electrocoagulation using a subtemporal approach. Ischemic area after stroke was evaluated by time-course analysis by magnetic resonance imaging (MRI) of the brain. C21 was administrated to mice 2 weeks before MCAO or immediately after MCAO treatment by intraperitoneal injection. Cerebral blood flow was evaluated by using 2D-laser speckle blood flow imaging system. Results: No significant remarkable change was observed in blood pressure in mice with or without C21 treatment. Pretreatment of C21 prevented ischemic brain damage 1 day after MCAO. In contrast, such preventive effect by C21 was not observed in AT 2 receptor-deficient mice. On the other hand, C21 treatment immediately after MCAO did not reduce ischemic area 1 day after MCAO, but remarkably reduced this 3 days after MCAO. Treatment with C21 prevented the reduced cerebral blood flow after MCAO. Conclusions: These findings indicate that AT 2 receptor stimulation by C21 prevents ischemic brain damage at least in part via maintaining cerebral blood flow even after stroke. Therefore, administration of C21 could work as a new therapeutical option in patients with stroke even in acute phase.

Cerebral Circulation and Cerebral Blood Flow

2019 ◽  
pp. 79-85
Author(s):  
Arnoley S. Abcejo ◽  
Jeffrey J. Pasternak
Keyword(s):  
Blood Flow ◽  
Cardiac Arrest ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neurologic Outcomes ◽  
The Us ◽  
Hospital Cardiac Arrest ◽  
Premonitory Symptoms

Cardiac arrest occurs suddenly, often without premonitory symptoms. Consciousness is lost within seconds to minutes because of insufficient cerebral blood flow in the midst of complete hemodynamic collapse. Anoxic-ischemic brain injury is most commonly caused by cardiac arrest, which is frequently lethal; of the US patients with out-of-hospital cardiac arrest treated by emergency medical services, almost 90% die. Among the patients who survive to hospital admission, inpatient mortality may be decreasing, but a substantial number of those survivors have poor neurologic outcomes from anoxic-ischemic brain injury.

Neurological monitoring

2019 ◽  
pp. 145-154
Author(s):  
Carl Waldmann ◽  
Andrew Rhodes ◽  
Neil Soni ◽  
Jonathan Handy
Keyword(s):  
Blood Flow ◽  
Intensive Care ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion ◽  
Brain Injuries ◽  
Icp Monitoring ◽  
Cerebral Function ◽  
Monitoring Methods ◽  
Neurological Assessment ◽  
Electroencephalogram Eeg

Dealing with neurological critically ill patients is one of the most challenging situations in intensive care. The range of conditions can go from carbon dioxide narcosis to status epilepticus or hypoxic or traumatic brain injuries. The key difficulty is the neurological assessment of these patients while they require general anaesthesia. This chapter discusses neurological monitoring and includes discussion on intracranial pressure (ICP) monitoring (including indications for ICP monitoring, methods of measuring ICP, complications of ICP monitoring, and ICP in normal and pathological conditions), intracranial perfusion (regulation of cerebral perfusion and measurement of cerebral blood flow), electroencephalogram (EEG) and cerebral function analysing monitoring (CFAM) (EEG, cerebral function monitors (CFM)/CFAM, EEG terminology, and clinical use in the intensive care unit), and other forms of neurological monitoring (tissue metabolism, cerebral blood flow and metabolism, and peripheral nerve and muscle electrophysiology).

Temporal profiles of cerebral blood flow in neonatal mice with hypoxic–ischemic brain injury

2011 ◽  
Vol 71 ◽  
pp. e403
Author(s):  
Makiko Ohshima ◽  
Masahiro Tsuji ◽  
Yukiko Kasahara ◽  
Akihiko Taguchi ◽  
Tomoaki Ikeda
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Hypoxic Ischemic Brain Injury ◽  
Temporal Profiles

scholarly journals Endothelial Nitric Oxide Synthase-Dependent Cerebral Blood Flow Augmentation by L-Arginine After Chronic Statin Treatment

2000 ◽  
Vol 20 (4) ◽  
pp. 709-717 ◽  
Author(s):  
Masaru Yamada ◽  
Zhihong Huang ◽  
Turgay Dalkara ◽  
Matthias Endres ◽  
Ulrich Laufs ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Nitric Oxide Synthase ◽  
Laser Doppler Flowmetry ◽  
Brain Blood Flow ◽  
Arginine Infusion ◽  
Doppler Flowmetry ◽  
Ischemic Brain ◽  
Oxide Synthase

Nitric oxide, a product of nitric oxide synthase activity, relaxes vascular smooth muscle and elevates brain blood flow. We evaluated the importance of eNOS to cerebral blood flow augmentation after L-arginine infusion and increases in flow after eNOS upregulation in SV-129 mice. Blood flow was measured by laser-Doppler flowmetry before and after L-arginine infusion (450 mg/kg during a 15-minute period) or measured by 14C-iodoamphetamine indicator fractionation or 14C-iodoantipyrine tissue equilibration techniques. rCBF increased by 26% (laser Doppler flowmetry) after L-arginine infusion but did not change in mutant mice deficient in eNOS expression. After eNOS upregulation by chronic simvastatin treatment (2 mg/kg subcutaneously, daily for 14 days), L-arginine amplified and sustained the hyperemia (38%) and increased absolute brain blood flow from 86 ± 7 to 119 ± 10 mL/100 g per minute. Furthermore, pretreatment with simvastatin enhanced blood flow within ischemic brain tissue after middle cerebral artery occlusion. Together, these findings suggest that eNOS activity is critical for blood flow augmentation during acute L-arginine infusion, and chronic eNOS upregulation combined with L-arginine administration provides a novel strategy to elevate cerebral blood flow in the normal and ischemic brain.

scholarly journals RheoSens; RheoPatch

2020 ◽  
Author(s):  
Tariq H. Khan
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Minimally Invasive ◽  
Brain Injuries ◽  
Tissue Oxygenation ◽  
Traumatic Brain Injuries ◽  
Invasive Device ◽  
The Brain ◽  
Minimally Invasive Device

Rheo Probe is a minimally invasive device, implanted in the brain matter for patients in a coma following brain haemorrage or traumatic brain injuries to measure cerebral blood flow, intracranial pressure, temperature and oxygenation parameters. Nearinfrared sensors assess levels of tissue oxygenation as well as cerebral blood flow by measuring oxygenated and deoxygenated hemoglobin based on spectrometry.

Cerebral blood flow augmentation using a cardiac-gated intracranial pulsating balloon pump in a swine model of elevated ICP

2020 ◽  
Vol 132 (5) ◽  
pp. 1606-1615
Author(s):  
Omer Doron ◽  
Tal Or ◽  
Limor Battino ◽  
Guy Rosenthal ◽  
Ofer Barnea
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Duty Cycle ◽  
Brain Injuries ◽  
Activation Parameters ◽  
Brain Perfusion ◽  
Physiological Parameters ◽  
Optimal Timing ◽  
Swine Model ◽  
Balloon Inflation

OBJECTIVEAugmenting brain perfusion or reducing intracranial pressure (ICP) dose is the end target of many therapies in the neuro-critical care unit. Many present therapies rely on aggressive systemic interventions that may lead to untoward effects. Previous studies have used a cardiac-gated intracranial balloon pump (ICBP) to model hydrocephalus or to flatten the ICP waveform. The authors sought to sought to optimize ICBP activation parameters to improve cerebral physiological parameters in a swine model of raised ICP.METHODSThe authors developed a cardiac-gated ICBP in which the volume, timing, and duty cycle (time relative to a single cardiac cycle) of balloon inflation could be altered. They studied the ICBP in a swine model of elevated ICP attained by continuous intracranial fluid infusion with continuous monitoring of systemic and cerebral physiological parameters, and defined two specific protocols of ICBP activation.RESULTSEleven swine were studied, 3 of which were studied to define the optimal timing, volume, and duty cycle of balloon inflation. Eight swine were studied with two defined protocols at baseline and with ICP gradually raised to a mean of 30.5 mm Hg. ICBP activation caused a consistent modification of the ICP waveform. Two ICBP activation protocols were used. Balloon activation protocol A led to a consistent elevation in cerebral blood flow (8%–25% above baseline, p < 0.00001). Protocol B resulted in a modest reduction of ICP over time (8%–11%, p < 0.0001) at all ICP levels. Neither protocol significantly affected systemic physiological parameters.CONCLUSIONSThe preliminary results indicate that optimized protocols of ICBP activation may have beneficial effects on cerebral physiological parameters, with minimal effect on systemic parameters. Further studies are warranted to explore whether ICBP protocols may be of clinical benefit in patients with brain injuries with increased ICP.

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