Differences in critical cerebral blood flow with age in swine

1991 ◽  
Vol 75 (1) ◽  
pp. 103-107 ◽  
Author(s):  
Jun Harada ◽  
Akira Takaku ◽  
Shunro Endo ◽  
Naoya Kuwayama ◽  
Osamu Fukuda
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Content Type ◽  
Neonatal Pigs ◽  
S 100 ◽  
Newborn Pigs ◽  
Electroencephalogram Eeg ◽  
The Brain ◽  
Fine Print

✓ Normal cerebral blood flow (CBF), critical CBF at a flat reading of the electroencephalogram (EEG), and reversibility of the flat EEG after reperfusion were investigated in a total of 59 pigs, including seven newborns (1 to 3 days of age), 38 juveniles (1 month old), and 14 adults (7 months old). The CBF was determined by the hydrogen clearance method; the EEG was recorded continuously and a power spectrum analysis was performed. Cerebral ischemia was produced by occlusion of both common carotid arteries and induction of hypotension (approximately 50 mm Hg). The flat EEG reversibility was investigated for 3 hours after reperfusion. As parameters of brain development, the neuronal density and the time at which the S-100 protein appeared in the brain were examined. Normal CBF was highest in neonatal pigs and decreased with age. The critical CBF at a flat EEG was lowest in newborn pigs and was elevated with development of the brain. Tolerance against cerebral ischemia was greatest in newborn pigs.

Cerebral blood flow measurements and electroencephalograms during carotid endarterectomy

1974 ◽  
Vol 41 (3) ◽  
pp. 310-320 ◽  
Author(s):  
Thoralf M. Sundt ◽  
Frank W. Sharbrough ◽  
Robert E. Anderson ◽  
John D. Michenfelder
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Carotid Endarterectomy ◽  
Carbon Dioxide Tension ◽  
Initial Slope ◽  
Flow Measurements ◽  
Content Type ◽  
Blood Flow Measurements ◽  
Electroencephalogram Eeg ◽  
Fine Print

✓ Ninety-three endarterectomies for carotid stenosis were monitored with cerebral blood flow (CBF) measurements, and 113 with both CBF measurements and a continuous electroencephalogram (EEG). Significant CBF increase occurred only when carotid endarterectomy was for a stenosis greater than 90%. A high correlation between CBF and EEG indicated when a shunt was required. To sustain a normal EEG, the CBF ascertained by the initial slope technique must be 18 ml/100 gm/min at an arterial carbon dioxide tension (PaCO2) of 40 torr. The degree of EEG change below this level during occlusion reflected the severity of reduced blood flow and was reversible with replacement of a shunt. The value and limitations of these monitoring techniques and a concept of ischemic tolerance and critical CBF are discussed.

Spinal cord stimulation reducing infarct volume in a model of focal cerebral ischemia in rats

2003 ◽  
Vol 99 (1) ◽  
pp. 131-137 ◽  
Author(s):  
Oren Sagher ◽  
Dah-Luen Huang ◽  
Richard F. Keep
Keyword(s):  
Spinal Cord ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
Spinal Cord Stimulation ◽  
Focal Cerebral Ischemia ◽  
Doppler Flowmetry ◽  
Content Type ◽  
Baseline Values ◽  
Fine Print

Object. The authors previously showed that spinal cord stimulation (SCS) increases cerebral blood flow in rats, indicating that this technique may be useful in the treatment of focal cerebral ischemia. In the present study, the neuroprotective potential of SCS in the setting of middle cerebral artery occlusion (MCAO) was investigated. Methods. The authors induced permanent, focal cerebral ischemia by using either suture-induced occlusion or direct division of the MCA in Sprague—Dawley rats. Electrical stimulation of the cervical spinal cord was performed during cerebral ischemia. Cerebral blood flow was assessed using both laser Doppler flowmetry (LDF) and quantitative radiotracer analysis. Stroke volumes were analyzed after 6 hours of ischemia. Spinal cord stimulation resulted in a 52.7 ± 13.3% increase in LDF values (nine animals). Following MCAO, LDF values decreased by 64.1 ± 3.6% from baseline values (10 animals). Spinal cord stimulation subsequently increased LDF values to 30.9 ± 13.5% below original baseline values. These findings were corroborated using radiotracer studies. Spinal cord stimulation in the setting of transcranial MCAO significantly reduced stroke volumes as well (from 203 ± 33 mm3 [control] to 32 ± 8 mm3 [MCAO plus SCS], seven animals in each group, p < 0.001). Similarly, after suture-induced MCAO, SCS reduced stroke volumes (from 307 ± 29 mm3 [control] to 78 ± 22 mm3 [MCAO plus SCS], 10 animals in each group, p < 0.001). Conclusions. A strategy of performing SCS for the prevention of critical ischemia is feasible and may have the potential for the treatment and prevention of stroke.

Pulsatile cerebral echo in diagnosis of brain death

1978 ◽  
Vol 48 (6) ◽  
pp. 866-875 ◽  
Author(s):  
Sumio Uematsu ◽  
Thomas D. Smith ◽  
A. Earl Walker
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Death ◽  
Simple Method ◽  
Cerebral Angiogram ◽  
Content Type ◽  
Cerebral Pathology ◽  
Conclusive Diagnosis ◽  
Electroencephalogram Eeg ◽  
Fine Print

✓ Conclusive diagnosis of brain death can be made by the demonstration of prolonged cessation of cerebral blood flow. This report describes a simple method to determine the presence or absence of the blood flow in the brain by recording the pulsatile midline echo on one channel of the electroencephalogram (EEG) or on any four-channel monitoring system in the intensive care unit. A firm transducer holder has been developed to eliminate artifacts caused by transducer motion. The pulsations of the midline echo are assumed to be the result of displacement of the midline structures by the arterial injection of each cardiac systole. Thus, the absence of these midline pulsatile echoes correlates with the absence of cerebral blood flow and, if the absence persists over 30 minutes in the presence of normal blood pressure, then the result is brain death. Twenty-eight cases of clinical brain death with electrocerebral silence of EEG and 18 obtunded patients with various types of cerebral pathology were examined by the echo-pulsation technique. Twenty-six of the 28 cases showed no pulsation of the midline echo. The validity of the technique was documented in four cases by four-vessel cerebral angiogram.

The effects of gammahydroxybutyric acid on canine cerebral blood flow and metabolism

1982 ◽  
Vol 57 (2) ◽  
pp. 197-202 ◽  
Author(s):  
Kent W. Baumann ◽  
Neal F. Kassell ◽  
Julie Olin ◽  
Thoru Yamada
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systemic Effect ◽  
High Dose ◽  
Vascular Effects ◽  
Content Type ◽  
Vascular Insufficiency ◽  
Gammahydroxybutyric Acid ◽  
The Brain ◽  
Fine Print

✓ Gammahydroxybutyric acid has been proposed as an alternative to high-dose barbiturate therapy for protecting the brain after ischemic or traumatic insult. The cerebral and systemic metabolic and vascular effects of gammahydroxybutyrate and its lactone analogue, gammabutyrolactone, are addressed in this paper. In anesthetized normal dogs, gammahydroxybutyrate or gammabutyrolactone was infused intravenously at a rate of 1 gm/kg/hr. Cerebral blood flow (CBF) decreased progressively with increasing doses of either agent. Cerebral metabolic rate of oxygen (CMRO2) increased initially with gammahydroxybutyrate, but not following gammabutyrolactone. Reduction in CBF exceeded that of CMRO2 at all doses in both series. The primary systemic effect noted was a severe, lethal metabolic acidosis resulting from infusion of gammabutyrolactone. Gammahydroxybutyrate did not cause a similar acidosis. The imbalance of the CBF-CMRO2 reduction following gammahydroxybutyrate administration suggests that it has no advantage over barbiturates in the management of patients with cerebral vascular insufficiency or intracranial hypertension.

A model of focal cortical contusion in gerbils

1982 ◽  
Vol 57 (2) ◽  
pp. 203-209 ◽  
Author(s):  
Alan Crockard ◽  
Joon Kang ◽  
Graeme Ladds
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Surrounding Tissue ◽  
Content Type ◽  
Time Period ◽  
Cortical Contusion ◽  
Capillary Bed ◽  
The Brain ◽  
Fine Print

✓ An experimental model of focal laceration and contusion in gerbils is described. Associated with this injury are systemic changes which are neurogenically mediated and result in an immediate reduction in blood pressure, bradycardia, and generalized reduction in cerebral blood flow. There is generalized edema, as judged by a decreased specific gravity in the brain, probably related to reduced blood flow; superimposed on this, there is an edema gradient which is maximal close to the injury. This, in turn, affects the local capillary bed and prevents any local increase in flow. A separate group studied over a longer time period (6 hours) did not reveal egress of Evans blue into the surrounding tissue and this is in contrast to reports from cold-injury studies.

Effect of mannitol on local cerebral blood flow after temporary complete cerebral ischemia in rats

1992 ◽  
Vol 76 (3) ◽  
pp. 486-492 ◽  
Author(s):  
Reizo Shirane ◽  
Philip R. Weinstein
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Ischemia ◽  
External Carotid ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Content Type ◽  
Arterial Blood ◽  
Permanent Occlusion ◽  
Fine Print

✓ The effects of pretreatment with mannitol on local cerebral blood flow (CBF) after permanent or temporary global cerebral ischemia were evaluated with 14C-iodoantipyrine autoradiography in rats under halothane-N2O endotracheal anesthesia. Blood pressure, pulse rate, arterial blood gas levels, and electroencephalographic (EEG) tracings were monitored throughout the experiments. After permanent occlusion of the basilar artery and both external carotid and pterygopalatine arteries, severe global ischemia was induced by permanent occlusion of the common carotid arteries (CCA's) or by a 30-minute temporary CCA occlusion followed by 5 minutes of reperfusion. Intravenous mannitol (25%, 1 gm/kg) or saline solution was administered 5 minutes before occlusion of the CCA's. Cerebral blood flow was measured in 24 anatomical regions. The EEG tracings flattened within 2 to 3 minutes after the onset of ischemia, and no recovery was observed during reperfusion. In the mannitol-treated rats and the saline-treated controls, autoradiographic studies after permanent occlusion showed no CBF in the forebrain or cerebellum, although brain-stem and spinal cord CBF values were normal. After 5 minutes of reperfusion, CBF in the cortex, basal ganglia, and white matter was 100% to 200% higher in mannitol-treated rats and 50% to 100% higher in saline-injected rats than in the nonischemic anesthetized control group. Heterogeneously distributed areas of no-reflow were seen in all saline-injected rats but were observed in none of the mannitol-treated rats. Pretreatment with mannitol prevented postischemic obstruction of the microcirculation during 5 minutes of recirculation after 30 minutes of severe temporary ischemia, but the EEG signals did not recover. Further studies of the functional and morphological responses to longer periods of postischemic recirculation are needed to verify the extent to which these mannitol-induced effects are protective.

Energy-requiring cell functions in the ischemic brain

1982 ◽  
Vol 56 (4) ◽  
pp. 482-497 ◽  
Author(s):  
Jens Astrup
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Global Cerebral Ischemia ◽  
Specific Inhibition ◽  
Ischemic Brain ◽  
Content Type ◽  
Cell Functions ◽  
The Brain ◽  
Fine Print

✓ The energy-requiring cell functions in the brain are described. The role of specific inhibition of these functions, and their critical low-supply levels of blood flow and oxygen are reviewed in relation to clinical management of focal and complete global cerebral ischemia.

Adenosine-induced modulation of excitatory amino acid transport across isolated brain arterioles

2003 ◽  
Vol 98 (3) ◽  
pp. 554-560 ◽  
Author(s):  
Gerald A. Grant ◽  
Joseph R. Meno ◽  
Thien-Son Nguyen ◽  
Kathe A. Stanness ◽  
Damir Janigro ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Amino Acid ◽  
Excitatory Amino Acid ◽  
Acid Transport ◽  
Content Type ◽  
Cerebral Arteriole ◽  
The Brain ◽  
Vectorial Transport ◽  
Fine Print

Object. Excitatory amino acid (EAA) uptake by neurons and glia acts synergistically with stereoselective transport across the blood—brain barrier (BBB) to maintain EAA homeostasis in the brain. The endogenous neuroprotectant adenosine counteracts many aspects of excitotoxicity by increasing cerebral blood flow and by producing pre- and postsynaptic actions on neurons. In the present study, the authors explored the effect of adenosine on EAA transport across the BBB. Methods. The effects of adenosine on the permeability of the BBB and transport of aspartate and glutamate across the BBB were studied in a well-characterized isolated penetrating cerebral arteriole preparation suitable for simultaneous investigations of changes in diameter and permeability. At concentrations within the physiological to low pathophysiological range (10−7–10−6 M), the net vectorial transport of [3H]l-glutamate or [3H]l-aspartate from blood to brain was significantly attenuated, whereas there was no effect of adenosine on paracellular BBB permeability to [14C]sucrose or [3H]d-aspartate. With higher concentrations of adenosine (10−4 M and 10−3 M) the net vectorial transport of [3H]l-glutamate and [3H]l-aspartate returned toward baseline. At 10−3 M, the permeability to [14C]sucrose was significantly altered, indicating a breakdown in the BBB. The effect of adenosine (10−6 M) was blocked by theophylline, a blocker of the A1 and A2 receptors of adenosine. Conclusions. Adenosine-mediated modulation of glutamate and aspartate transport across the BBB is a novel physiological finding.

Early changes measured by magnetic resonance imaging in cerebral blood flow, blood volume, and blood-brain barrier permeability following dexamethasone treatment in patients with brain tumors

1999 ◽  
Vol 90 (2) ◽  
pp. 300-305 ◽  
Author(s):  
Leif Østergaard ◽  
Fred H. Hochberg ◽  
James D. Rabinov ◽  
A. Gregory Sorensen ◽  
Michael Lev ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Magnetic Resonance ◽  
Brain Tumors ◽  
Mr Imaging ◽  
Blood Volume ◽  
Cerebral Blood Volume ◽  
Clinical Effects ◽  
Content Type ◽  
Fine Print

Object. In this study the authors assessed the early changes in brain tumor physiology associated with glucocorticoid administration. Glucocorticoids have a dramatic effect on symptoms in patients with brain tumors over a time scale ranging from minutes to a few hours. Previous studies have indicated that glucocorticoids may act either by decreasing cerebral blood volume (CBV) or blood-tumor barrier (BTB) permeability and thereby the degree of vasogenic edema.Methods. Using magnetic resonance (MR) imaging, the authors examined the acute changes in CBV, cerebral blood flow (CBF), and BTB permeability to gadolinium-diethylenetriamine pentaacetic acid after administration of dexamethasone in six patients with brain tumors. In patients with acute decreases in BTB permeability after dexamethasone administration, changes in the degree of edema were assessed using the apparent diffusion coefficient of water.Conclusions. Dexamethasone was found to cause a dramatic decrease in BTB permeability and regional CBV but no significant changes in CBF or the degree of edema. The authors found that MR imaging provides a powerful tool for investigating the pathophysiological changes associated with the clinical effects of glucocorticoids.

Transcorneal stimulation of trigeminal nerve afferents to increase cerebral blood flow in rats with cerebral vasospasm: a noninvasive method to activate the trigeminovascular reflex

2002 ◽  
Vol 97 (5) ◽  
pp. 1179-1183 ◽  
Author(s):  
Basar Atalay ◽  
Hayrunnisa Bolay ◽  
Turgay Dalkara ◽  
Figen Soylemezoglu ◽  
Kamil Oge ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Vasospasm ◽  
Trigeminal Nerve ◽  
Nerve Endings ◽  
Noninvasive Method ◽  
Direct Stimulation ◽  
Content Type ◽  
Fine Print ◽  
Stimulation Of

Object. The goal of this study was to investigate whether stimulation of trigeminal afferents in the cornea could enhance cerebral blood flow (CBF) in rats after they have been subjected to experimental subarachnoid hemorrhage (SAH). Cerebral vasospasm following SAH may compromise CBF and increase the risks of morbidity and mortality. Currently, there is no effective treatment for SAH-induced vasospasm. Direct stimulation of the trigeminal nerve has been shown to dilate constricted cerebral arteries after SAH; however, a noninvasive method to activate this nerve would be preferable for human applications. The authors hypothesized that stimulation of free nerve endings of trigeminal sensory fibers in the face might be as effective as direct stimulation of the trigeminal nerve. Methods. Autologous blood obtained from the tail artery was injected into the cisterna magna of 10 rats. Forty-eight and 96 hours later (five rats each) trigeminal afferents were stimulated selectively by applying transcorneal biphasic pulses (1 msec, 3 mA, and 30 Hz), and CBF enhancements were detected using laser Doppler flowmetry in the territory of the middle cerebral artery. Stimulation-induced changes in cerebrovascular parameters were compared with similar parameters in sham-operated controls (six rats). Development of vasospasm was histologically verified in every rat with SAH. Corneal stimulation caused an increase in CBF and blood pressure and a net decrease in cerebrovascular resistance. There were no significant differences between groups for these changes. Conclusions. Data from the present study demonstrate that transcorneal stimulation of trigeminal nerve endings induces vasodilation and a robust increase in CBF. The vasodilatory response of cerebral vessels to trigeminal activation is retained after SAH-induced vasospasm.

Sign in / Sign up

Export Citation Format

Share Document