Cerebrovascular and metabolic effects on the rat brain of focal Nd:YAG laser irradiation

1990 ◽  
Vol 73 (6) ◽  
pp. 909-917 ◽  
Author(s):  
Marika Kiessling ◽  
Eberhard Herchenhan ◽  
Hans R. Eggert
Keyword(s):  
Blood Flow ◽  
Protein Synthesis ◽  
Laser Irradiation ◽  
Nd:Yag Laser ◽  
Vasogenic Edema ◽  
Coagulation Necrosis ◽  
Protein Synthesis Inhibition ◽  
Irradiation Site ◽  
Content Type ◽  
Fine Print

✓ To investigate the effects of focal neodymium:yttrium-aluminum-garnet (Nd:YAG) laser irradiation (λ = 1060 nm) on regional cerebral blood flow, cerebral protein synthesis, and blood-brain barrier permeability, the parietal brain surface of 44 rats was irradiated with a focused laser beam at a constant output energy of 30 J. Survival times ranged from 5 minutes to 48 hours. Laser irradiation immediately caused well-defined cortical coagulation necrosis. Within 5 minutes after unilateral irradiation, 14C-iodoantipyrine autoradiographs demonstrated severely reduced blood flow to the irradiation site and perilesional neocortex, but a distinct reactive hyperemia in all other areas of the forebrain. Apart from a persistent ischemic focus in the vicinity of the cortical coagulation necrosis, blood flow alterations in remote areas of the brain subsided within 3 hours after irradiation. Autoradiographic assessment of 3H-tyrosine incorporation into brain proteins revealed rapid onset and prolonged duration of protein synthesis inhibition in perifocal morphologically intact cortical and subcortical structures. Impairment of amino acid incorporation proved to be completely reversible within 48 hours. Immunoautoradiographic visualization of extravasated plasma proteins using 3H-labeled rabbit anti-rat immunoglobulins showed that, up to 1 hour after irradiation, immunoreactive proteins were confined to the neocortex at the irradiation site. At 4 hours, vasogenic edema was present in the vicinity of the irradiation site and the subcortical white matter, and, at later stages (16 to 36 hours), also extended into the contralateral hemisphere. Although this was followed by a gradual decrease in labeling intensity, resolution of edema was still not complete after 48 hours. Analysis of sequential functional changes in conjunction with morphological alterations indicates that the evolution of morphological damage after laser irradiation does not correlate with the time course and spatial distribution of protein synthesis inhibition or vasogenic edema. Although the central coagulation necrosis represents a direct effect of radiation, the final size of the laser-induced lesion is determined by a delayed colliquation necrosis due to persistent perifocal ischemia. Extent and severity of ischemia in a zone with initial preservation of neuroglial cells can be explained by the optical properties of the Nd:YAG laser; extensive scattering of light within brain parenchyma associated with a high blood-to-brain absorption ratio selectively affects blood vessels outside the irradiation focus.

Cerebral blood flow and glucose metabolism in experimental brain edema

1989 ◽  
Vol 71 (6) ◽  
pp. 868-874 ◽  
Author(s):  
Leslie N. Sutton ◽  
David Barranco ◽  
Joel Greenberg ◽  
Stephen Dante ◽  
Sandra Florin ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
White Matter ◽  
Vasogenic Edema ◽  
Tissue Water ◽  
Content Type ◽  
Control Value ◽  
Experimental Brain Edema ◽  
Fine Print ◽  
Edematous Brain

✓ The relationship between cerebral blood flow (CBF) and cerebral metabolic rate of glucose (CMR gl) in the white matter was studied in a plasma infusion model of vasogenic edema in cats. Local CBF, as determined by iodoantipyrine testing, was found to be significantly decreased in edematous white matter (mean ± standard error of the mean: 17.3 ± 1.5 ml/100 gm/min) when compared with CBF in the contralateral control white matter (24.8 ± 1.8 ml/100 gm/min). When the values for edematous brain were corrected for dilution, however, the local CBF averaged 25.3 ± 1.7 ml/100 gm/min, which was similar to the control value. Local CMRgl was found to be significantly increased in plasma-infused white matter (16.3 ± 2.2 µmol/100 gm/min) compared with that in control white matter (10.7 ± 1.3 µmol/100 gm/min). This difference remained, despite correction for dilution and recalculation of local CMRgl values based on altered kinetic constants found in edematous brain. A similar increase in local CMRgl was noted with saline-infusion edema. It is concluded that the increased tissue water level does not alter CBF, but does induce an increase in anaerobic metabolism.

Experiences with surgical thrombosis of intracranial berry aneurysms and carotid cavernous fistulas

1974 ◽  
Vol 41 (6) ◽  
pp. 657-670 ◽  
Author(s):  
Sean Mullan
Keyword(s):  
Blood Flow ◽  
Intracranial Aneurysm ◽  
Carotid Cavernous Fistula ◽  
Content Type ◽  
Cavernous Fistula ◽  
Carotid Blood Flow ◽  
Giant Intracranial Aneurysm ◽  
Surgical Methods ◽  
Carotid Cavernous Fistulas ◽  
Fine Print

✓ The results of 61 cases of stereotaxic thrombosis of intracranial berry aneurysms indicate that the technique in selected cases is comparable to, but not necessarily superior to standard surgical methods. The results of wire-induced thrombosis in 15 cases of giant intracranial aneurysm suggest that this method is effective in situations where clipping and encapsulation are inapplicable. The results of thrombosis in six cases of carotid cavernous fistula suggest that intracavernous wire thrombosis may prove to be the treatment of choice in that it seals the fistula without impairing carotid blood flow.

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.

Effect of sympathectomy on spinal blood flow autoregulation and posttraumatic ischemia

1982 ◽  
Vol 56 (5) ◽  
pp. 706-710 ◽  
Author(s):  
Wise Young ◽  
Vincent DeCrescito ◽  
John J. Tomasula
Keyword(s):  
Blood Flow ◽  
Spinal Injury ◽  
Sympathetic Ganglia ◽  
Control Group ◽  
Content Type ◽  
Systemic Pressure ◽  
Sympathetic Regulation ◽  
Mean Systemic Pressure ◽  
Paravertebral Sympathetic Ganglia ◽  
Fine Print

✓ The hypothesis that the paravertebral sympathetic ganglia play a role in spinal blood flow regulation was tested in cats. Five cats were subjected to paravertebral sympathectomy, two to combined sympathectomy-adrenalectomy, three to adrenalectomy alone, and five controls received no treatment. Laminectomy was carried out to expose the T4–10 cord, and autoregulation was tested by measuring blood flow from the lateral columns with the hydrogen clearance technique during manipulation of systemic pressure with intravenous saline infusion and nitroprusside administration. The cord was then contused at T-7 with a 400 gm-cm impact injury. Posttraumatic blood flow was recorded, and neurophysiological function was assessed with somatosensory evoked potential (SEP) monitoring. Before injury, blood flow in the untreated (control) group had no consistent relationship with mean systemic pressure over the range 80 to 160 mm Hg. In contrast, in all cats with paravertebral sympathectomy, whether accompanied by adrenalectomy or not, blood flows increased with systemic pressure (correlation coefficient 0.86, p < 0.01). After injury, the control and adrenalectomized cats showed blood flow decreases of > 60% to 4 to 6 ml/100 gm/min (p < 0.01) by 2 to 3 hours. However, cats with paravertebral sympathectomy maintained blood flow above 9 ml/100 gm/min for up to 3 hours after injury. All the sympathectomized cats recovered their SEP by the 3rd hour after injury, compared with none of the controls. Thus, in the absence of the paravertebral sympathetic ganglia, spinal blood flow autoregulation was impaired and the typical posttraumatic loss in blood flow did not occur. The sympathectomy also protected the spinal cords from the neurophysiological loss usually seen in 400 gm-cm injury. The data suggest the need for caution in using acetylcholine blocking agents to paralyze animals in experimental spinal injury, since these agents alter sympathetic activity and may influence the injury process. The spinal cord is an excellent model in which to investigate sympathetic regulation of central nervous system blood flow.

Nonhyperemic blood flow restoration and brain edema in experimental focal cerebral ischemia

1989 ◽  
Vol 70 (1) ◽  
pp. 73-80 ◽  
Author(s):  
Toshihiko Kuroiwa ◽  
Makoto Shibutani ◽  
Riki Okeda
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Brain Edema ◽  
Focal Cerebral Ischemia ◽  
Reactive Hyperemia ◽  
Diffusion Method ◽  
Left Middle Cerebral Artery ◽  
Content Type ◽  
Bbb Opening ◽  
Fine Print

✓ The effect of suppression of postischemic reactive hyperemia on the blood-brain barrier (BBB) and ischemic brain edema after temporary focal cerebral ischemia was studied in cats under ketamine and alpha-chloralose anesthesia. Regional cerebral blood flow (rCBF) was measured by a thermal diffusion method and a hydrogen clearance method. The animals were separated into three groups. In Group A, the left middle cerebral artery (MCA) was occluded for 6 hours. In Group B, the MCA was occluded for 3 hours and then reperfused for 3 hours; postischemic hyperemia was suppressed to the preischemic level by regulating the degree of MCA constriction. In Group C, the MCA was occluded for 3 hours and reperfused for 3 hours without suppressing the postischemic reactive hyperemia. The brain was removed and cut coronally at the site of rCBF measurement. The degree of ischemic edema was assessed by gravimetry in samples taken from the coronal section and correlated with the degree of BBB disruption at the corresponding sites, evaluated by densitometric determination of Evans blue discoloration. The findings showed that 1) ischemic edema was significantly exacerbated by postischemic hyperemia during reperfusion in parallel with the degree of BBB opening to serum proteins, and 2) suppression of postischemic hyperemia significantly reduced the exacerbation of ischemic edema and BBB opening. These findings indicate that blood flow may be restored without significant exacerbation of postischemic edema by the suppression of postischemic hyperemia in focal cerebral ischemia.

Improvement in cerebral blood flow and metabolism following subarachnoid hemorrhage in response to prophylactic administration of the hydroxyl radical scavenger, AVS, (±)-N,N′-propylenedinicotinamide: a positron emission tomography study in rats

2000 ◽  
Vol 92 (6) ◽  
pp. 1009-1015 ◽  
Author(s):  
Seiji Yamamoto ◽  
Weiyu Teng ◽  
Shigeru Nishizawa ◽  
Takeharu Kakiuchi ◽  
Hideo Tsukada
Keyword(s):  
Positron Emission Tomography ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Emission Tomography ◽  
Radical Scavenger ◽  
Content Type ◽  
Prophylactic Administration ◽  
Positron Emission ◽  
Hydroxyl Radical Scavenger ◽  
Fine Print

Object. The hydroxyl radical scavenger (±)-N,N′-propylenedinicotinamide (AVS) has been shown to ameliorate the occurrence of vasospasm following experimental subarachnoid hemorrhage (SAH) and to reduce the incidence of delayed ischemic neurological deficits (DINDs) in patients with SAH. The authors investigated whether prophylactic administration of AVS could improve cerebral blood flow (CBF) and cerebral glucose utilization (CGU) following SAH in rats.Methods. Anesthetized rats were subjected to intracisternal injection of blood (SAH group) or saline (control group). Either AVS (1 mg/kg/min) or saline (vehicle group) was continuously injected into the rat femoral vein. Forty-eight hours later, positron emission tomography scanning was used with the tracers 15O-H2O and 18F-2-fluoro-d-glucose to analyze quantitatively CBF and CGU, respectively, in the frontoparietal and occipital regions (12 regions of interest/group).In SAH rats receiving only vehicle, CBF decreased significantly (p < 0.05, Tukey's test) and CGU tended to decrease, compared with values obtained in control (non-SAH) rats receiving vehicle. In rats that were subjected to SAH, administration of AVS significantly (p < 0.05, Tukey's test) improved CBF and CGU in both the frontoparietal and occipital regions compared with administration of vehicle alone.Conclusions. Prophylactic administration of AVS improves CBF and CGU in the rat brain subjected to SAH, and can be a good pharmacological treatment for the prevention of DINDs following SAH.

An experimental study of the acute stage of subarachnoid hemorrhage

1983 ◽  
Vol 59 (6) ◽  
pp. 917-924 ◽  
Author(s):  
Ken Kamiya ◽  
Hideyuki Kuyama ◽  
Lindsay Symon
Keyword(s):  
Blood Flow ◽  
Subarachnoid Hemorrhage ◽  
Acute Stage ◽  
Flow Measurements ◽  
Content Type ◽  
Baboon Model ◽  
Differential Increase ◽  
Blood Flow Measurements ◽  
Fine Print ◽  
Made In

✓ A baboon model of subarachnoid hemorrhage (SAH) has been developed to study the changes in cerebral blood flow (CBF), intracranial pressure (ICP), and cerebral edema associated with the acute stage of SAH. In this model, hemorrhage was caused by avulsion of the posterior communicating artery via a periorbital approach, with the orbit sealed and ICP restored to normal before SAH was produced. Local CBF was measured in six sites in the two hemispheres, and ICP monitored by an implanted extradural transducer. Following sacrifice of the animal, the effect of the induced SAH on ICP, CBF, autoregulation, and CO2 reactivity in the two hemispheres was assessed. Brain water measurements were also made in areas of gray and white matter corresponding to areas of blood flow measurements, and also in the deep nuclei. Two principal patterns of ICP change were found following SAH; one group of animals showed a return to baseline ICP quite quickly and the other maintained high ICP for over an hour. The CBF was reduced after SAH to nearly 20% of control values in all areas, and all areas showed impaired autoregulation. Variable changes in CO2 reactivity were evident, but on the side of the hemorrhage CO2 reactivity was predominantly reduced. Differential increase in pressure lasting for over 7 minutes was evident soon after SAH on the side of the ruptured vessel. There was a significant increase of water in all areas, and in cortex and deep nuclei as compared to control animals.

The effect of total parenteral nutrition on vasogenic edema development following cold injury in rats

1989 ◽  
Vol 70 (4) ◽  
pp. 623-627 ◽  
Author(s):  
David J. Combs ◽  
Linda Ott ◽  
Pamela S. McAninch ◽  
Robert J. Dempsey ◽  
Byron Young
Keyword(s):  
Parenteral Nutrition ◽  
Total Parenteral Nutrition ◽  
Glucose Level ◽  
Vasogenic Edema ◽  
Serum Glucose ◽  
Serum Osmolality ◽  
Cold Injury ◽  
Serum Glucose Level ◽  
Content Type ◽  
Fine Print

✓ Total parenteral nutrition (TPN) has been shown to decrease mortality and to increase the rate of recovery in head-injured patients. However, a recent short-term animal experiment has raised concern over the potential enhancement of vasogenic edema by TPN. The experiment described here was undertaken to examine longer-term effects of TPN infusion on vasogenic edema development. Twenty-four rats received an infusion of a TPN solution (35% glucose) or 0.9% saline at 4 ml/kg/hr for 4 or 26 hours following cold injury. In the 4-hour experiment, TPN increased the serum glucose level to 772 ± 57 mg/dl compared to 160 ± 14 mg/dl in the saline-treated animals (p = 0.0001) and increased serum osmolality to 312 ± 3 mOsm/kg compared to 291 ± 3 mOsm/kg in the saline-treated group (p = 0.0006). In the 26-hour experiment, TPN-infused rats were also hyperglycemic and hyperosmotic by 4 hours postinjury and remained hyperglycemic at 26 hours postinjury (serum glucose level 374 ± 97 mg/dl compared to 141 ± 3 mg/dl in saline-treated animals; p = 0.0371). Although by 26 hours the TPN-infused rats appeared hyperosmotic compared to the saline-treated rats, high variability in the TPN group prevented statistical confirmation of this observation (serum osmolality 337 ± 35 mOsm/kg in the TPN group compared to 287 ± 6 mOsm/kg in the saline group). A three-way analysis of variance with repeated measures was used to analyze the effect of infusion (saline vs. TPN), time (4 vs. 26 hours), and cold injury on the specific gravity of the five brain regions studied. Cold injury significantly increased edema development in the injured versus uninjured hemisphere for every region studied (p ≤ 0.0034, all five regions), and edema development increased significantly between 4 and 26 hours in three of the five regions (p ≤ 0.0207, all three regions). The infusion fluid was not a significant factor in any of the analyses. In conclusion, TPN infusion produced hyperglycemia and hyperosmolality in cold-injured rats but did not enhance vasogenic edema development in any brain region studied.

Volumetric thermal devascularization of large meningiomas

2004 ◽  
Vol 101 (5) ◽  
pp. 779-786 ◽  
Author(s):  
Amami Kato ◽  
Yasunori Fujimoto ◽  
Masaaki Taniguchi ◽  
Naoya Hashimoto ◽  
Azuma Hirayama ◽  
...  
Keyword(s):  
Thermal Ablation ◽  
Histopathological Examination ◽  
Three Dimensional ◽  
Target Volume ◽  
Coagulation Necrosis ◽  
Radiofrequency Energy ◽  
Content Type ◽  
Dimensional Reconstruction ◽  
Tumor Parenchyma ◽  
Fine Print

Object. Controlling hemorrhage is crucial in the safe and efficient removal of large meningiomas. Intravascular embolization is not always a satisfactory means of accomplishing this goal because of the procedure's hemostatic effect and risk of complications. The authors in this study used a volumetric thermal ablation technique incorporating radiofrequency energy, image guidance, and local temperature control to devascularize tumor tissue. Methods. Five patients with large meningiomas were treated. The target and orientation of the radiofrequency thermal ablation (RFTA) were simulated preoperatively to maximize devascularization of the lesion without thermal injury to adjacent critical structures. Image fusion, three-dimensional reconstruction, and image-guided methods provided for optimized trajectories and targets for insertion of the RFTA needle. During ablation, local temperatures of the tissue being cauterized were monitored continuously to limit the ablated lesion to within the target volume. The effects of devascularization and the softening of the tumor parenchyma facilitated lesion removal. The intracranial ablated meningioma changed into necrotic tissue and shrank within a few months. Histopathological examination of the ablated lesion revealed sharply demarcated coagulation necrosis. Conclusions. Volumetric thermal devascularization can be applied safely in the treatment of large meningiomas to facilitate surgical manipulation of the lesion as well as to reduce its size palliatively. The procedure's usefulness should be studied further in a larger number of cases with different tumor characteristics.

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