scholarly journals Reversal Of Impaired Blood Flow Of The Basal Ganglion From The Prior Focal Perfusion Defect In A Case Of Ischemic Infarction: Observation During The Two Stages Of Administration Of Intravenous Laser Irradiation Of Blood Shin-Tsu Chang1*, Jui-Hsiang Sung2

2019 ◽  
Vol 2 (1) ◽  
pp. 01-05
Author(s):  
Shin-Tsu Chang ◽  
Keyword(s):  
Blood Flow ◽  
Laser Irradiation ◽  
Basal Ganglion ◽  
Perfusion Defect ◽  
Ischemic Infarction ◽  
Two Stages

5-Hydroxytryptamine dominates over thromboxane A2 in reducing collateral blood flow by activated platelets

1993 ◽  
Vol 265 (1) ◽  
pp. H158-H164 ◽  
Author(s):  
W. Loots ◽  
F. De Clerck
Keyword(s):  
Blood Flow ◽  
Platelet Activation ◽  
Perfusion Defect ◽  
Activation Process ◽  
Collateral Blood Flow ◽  
Peripheral Vascular ◽  
Similar Extent ◽  
Receptor Antagonism ◽  
Prostaglandin Endoperoxide ◽  
Activated Platelets

Intra-aortic infusion of collagen (100 micrograms/kg in 1 min) elicited an extensive platelet activation and transient but marked reductions of blood flow and increases of peripheral vascular resistance, both responses being more pronounced in collaterals than in normal arterial beds in feline hind legs. Blockade of 5-hydroxytryptamine (5-HT) subtype 2 (5-HT2) receptors for 5-HT (ketanserin or ritanserin, 0.63 mg/kg iv, -10 min) or amine depletion (reserpine, 0.1 mg/kg im, -10 days, + parachlorophenylalanine 100 mg/kg sc daily for 3 days), but not cyclooxygenase inhibition (indomethacin, 5 mg/kg iv) or thromboxane (Tx) A2/prostaglandin endoperoxide receptor antagonism (sulotroban, 2.5 mg/kg iv), largely prevented the collagen-induced perfusion defect without interfering substantially with the platelet activation process. TxA2 synthase inhibition, alone (dazoxiben, 5 mg/kg iv) or combined with TxA2-prostaglandin endoperoxide receptor antagonism (ridogrel, 2.5 mg/kg iv), partially reduced the collagen-induced perfusion defect and limited to a similar extent the initial platelet aggregation and release of 5-hydroxyindoles and TxB2 while increasing plasma levels of prostacyclin. These results suggest that platelet-derived 5-HT dominates over TxA2 in reducing blood flow in collateral-dependent tissue of the cat hindlimb.

Local Cerebral Blood Flow and Oxygen Consumption in Evolving Irreversible Ischemic Infarction

1983 ◽  
pp. 120-125 ◽  
Author(s):  
J. C. Baron ◽  
D. Rougemont ◽  
P. Lebrun-Grandié ◽  
M. G. Bousser ◽  
E. Cabanis ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Oxygen Consumption ◽  
Local Cerebral Blood Flow ◽  
Ischemic Infarction

scholarly journals Hyperlipidemia Disrupts Cerebrovascular Reflexes and Worsens Ischemic Perfusion Defect

2013 ◽  
Vol 33 (6) ◽  
pp. 954-962 ◽  
Author(s):  
Cenk Ayata ◽  
Hwa Kyoung Shin ◽  
Ergin Dileköz ◽  
Dmitriy N Atochin ◽  
Satoshi Kashiwagi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Apolipoprotein E ◽  
Knockout Mice ◽  
Perfusion Defect ◽  
Laser Speckle ◽  
Wild Type ◽  
Apolipoprotein E Knockout Mice ◽  
The Impact ◽  
Cerebrovascular Reflexes

Hyperlipidemia is a highly prevalent risk factor for coronary and cervical atherosclerosis and stroke. However, even in the absence of overt atherosclerosis, hyperlipidemia disrupts endothelial and smooth muscle function. We investigated the impact of hyperlipidemia on resting-brain perfusion, fundamental cerebrovascular reflexes, and dynamic perfusion defect during acute focal ischemia in hyperlipidemic apolipoprotein E knockout mice before the development of flow-limiting atherosclerotic stenoses. Despite elevated blood pressures, absolute resting cerebral blood flow was reduced by 20% in apolipoprotein E knockout compared with wild type when measured by [14C]-iodoamphetamine technique. Noninvasive, high spatiotemporal resolution laser speckle flow imaging revealed that the lower autoregulatory limit was elevated in apolipoprotein E knockout mice (60 vs. 40 mm Hg), and cortical hyperemic responses to hypercapnia and functional activation were attenuated by 30% and 64%, respectively. Distal middle cerebral artery occlusion caused significantly larger perfusion defects and infarct volumes in apolipoprotein E knockout compared with wild type. Cerebrovascular dysfunction showed a direct relationship to the duration of high-fat diet. These data suggest that hyperlipidemia disrupts cerebral blood flow regulation and diminishes collateral perfusion in acute stroke in the absence of hemodynamically significant atherosclerosis.

Targeted increase in cerebral blood flow by transcranial near-infrared laser irradiation

2010 ◽  
Vol 42 (6) ◽  
pp. 566-576 ◽  
Author(s):  
Yoichi Uozumi ◽  
Hiroshi Nawashiro ◽  
Shunichi Sato ◽  
Satoko Kawauchi ◽  
Katsuji Shima ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Laser Irradiation ◽  
Near Infrared ◽  
Infrared Laser ◽  
Infrared Laser Irradiation

scholarly journals Effects of transcranial near-infrared laser irradiation on cerebral blood flow in mice

Nosotchu ◽  
2010 ◽  
Vol 32 (6) ◽  
pp. 559-562
Author(s):  
Hiroshi Nawashiro ◽  
Youichi Uozumi ◽  
Shunichi Sato ◽  
Satoko Kawauchi ◽  
Hiroaki Kobayashi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Laser Irradiation ◽  
Near Infrared ◽  
Infrared Laser ◽  
Infrared Laser Irradiation

scholarly journals Microvascular blood flow dynamics associated with photodynamic therapy, pulsed dye laser irradiation and combined regimens

2006 ◽  
Vol 38 (5) ◽  
pp. 532-539 ◽  
Author(s):  
Tia K. Smith ◽  
Bernard Choi ◽  
Julio C. Ramirez-San-Juan ◽  
J. Stuart Nelson ◽  
Kathryn Osann ◽  
...  
Keyword(s):  
Blood Flow ◽  
Photodynamic Therapy ◽  
Laser Irradiation ◽  
Dye Laser ◽  
Flow Dynamics ◽  
Pulsed Dye Laser ◽  
Microvascular Blood Flow ◽  
Blood Flow Dynamics

Optothermal mathematical model and experimental studies for laser irradiation of arteries in the presence of blood flow

1989 ◽  
Vol 28 (12) ◽  
pp. 2263 ◽  
Author(s):  
Diana Decker-Dunn ◽  
Douglas A. Christensen ◽  
William Mackie ◽  
Jolene Fox ◽  
G. Michael Vincent
Keyword(s):  
Mathematical Model ◽  
Blood Flow ◽  
Laser Irradiation ◽  
Experimental Studies

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.

scholarly journals Changes of blood flow in the cerebral cortex after subcortical ischemic infarction.

Stroke ◽  
1989 ◽  
Vol 20 (2) ◽  
pp. 211-216 ◽  
Author(s):  
E Højer-Pedersen ◽  
O F Petersen
Keyword(s):  
Blood Flow ◽  
Cerebral Cortex ◽  
Ischemic Infarction
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