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  • 1
    Online Resource
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    Hypothermia effects on neurovascular coupling and cerebral metabolic rate of oxygen
    Elsevier BV ; 2008
    In:  NeuroImage Vol. 40, No. 4 ( 2008-05), p. 1523-1532
    Details
    In: NeuroImage, Elsevier BV, Vol. 40, No. 4 ( 2008-05), p. 1523-1532
    Type of Medium: Online Resource
    ISSN: 1053-8119
    URL: Article
    DOI: 10.1016/j.neuroimage.2008.01.041
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1471418-8
    SSG: 5,2
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  • 2
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    Ion changes in spreading ischaemia induce rat middle cerebral artery constriction in the absence of NO
    Oxford University Press (OUP) ; 2005
    In:  Brain Vol. 128, No. 9 ( 2005-09-01), p. 2042-2051
    Details
    In: Brain, Oxford University Press (OUP), Vol. 128, No. 9 ( 2005-09-01), p. 2042-2051
    Type of Medium: Online Resource
    ISSN: 1460-2156 , 0006-8950
    URL: Article
    DOI: 10.1093/brain/awh545
    RVK:
    XA 10000
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2005
    detail.hit.zdb_id: 1474117-9
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  • 3
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    Role of Nitric Oxide Synthase Inhibition in Leukocyte-Endothelium Interaction in the Rat Pial Microvasculature
    SAGE Publications ; 1996
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 16, No. 6 ( 1996-11), p. 1143-1152
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 16, No. 6 ( 1996-11), p. 1143-1152
    Abstract: We investigated the role of nitric oxide (NO) in leukocyte-endothelium interaction, blood-brain barrier (BBB) function and oxygen free-radical production in the rat pial microcirculation. In a closed cranial window preparation (dura removed) over the parietal cortex of pentobarbital-anesthetized Wistar rats, NO synthase (NOS) was inhibited by systemic and/or topical application of N ω -nitro-l-arginine (l-NNA) under physiological conditions and during leukotriene B 4 (LTB 4 ) activation. Circulating leukocytes were labeled by intravenous injection of rhodamine 6G. We used a confocal laser scanning microscope (CLSM) and studied leukocyte rolling and sticking in pial veins and arteries before and after NOS inhibition. At the end of the experiments, sodium-fluorescein was injected intravenously to test BBB integrity. Brain cortex oxygen free-radical production was investigated in the cranial window preparation using lucigenin-enhanced chemiluminescence (CL). l-NNA application did not lead to significant changes in leukocyte-endothelium interaction, BBB function, and oxygen free-radical production under physiological conditions [leukocyte-endothelium interaction: control (n = 5), l-NNA systemically (n = 5), l-NNA topically (n = 5): at baseline rollers/100 μm: 0.76 ± 0.55, 0.64 ± 0.94, 0.44 ± 0.55 and stickers/100 μm: 0.90 ± 0.28, 0.76 ± 0.24, 0.84 ± 0.42; at 60 min rollers/100 μm: 1.49 ± 0.66, 1.21 ± 0.99, 0.67 ± 0.66 and stickers/100 μm: 1.04 ± 0.20, 1.19 ± 0.23, 1.21 ± 0.54; oxygen free-radical production (n = 4): CL count before l-NNA application 35 ± 17 cps, after 1 h of topical superfusion of l-NNA 38 ± 14 cps; p 〈 0.05]. In contrast to the results achieved under physiological conditions, a significant further increase of rolling leukocytes and BBB permeability occurred due to NOS inhibition under LTB 4 -activated conditions [76 ± 47% significant ( p ≤ 0.01, n = 7) further increase of rollers/100 μm due to 60 min l-NNA application following the activation period of 120 min LTB 4 superfusion]. Our results support a modulatory role for NO in leukocyte-endothelium interaction and BBB permeability in the pial microcirculation when this interaction is increased.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/00004647-199611000-00008
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1996
    detail.hit.zdb_id: 2039456-1
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  • 4
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    Heparin Inhibits Leukocyte Rolling in Pial Vessels and Attenuates Inflammatory Changes in a Rat Model of Experimental Bacterial Meningitis
    SAGE Publications ; 1997
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 17, No. 11 ( 1997-11), p. 1221-1229
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 17, No. 11 ( 1997-11), p. 1221-1229
    Abstract: Heparin is a natural proteoglycan that was first described in 1916. In addition to its well characterized effect on blood coagulation, it is becoming clear that heparin also modulates inflammatory processes on several levels, including the interference with leukocyte–endothelium interaction. Anecdotal observations suggest a better clinical outcome of heparin-treated patients with bacterial meningitis. The authors demonstrate that heparin, a glycosaminoglycan, inhibits significantly in the early phase of experimental pneumococcal meningitis the increase of 1) regional cerebral blood flow (125 ± 18 versus 247 ± 42%), 2) intracranial pressure (4.5 ± 2.0 versus 12.1 ± 2.2 mm Hg), 3) brain edema (brain water content: 78.23 ± 0.33 versus 79.49 ± 0.46%), and 4) influx of leukocytes (571 ± 397 versus 2400 ± 875 cells/μL) to the cerebrospinal fluid compared with untreated rats. To elucidate the possible mechanism of this observation, the authors investigated for the first time leukocyte rolling in an inflammatory model in brain venules by confocal laser scanning microscopy in vivo. Heparin significantly attenuates leukocyte rolling at 2, 3, and 4 hours (2.8 ± 1.3 versus 7.9 ± 3.2/100 μm/min), as well as leukocyte sticking at 4 hours (2.1 ± 0.4 versus 3.5 ± 1.0/100 μm/min) after meningitis induction compared with untreated animals. The authors conclude that heparin can modulate acute central nervous system inflammation and, in particular, leukocyte–endothelium interaction, a key process in the cascade of injury in bacterial meningitis. They propose to evaluate further the potential of heparin in central nervous system inflammation in basic and clinical studies.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/00004647-199711000-00011
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1997
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  • 5
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    Cerebrovascular Vasodilation to Extraluminal Acidosis Occurs via Combined Activation of ATP-Sensitive and Ca 2+ -Activated Potassium Channels
    SAGE Publications ; 2003
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 23, No. 10 ( 2003-10), p. 1227-1238
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 23, No. 10 ( 2003-10), p. 1227-1238
    Abstract: Albeit controversely discussed, it has been suggested by several authors that nitric oxide (NO) serves as a permissive factor in the cerebral blood flow response to systemic hypercapnia. Potassium channels are important regulators of cerebrovascular tone and may be modulated by a basal perivascular NO level. To elucidate the functional targets of the proposed NO modulation during hypercapnia-induced vasodilation, the authors performed experiments in isolated, cannulated, and pressurized rat middle cerebral arteries (MCA). Extracellular pH was reduced from 7.4 to 7.0 in the extraluminal bath to induce NO dependent vasdilation. Acidosis increased vessel diameter by 35 ± 10%. In separate experiments, ATP-sensitive potassium channels (K ATP ) were blocked by extraluminal application of glibenclamide (Glib), Ca 2+ -activated potassium channels (K Ca ) by tetraethylammonium (TEA), voltage-gated potassium channels (K v ) by 4-aminopyridine, and inward rectifier potassium channels (K IR ) by BaCl 2 . Na + -K + -ATP-ase was inhibited by ouabain. Application of TEA slightly constricted the arteries at pH 7.4 and slightly but significantly attenuated the vasodilation to acidosis. Inhibition of the other potassium channels or Na + -K + -ATP-ase had no effect. Combined blockade of K ATP and K Ca channels further reduced resting diameter, and abolished acidosis induced vasodilation. The authors conclude that mainly K Ca channels are active under resting conditions. K ATP and K Ca channels are responsible for vasodilation to acidosis. Activity of one of these potassium channel families is sufficient for vasodilation to acidosis, and only combined inhibition completely abolishes vasodilation. During NO synthase inhibition, dilation to the K ATP channel opener pinacidil or the K Ca channel opener NS1619 was attenuated or abolished, respectively. The authors suggest that a basal perivascular NO level is necessary for physiologic K ATP and K Ca channel function in rat MCA. Future studies have to elucidate whether this NO dependent effect on K ATP and K Ca channel function is a principle mechanism of NO induced modulation of cerebrovascular reactivity and whether the variability of findings in the literature concerning a modulatory role of NO can be explained by different levels of vascular NO/cGMP concentrations within the cerebrovascular tree.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1097/01.WCB.0000088764.02615.B7
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2003
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  • 6
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    Pharmacological Uncoupling of Activation Induced Increases in CBF and CMRO 2
    SAGE Publications ; 2010
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 30, No. 2 ( 2010-02), p. 311-322
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 30, No. 2 ( 2010-02), p. 311-322
    Abstract: Neurovascular coupling provides the basis for many functional neuroimaging techniques. Nitric oxide (NO), adenosine, cyclooxygenase, CYP450 epoxygenase, and potassium are involved in dilating arterioles during neuronal activation. We combined inhibition of NO synthase, cyclooxygenase, adenosine receptors, CYP450 epoxygenase, and inward rectifier potassium (Kir) channels to test whether these pathways could explain the blood flow response to neuronal activation. Cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO 2 ) of the somatosensory cortex were measured during forepaw stimulation in 24 rats using a laser Doppler/spectroscopy probe through a cranial window. Combined inhibition reduced CBF responses by two-thirds, somatosensory evoked potentials and activation-induced CMRO 2 increases remained unchanged, and deoxy-hemoglobin (deoxy-Hb) response was abrogated. This shows that in the rat somatosensory cortex, one-third of the physiological blood flow increase is sufficient to prevent microcirculatory increase of deoxy-Hb concentration during neuronal activity. The large physiological CBF response is not necessary to support small changes in CMRO 2 . We speculate that the CBF response safeguards substrate delivery during functional activation with a considerable ‘safety factor’. Reduction of the CBF response in pathological states may abolish the BOLD–fMRI signal, without affecting underlying neuronal activity.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/jcbfm.2009.211
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2010
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  • 7
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    Global Cerebral Ischemia in the Rat: Online Monitoring of Oxygen Free Radical Production Using Chemiluminescence in vivo
    SAGE Publications ; 1995
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 15, No. 6 ( 1995-11), p. 929-940
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 15, No. 6 ( 1995-11), p. 929-940
    Abstract: Using online in vivo chemiluminescence (CL), we studied for the first time continuously the production of reactive oxygen species (ROS) after global cerebral ischemia and the relationship of ROS production to CBF. In anesthetized rats equipped with a closed cranial window, the CL enhancer, lucigenin (1 m M), was superfused onto the brain topically. CL was measured through the cranial window with a cooled photomultiplier, and CBF was measured simultaneously with laser–Doppler flowmetry. Reperfusion after 10 min (n = 8) of global cerebral ischemia led to a CL peak to 188 ± 77% (baseline = 100%) within 10 ± 4 min. After 2 h of reperfusion, CL had returned to 102 ± 28%. Reperfusion after 20 min (n = 8) of ischemia increased CL to 225 ± 48% within 12 ± 3 min. After 2 h, CL was still increased (150 ± 44%, p 〈 0.05 compared with 10 min of ischemia). CL after 10 min of ischemia was neither affected by brain topical free CuZn-superoxide dismutase (SOD) (100 U/ml, n = 3) nor by i.v. administration of free CuZn-SOD (104 U/kg, followed by 104 U/kg/h, n = 3). The CBF hyperperfusion peak on reperfusion preceded the CL peak in all experiments by several minutes. In additional in vitro experiments we investigated the source of CL: Intracellular loading of lucigenin was demonstrated in cultured CNS cells, and a very similar pattern of CL as in the in vivo preparation after ischemia developed in rat brain slices after 15 min of hypoxia, which was unaffected by free CuZn-SOD (100 U/ml) but strongly attenuated by liposome-entrapped CuZn-SOD. We conclude that lucigenin-enhanced CL is a promising tool to study ROS production continuously from the in vivo brain of experimental animals and brain slices, and that the CL signal most likely derives from the intracellular production of superoxide. The production of ROS is preceded by reperfusion, is burst-like, and is dependent on the duration of the ischemic interval.
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/jcbfm.1995.118
    Language: English
    Publisher: SAGE Publications
    Publication Date: 1995
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  • 8
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    The cerebrovascular response to elevated potassium – role of nitric oxide in the in vitro model of isolated rat middle cerebral arteries
    Elsevier BV ; 2001
    In:  Neuroscience Letters Vol. 306, No. 1-2 ( 2001-6), p. 61-64
    Details
    In: Neuroscience Letters, Elsevier BV, Vol. 306, No. 1-2 ( 2001-6), p. 61-64
    Type of Medium: Online Resource
    ISSN: 0304-3940
    URL: Article
    DOI: 10.1016/S0304-3940(01)01878-X
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2001
    detail.hit.zdb_id: 1498535-4
    SSG: 12
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  • 9
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    Nitric oxide: a modulator, but not a mediator, of neurovascular coupling in rat somatosensory cortex
    American Physiological Society ; 1999
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 277, No. 2 ( 1999-08-01), p. H799-H811
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 277, No. 2 ( 1999-08-01), p. H799-H811
    Abstract: We investigated the role of nitric oxide (NO)/cGMP in the coupling of neuronal activation to regional cerebral blood flow (rCBF) in α-chloralose-anesthetized rats. Whisker deflection (60 s) increased rCBF by 18 ± 3%. NO synthase (NOS) inhibition by N ω -nitro-l-arginine (l-NNA; topically) reduced the rCBF response to 9 ± 4% and resting rCBF to 80 ± 8%. NO donors [ S-nitroso- N-acetylpenicillamine (SNAP; 50 μM), 3-morpholinosydnonimine (10 μM)] or 8-bromoguanosine 3′,5′-cyclic-monophosphate (8-BrcGMP; 100 μM)] restored resting rCBF andl-NNA-induced attenuation of the whisker response in the presence ofl-NNA, whereas the NO-independent vasodilator papaverine (1 mM) had no effect on the whisker response. Basal cGMP levels were decreased to 35% byl-NNA and restored to 65% of control by subsequent SNAP superfusion. Inhibition of neuronal NOS by 7-nitroindazole (7-NI; 40 mg/kg ip) or soluble guanylyl cyclase by 1 H-[1,2,4] oxadiazolo[4,3-a]quinoxalin-1-one (ODQ; 100 μM) significantly reduced resting rCBF to 86 ± 8 and 92 ± 10% and whisker rCBF response to 7 ± 4 and 12 ± 3%, respectively. ODQ reduced tissue cGMP to 54%. 8-BrcGMP restored the whisker response in the presence of 7-NI or ODQ. We conclude that NO, produced by neuronal NOS, is a modulator in the coupling of neuronal activation and rCBF in rat somatosensory cortex and that this effect is mainly mediated by cGMP.l-NNA-induced vasomotion was significantly reduced during increased neuronal activity and after restoration of basal NO levels, but not after restoration of cGMP.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.1999.277.2.H799
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1999
    detail.hit.zdb_id: 1477308-9
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  • 10
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    Neuroprotective effects of creatine in a mouse model of stroke: An experimental MRI study
    SAGE Publications ; 2005
    In:  Journal of Cerebral Blood Flow & Metabolism Vol. 25, No. 1_suppl ( 2005-08), p. S6-S6
    Details
    In: Journal of Cerebral Blood Flow & Metabolism, SAGE Publications, Vol. 25, No. 1_suppl ( 2005-08), p. S6-S6
    Type of Medium: Online Resource
    ISSN: 0271-678X , 1559-7016
    URL: Article
    DOI: 10.1038/sj.jcbfm.9591524.0006
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2005
    detail.hit.zdb_id: 2039456-1
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