Clinical visualization of cerebral vasodilatation by desflurane

AbstractInhibition of RhoA-ROCK pathway is involved in the H2S-induced cerebral vasodilatation and H2S-mediated protection on endothelial cells against oxygen-glucose deprivation/reoxygenation injury. However, the inhibitory mechanism of H2S on RhoA-ROCK pathway is still unclear. The aim of this study was to investigate the target and mechanism of H2S in inhibition of RhoA/ROCK. GST-RhoAwild and GST-RhoAS188A proteins were constructed and expressed, and were used for phosphorylation assay in vitro. Recombinant RhoAwild-pEGFP-N1 and RhoAS188A-pEGFP-N1 plasmids were constructed and transfected into primary hippocampal nerve cells (HNCs) to evaluate the neuroprotective mechanism of endothelial H2S by using transwell co-culture system with endothelial cells from cystathionine-γ-lyase knockout (CSE−/−) mice and 3-mercaptopyruvate sulfurtransferase knockout (3-MST−/−) rats, respectively. We found that NaHS, exogenous H2S donor, promoted RhoA phosphorylation at Ser188 in the presence of cGMP-dependent protein kinase 1 (PKG1) in vitro. Besides, both exogenous and endothelial H2S facilitated the RhoA phosphorylation at Ser188 in HNCs, which induced the reduction of RhoA activity and membrane transposition, as well as ROCK2 activity and expression. To further investigate the role of endothelial H2S on RhoA phosphorylation, we detected H2S release from ECs of CSE+/+ and CSE−/− mice, and 3-MST+/+ and 3-MST−/− rats, respectively, and found that H2S produced by ECs in the culture medium is mainly catalyzed by CSE synthase. Moreover, we revealed that both endothelial H2S, mainly catalyzed by CSE, and exogenous H2S protected the HNCs against hypoxia-reoxygenation injury via phosphorylating RhoA at Ser188.

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Mechanisms of cerebral vasodilatation in hypoxia

Journal of Applied Physiology ◽

10.1152/jappl.1970.29.2.223 ◽

1970 ◽

Vol 29 (2) ◽

pp. 223-229 ◽

Cited By ~ 139

Author(s):

K. Kogure ◽

P. Scheinberg ◽

O. M. Reinmuth ◽

M. Fujishima ◽

R. Busto

Keyword(s):

Cerebral Vasodilatation

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Mechanisms of Hypoxic and Hypercapnic Cerebral Vasodilatation

The Human Brain Circulation ◽

10.1007/978-1-4612-0303-2_15 ◽

1994 ◽

pp. 195-209 ◽

Cited By ~ 2

Author(s):

William J. Pearce

Keyword(s):

Cerebral Vasodilatation

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Indication for cholinergically mediated cerebral vasodilatation during static exercise in humans

The FASEB Journal ◽

10.1096/fasebj.24.1_supplement.979.7 ◽

2010 ◽

Vol 24 (S1) ◽

Author(s):

Thomas Seifert ◽

James P Fisher ◽

Colin N Young ◽

Doreen Hartwich ◽

Paul J Fadel ◽

...

Keyword(s):

Static Exercise ◽

Cerebral Vasodilatation ◽

Exercise In Humans

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Neuronal nitric oxide mediates cerebral vasodilatation during acute hypertension

Brain Research ◽

10.1016/j.brainres.2007.01.008 ◽

2007 ◽

Vol 1139 ◽

pp. 126-132 ◽

Cited By ~ 35

Author(s):

William T. Talman ◽

Deidre Nitschke Dragon

Keyword(s):

Nitric Oxide ◽

Acute Hypertension ◽

Cerebral Vasodilatation

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Global Cerebral Vasodilatation Elicited by Focal Electrical Stimulation within the Dorsal Medullary Reticular Formation in Anesthetized Rat

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1983.41 ◽

1983 ◽

Vol 3 (3) ◽

pp. 270-279 ◽

Cited By ~ 34

Author(s):

Costantino Iadecola ◽

Masatsugu Nakai ◽

Ehud Arbit ◽

Donald J. Reis

Keyword(s):

Electrical Stimulation ◽

Reticular Formation ◽

Medial Longitudinal Fasciculus ◽

Medullary Reticular Formation ◽

Tissue Samples ◽

The Central Nervous System ◽

Cerebral Vasodilatation ◽

Cervical Sympathetic ◽

Global Increase ◽

Stimulation Of

We examined the effects of electrical stimulation of a restricted area of the dorsal medullary reticular formation (DMRF) on regional cerebral blood flow (CBF) in anesthetized (by chloralose), paralyzed (by curare) rats. CBF was measured in tissue samples by the Kety principle, with 14C-iodoantipyrine as indicator. Stimulation of DMRF elicited a widespread, significant increase in CBF in 12 of 13 areas. The increase in flow was greatest in cerebral cortex, up to 240% of control. However, it was also substantially increased in selected regions of telencephalon, diencephalon, mesencephalon, and lower brainstem, but not cerebellum. In contrast, electrical stimulation of the midline (interstitial nucleus of the medial longitudinal fasciculus) 1 mm medial to the DMRF did not change CBF. The increase in CBF evoked by DMRF stimulation persisted after transection of the spinal cord at C1 or cervical sympathetic trunk. We conclude that excitation of neurons originating in or passing through the DMRF can elicit a potent and virtually global increase of CBF. The effect appears to be mediated by intrinsic pathways of the central nervous system.

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Role of inwardly rectifying K+ channels in K+-induced cerebral vasodilatation in vivo

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.2000.279.6.h2704 ◽

2000 ◽

Vol 279 (6) ◽

pp. H2704-H2712 ◽

Cited By ~ 39

Author(s):

Sophocles Chrissobolis ◽

James Ziogas ◽

Yi Chu ◽

Frank M. Faraci ◽

Christopher G. Sobey

Keyword(s):

Basilar Artery ◽

Channel Activity ◽

Atpase Inhibitor ◽

Kir Channel ◽

Cerebral Vasodilatation ◽

Nos Inhibitor ◽

Oxide Synthase ◽

Inwardly Rectifying

We tested whether activation of inwardly rectifying K+ (Kir) channels, Na+-K+-ATPase, or nitric oxide synthase (NOS) play a role in K+-induced dilatation of the rat basilar artery in vivo. When cerebrospinal fluid [K+] was elevated from 3 to 5, 10, 15, 20, and 30 mM, a reproducible concentration-dependent vasodilator response was elicited (change in diameter = 9 ± 1, 27 ± 4, 35 ± 4, 43 ± 12, and 47 ± 16%, respectively). Responses to K+ were inhibited by ∼50% by the Kir channel inhibitor BaCl2 (30 and 100 μM). In contrast, neither ouabain (1–100 μM, a Na+-K+-ATPase inhibitor) nor N G-nitro-l-arginine (30 μM, a NOS inhibitor) had any effect on K+-induced vasodilatation. These concentrations of K+ also hyperpolarized smooth muscle in isolated segments of basilar artery, and these hyperpolarizations were virtually abolished by 30 μM BaCl2. RT-PCR experiments confirmed the presence of mRNA for Kir2.1 in the basilar artery. Thus K+-induced dilatation of the basilar artery in vivo appears to partly involve hyperpolarization mediated by Kir channel activity and possibly another mechanism that does not involve hyperpolarization, activation of Na+-K+-ATPase, or NOS.

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Mechanisms underlying response to hypercapnia and bicarbonate of isolated dog cerebral arteries

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.257.1.h141 ◽

1989 ◽

Vol 257 (1) ◽

pp. H141-H146 ◽

Cited By ~ 3

Author(s):

N. Toda ◽

Y. Hatano ◽

K. Mori

Keyword(s):

Superoxide Dismutase ◽

Cerebral Arteries ◽

Extracellular Ph ◽

Na Pump ◽

Prostaglandin F2 Alpha ◽

Electrogenic Na Pump ◽

Cerebral Vasodilatation ◽

High Level ◽

Arterial Tone ◽

Hcl Solution

In helical strips of dog cerebral arteries contracted with K+ or prostaglandin F2 alpha, the increase in CO2 from 5 to 15% in the gas aerating the bathing media produced a persistent relaxation in association with a rise of PCO2 and a fall of pH and PO2. Elevation of the NaHCO3 concentration from 25 to 75 mM in the bathing media under hypercapnia almost reversed the arterial tone when the osmolarity was balanced; the pH was completely reversed, whereas PCO2 was maintained at the high level. When 50 mM NaHCO3 were applied to the hypercapnic media without having the osmolarity balanced, the arteries relaxed further. Infusions of the HCl solution lowered the pH and relaxed the arterial strips; however, such a relaxation was significantly less than that caused by hypercapnia-induced acidosis. Relaxant responses to hypercapnia were attenuated by treatment with ouabain but were not influenced by amiloride and superoxide dismutase or by removal of endothelium. Relaxations due to hypertonic NaHCO3 were abolished or reversed to contractions by ouabain and were reduced by treatment with amiloride. It may be concluded that the hypercapnia-induced cerebroarterial relaxation is associated mainly with a fall of extracellular pH and is mediated partly by an activation of the electrogenic Na+ pump. Cerebral vasodilatation by increased osmolarity with NaHCO3 appears to result from stimulated Na+-H+ exchange and activated Na+ pump.

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Selective β1-Antagonism with Bisoprolol Is Associated with Fewer Postoperative Strokes than Atenolol or Metoprolol

Anesthesiology ◽

10.1097/aln.0b013e3182a17f12 ◽

2013 ◽

Vol 119 (4) ◽

pp. 777-787 ◽

Cited By ~ 72

Author(s):

Catherine Ashes ◽

Saul Judelman ◽

Duminda N. Wijeysundera ◽

Gordon Tait ◽

C. David Mazer ◽

...

Keyword(s):

Animal Studies ◽

Secondary Analysis ◽

Secondary Outcome ◽

Matched Cohort ◽

Postoperative Stroke ◽

Selective Agents ◽

Cerebral Vasodilatation ◽

Β Blocker ◽

Β Blockers ◽

Independent Association

Abstract Background: Perioperative metoprolol increases postoperative stroke. Animal studies indicate that the mechanism may be related to attenuated β2-adrenoreceptor-mediated cerebral vasodilatation. The authors therefore conducted a cohort to study whether the highly β1-specific β-blocker (bisoprolol) was associated with a reduced risk of postoperative stroke compared with less selective β-blockers (metoprolol or atenolol). Methods: The authors conducted a single-center study on 44,092 consecutive patients with age 50 yr or more having noncardiac, nonneurologic surgery. The primary outcome was stroke within 7 days of surgery. The secondary outcome was a composite of all-cause mortality, postoperative myocardial injury, and stroke. A propensity score-matched cohort was created to assess the independent association between bisoprolol and less β1-selective agents metoprolol or atenolol. A secondary analysis using logistic regression, based on previously identified confounders, also compared selective β1-antagonism. Results: Twenty-four percent (10,756) of patients were exposed to in-hospital β-blockers. A total of 88 patients (0.2%) suffered a stroke within 7 days of surgery. The matched cohort consisted of 2,462 patients, and the pairs were well matched for all variables. Bisoprolol was associated with fewer postoperative strokes than the less selective agents (odds ratio = 0.20; 95% CI, 0.04–0.91). Multivariable risk-adjustment in the β-blockers-exposed patients comparing bisoprolol with the less selective agents was associated with a similarly reduced stroke rate. Conclusions: The use of metoprolol and atenolol is associated with increased risks of postoperative stroke, compared with bisoprolol. These findings warrant confirmation in a pragmatic randomized trial.

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