scholarly journals Relationship between Inward Rectifier Potassium Current Impairment and Brain Injury after Cerebral Ischemia/Reperfusion

1999 ◽  
Vol 19 (12) ◽  
pp. 1309-1315 ◽  
Author(s):  
Michèle Bastide ◽  
Régis Bordet ◽  
Qian Pu ◽  
Emmanuel Robin ◽  
François Puisieux ◽  
...  
Keyword(s):  
Brain Injury ◽  
Ischemia Reperfusion ◽  
Cerebral Arteries ◽  
Inward Rectifier ◽  
Inward Rectification ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Middle Cerebral Arteries ◽  
External Potassium ◽  
The Relationship

Functional alterations of barium-sensitive potassium inward rectifier (Kir) current, which is involved in the vasodilation of middle cerebral arteries (MCA) in rat brain, have been described during brain ischemiaireperfusion (I/R). The authors investigate the effects of I/R on Kir current recorded in isolated myocytes from MCA of control rats and from contralateral and ipsilateral MCA of ischemic rats by the whole-cell patch-clamp technique, and the relationship between its alteration and The severity of brain injury. The vascular smooth muscle cells exhibited similar morphologic features in all conditions, and the Kir was present in the three groups of myocytes, exhibiting a characteristic inward rectification and a normal external potassium dependence. The Kir density was significantly reduced in cell of MCA ipsilateral to occlusion with a maximum at −135 mV, whereas there was no difference between control and contralateral cells. This alteration in Kir density in occluded MCA was significantly correlated with severity of brain injury and brain edema. These results suggest that the alteration of Kir density in MCA myocytes after I/R and the consecutive impaired dilation of MCA may contribute to aggravation of the brain injury.

scholarly journals Protective Effect and Mechanism of Total Flavones fromRhododendron simsiiPlanch Flower on Cultured Rat Cardiomyocytes with Anoxia and Reoxygenation

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Yi Jiao ◽  
Yi-Fei Fan ◽  
Yu-Ling Wang ◽  
Jun-Yan Zhang ◽  
Shuo Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Protective Effect ◽  
Cell Viability ◽  
Ischemia Reperfusion ◽  
Cellular Damage ◽  
Protective Mechanism ◽  
Patch Clamp Technique ◽  
Rat Cardiomyocytes ◽  
Whole Cell Patch Clamp ◽  
Myocardial Ischemia Reperfusion

Many flavonoids have cardioprotection against myocardial ischemia/reperfusion (I/R) injury. Total flavones fromRhododendron simsiiPlanch flower (TFR) can protect myocardial ischemic injuries. However, its protective mechanism is still unknown. The present study was designed to investigate the mechanism of TFR on myocardial I/R and anoxia/reoxygenation (A/R) injuries. Rat model of myocardial I/R injury was made, and myocardial infarction was determined. A/R injury was induced in cultured rat cardiomyocytes; cellular damage was evaluated by measuring cell viability, LDH and cTnT releases, and MDA content. Expressions of ROCK1and ROCK2protein were examined by Western blot analysis, and K+currents were recorded by using whole-cell patch clamp technique. TFR 20~80 mg/kg markedly reduced I/R-induced myocardial infarction. TFR 3.7~300 mg/L significantly inhibited A/R-induced reduction of cell viability, LDH and cTnT releases, and MDA production. Exposure to A/R significantly increased ROCK1and ROCK2expressions in rat cardiomyocytes, but TFR 33.3~300 mg/L obviously inhibited this increase. 300 mg/L TFR significantly augmented inward rectifier K+current and other K+currents in rat cardiomyocytes. These results indicate that TFR has a protective effect on rat cardiomyocytes A/R damage, and the protective mechanism may be engaged with the inhibition of ROCK1and ROCK2and activation of K+channels.

Traumatic Brain Injury Reduces Myogenic Responses in Pressurized Rodent Middle Cerebral Arteries

1999 ◽  
Vol 16 (12) ◽  
pp. 1177-1186 ◽  
Author(s):  
BABU P. MATHEW ◽  
DOUGLAS S. DeWITT ◽  
ROBERT M. BRYAN ◽  
RICHARD D. BUKOSKI ◽  
DONALD S. PROUGH
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cerebral Arteries ◽  
Middle Cerebral Arteries ◽  
Myogenic Responses

scholarly journals Delayed Cerebrovascular Protective Effect of Lipopolysaccharide in Parallel to Brain Ischemic Tolerance

2003 ◽  
Vol 23 (4) ◽  
pp. 399-405 ◽  
Author(s):  
Michèle Bastide ◽  
Patrick Gelé ◽  
Olivier Pétrault ◽  
Qian Pu ◽  
Audrey Caliez ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Infarct Volume ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Muscle Relaxation ◽  
Cerebral Arteries ◽  
Inward Rectifier ◽  
Ischemic Tolerance ◽  
Smooth Muscle Relaxation ◽  
Vascular Protection

Cerebrovascular abnormalities, in endothelium and smooth muscle compartments, occur in the course of cerebral ischemia–reperfusion as evidenced by the impairment of endothelium-dependent relaxation and decrease in potassium inward rectifier density in occluded middle cerebral arteries (MCAs). The authors investigated whether a delayed vascular protection occurred in a model of brain ischemic tolerance. A low dose of lipopolysaccharide (0.3 mg/kg) administered 72 h before MCA occlusion induced a significant decrease in infarct volume. In parallel to this delayed neuroprotective effect, lipopolysaccharide prevented the ischemia–reperfusion–induced impairment of endothelium relaxation. In addition, lipopolysaccharide prevented the postischemic alteration of potassium inward rectifier–dependent smooth muscle relaxation as well as the decrease in potassium inward rectifier density measured by patch-clamp in dissociated vascular smooth muscle cells originated from the occluded MCA. These results suggest that during brain ischemic tolerance, lipopolysaccharide is able to induce both a delayed neuroprotective and vasculoprotective effect.

Characterization of Outward Currents Induced by 5-HT in Neurons of Rat Dorsolateral Septal Nucleus

2001 ◽  
Vol 85 (4) ◽  
pp. 1453-1460 ◽  
Author(s):  
Kei Yamada ◽  
Hiroshi Hasuo ◽  
Masaru Ishimatsu ◽  
Takashi Akasu
Keyword(s):  
Protein Kinase ◽  
G Protein ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Inward Rectifier ◽  
Inward Rectification ◽  
Septal Nucleus ◽  
Whole Cell Patch Clamp ◽  
Outward Currents ◽  
Artificial Cerebrospinal Fluid

Properties of the 5-hydroxytryptamine (5-HT)-induced current ( I 5-HT) were examined in neurons of rat dorsolateral septal nucleus (DLSN) by using whole cell patch-clamp techniques. I 5-HT was associated with an increase in the membrane conductance of DLSN neurons. The reversal potential of I 5-HT was −93 ± 6 (SE) mV ( n = 7) in the artificial cerebrospinal fluid (ACSF) and was changed by 54 mV per decade change in the external K+ concentration, indicating that I 5-HT is carried exclusively by K+. Voltage dependency of the K+ conductance underlying I 5-HT was investigated by using current-voltage relationship. I 5-HTshowed a linear I-V relation in 63%, inward rectification in 21%, and outward rectification in 16% of DLSN neurons. (±)-8-Hydroxy-dipropylaminotetralin hydrobromide (30 μM), a selective 5-HT1A receptor agonist, also produced outward currents with three types of voltage dependency. Ba2+ (100 μM) blocked the inward rectifier I 5-HT but not the outward rectifier I 5-HT. In I 5-HT with linear I-Vrelation, blockade of the inward rectifier K+current by Ba2+ (100 μM) unmasked the outward rectifier current in DLSN neurons. These results suggest that I 5-HT with linear I-Vrelation is the sum of inward rectifier and outward rectifier K+ currents in DLSN neurons. Intracellular application of guanosine-5′- O-(3-thiotriphosphate) (300 μM) and guanosine-5′- O-(2-thiodiphosphate) (5 mM), blockers of G protein, irreversibly depressed I 5-HT. Protein kinase C (PKC) 19-36 (20 μM), a specific PKC inhibitor, depressed the outward rectifier I 5-HT but not the inward rectifier I 5-HT. I 5-HT was depressed by N-ethylmaleimide, which uncouples the G-protein-coupled receptor from pertussis-toxin-sensitive G proteins. H-89 (10 μM) and adenosine 3′,5′-cyclic monophosphothioate Rp-isomer (300 μM), protein kinase A inhibitors, did not depress I 5-HT. Phorbol 12-myristate 13-acetate (10 μM), an activator of PKC, produced an outward rectifying K+ current. These results suggest that both 5-HT-induced inward and outward rectifying currents are mediated by a G protein and that PKC is probably involved in the transduction pathway of the outward rectifying I 5-HT in DLSN neurons.

Magnesium shifts voltage dependence of activation of delayed rectifier I(K) in guinea pig ventricular myocytes

1997 ◽  
Vol 272 (3) ◽  
pp. H1292-H1301 ◽  
Author(s):  
B. A. Williams ◽  
G. N. Beatch
Keyword(s):  
Guinea Pig ◽  
Ventricular Myocytes ◽  
Inward Rectification ◽  
Delayed Rectifier ◽  
Maximal Effect ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
K Current ◽  
Dose Dependent Decrease ◽  
20 Nm

The sensitivity of the delayed rectifier K+ current (I(K)) to intracellular Mg2+ was investigated in guinea pig ventricular myocytes using the whole cell patch-clamp technique. An increase in free intracellular Mg2+ concentration ([Mg2+]i) led to a dose-dependent decrease in I(K) with a half-maximal effect of approximately 20 nM. Activation of I(K) was shifted toward more positive voltages on increasing [Mg2+]i, but little effect was observed on activation and deactivation kinetics. Isoproterenol increased I(K) and was partially reversible in both control and 100 nM [Mg2+]i. The antiarrhythmic drug dofetilide was used to separate I(K) into its two components, rapidly activating (I(Kr)) and slowly activating (I(Ks)). The magnitude of both components decreased to a similar extent with an increase in [Mg2+]i. As [Mg2+]i was reduced, however, the number of experiments in which the dofetilide-sensitive current I(Kr) displayed inward rectification was reduced. In contrast to results previously reported for frog myocytes, it is unlikely that Mg2+ effects on guinea pig I(K) are mediated by a protein phosphatase.

Comparison of Ito in young and adult human atrial myocytes: evidence for developmental changes

1995 ◽  
Vol 268 (3) ◽  
pp. H1335-H1342 ◽  
Author(s):  
W. J. Crumb ◽  
J. D. Pigott ◽  
C. W. Clarkson
Keyword(s):  
Current Density ◽  
Outward Current ◽  
Inward Rectifier ◽  
Developmental Changes ◽  
Transient Outward Current ◽  
Atrial Myocytes ◽  
Patch Clamp Technique ◽  
Whole Cell Patch Clamp ◽  
Age Related ◽  
Age Related Changes

In an effort to understand the ionic basis for the developmental changes that have been reported to occur in the configuration of the human atrial action potential, we characterized the transient outward current (Ito) and the inward rectifier current in atrial myocytes isolated from 20 young (ages 1 day-2.5 yr) and 8 adult (11–68 yr) human hearts using the whole cell patch-clamp technique. We found evidence for statistically significant (P < 0.05) age-related changes in the Ito, including 1) the presence of an Ito in only 67% of the cells isolated from young hearts vs. 100% of the cells isolated from adult hearts, 2) an almost twofold increase in the current density of Ito in adult cells vs. young cells, and 3) recovery kinetics that are approximately twofold slower in young myocytes relative to adult myocytes. In contrast, there were no age-related changes found in the current density of the inward rectifier current or the sustained current measured after the decay of Ito. These results suggest important current-dependent changes that occur with age in human atria.

scholarly journals Brain Injury after Transcatheter Aortic Valve Replacement for Bicuspid Versus Tricuspid Aortic Valve Stenosis

2020 ◽  
Author(s):  
Jiaqi Fan ◽  
Xian Fang ◽  
Chunhui Liu ◽  
Gangjie Zhu ◽  
Cody R. Hou ◽  
...  
Keyword(s):  
Brain Injury ◽  
Aortic Valve ◽  
Aortic Valve Replacement ◽  
Valve Replacement ◽  
Transcatheter Aortic Valve Replacement ◽  
Cerebral Arteries ◽  
Lesion Volume ◽  
Tricuspid Aortic Valve ◽  
Transcatheter Aortic Valve ◽  
Middle Cerebral Arteries

AbstractBackgroundsThe risk of brain injury in bicuspid aortic valve (BAV) patients following transcatheter aortic valve replacement (TAVR) is currently unknown.Methods and ResultsA total of 204 consecutive severe aortic stenosis patients who underwent TAVR were enrolled. 83 (40.7%) patients were BAV patients and the other 121 patients were tricuspid aortic valve (TAV) patients. All patients received diffusion-weighted magnetic resonance imaging (DW-MRI) at baseline, 2 to 7 days after TAVR. Mean ages (mean ± SD: 75.8 ± 6.7 years vs. 78.9 ± 6.6 years, p = 0.004) and STS scores (6.0 ± 3.7 vs. 7.1 ± 4.2, p = 0.044) of the BAV and TAV patients were significantly different, while the stroke rates (2.4% vs. 1.7%, p = 0.704) were comparable between two groups. BAV patients were associated with higher number of new lesions (5.69 ± 6.22 vs. 3.50 ± 4.16, p = 0.008), total lesion volume [median(interquartile range): 290(70-930) mm3 vs. 140(35-480) mm3, p = 0.008], and the volume per lesion [70.0(45.0-115.0) mm3 vs. 57.5(24.5-93.0) mm3, p = 0.037] in DW-MRI. Moreover, the proportion of patients with lesions larger than 1cm3 (28.6% vs. 10.9%, p = 0.005) and the number of new lesions in the middle cerebral arteries zone (1.46 ± 2.07 vs. 0.98 ± 1.84, p = 0.039) and intermediate zone between the anterior cerebral and middle cerebral arteries (ACA/MCA) (1.07 ± 1.68 vs. 0.50 ± 1.05, p = 0.007), and between the vertebral artery and basilar artery (VA/BA) (1.01 ± 1.35 vs. 0.77 ± 1.44, p = 0.033) were higher in BAV patients than in TAV patients.ConclusionsBAV patients may encounter more severe brain injuries not only due to greater number of lesions but also due to larger lesion size, especially in the ACA/MCA, MCA and VA/BA lesions zone.

Sign in / Sign up

Export Citation Format

Share Document