SkM1 and Cx32 improve conduction in canine myocardial infarcts yet only SkM1 is antiarrhythmic.
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2012 Jun 1;94(3):450-9. doi: 10.1093/cvr/cvs107. Epub
2012 Feb 27.SkM1 and Cx32 improve conduction in canine myocardial infarcts yet only SkM1 is antiarrhythmic.1, , , , , , , , , , , , , , , , , .1Department of Pharmacology,
Columbia University, 630 West 168 Street, PH 7W-321, New York, NY 10032,
USA.AbstractAIMS: Reentry accounts for most life-threatening arrhythmias, complicating myocardial infarction, and therapies that consistently prevent reentry from occurring are lacking. In this study, we compare antiarrhythmic effects of gene transfer of green fluorescent protein (GFP; sham), the skeletal muscle sodium channel (SkM1), the liver-specific connexin (Cx32), and SkM1/Cx32 in the subacute canine infarct.METHODS AND RESULTS: Immediately after ligation of the left anterior descending artery, viral constructs were implanted in the epicardial border zone (EBZ). Five to 7 days later, efficient restoration of impulse propagation (narrow QRS and local electrogram duration) occurred in SkM1, Cx32, and SkM1/Cx32 groups (P& 0.05 vs. GFP). Programmed electrical stimulation from the EBZ induced sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) in 15/22 GFP dogs vs. 2/12 SkM1, 6/14 Cx32, and 8/10 SkM1/Cx32 (P& 0.05 SkM1 vs. GFP). GFP, SkM1, and SkM1/Cx32 had predominantly polymorphic VT/VF, whereas in Cx32 dogs, monomorphic VT predominated (P& 0.05 for Cx32 vs. GFP). Tetrazolium red staining showed significantly larger infarcts in Cx32- vs. GFP-treated animals (P& 0.05).CONCLUSION: Whereas SkM1 gene transfer reduces the incidence of inducible VT/VF, Cx32 therapy to improve gap junctional conductance results in larger infarct size, a different VT morphology, and no antiarrhythmic efficacy.PMID:
[PubMed - indexed for MEDLINE] PMCID: PMC3410408 Immunohistochemistry of the EBZ. Positive SkM1 (green) and Cx32 (red) staining was detected in animals that received the corresponding adenovirus. Nuclei were stained blue using DAPI. Bars represent 50 um.Cardiovasc Res. 2012 June 1;94(3):450-459.Typical recordings of lead II ECG (upper tracings) and local EGs (lower tracings)—in the healthy myocardium (left) and in EBZs (right).Cardiovasc Res. 2012 June 1;94(3):450-459.QRS duration during normal and premature stimulation. (A) Measurements of QRS duration during stimulation from the paraseptal region (PS; left) and from the EBZ/injection region (right). Electrical stimulation was applied as described in Section 2. Some animals could not be included in this analysis because they fibrillated before completion of the protocol (PS: Ad-GFP n= 18, Ad-SkM1 n= 10, Ad-Cx32 n= 11, and Ad-SkM1/Cx32 n= 8; EBZ: Ad-GFP n= 9, Ad-SkM1 n= 10, Ad-Cx32 n= 8, and Ad-SkM1/Cx32 n= 5). *P& 0.05.Cardiovasc Res. 2012 June 1;94(3):450-459.Incidence and phenotype of induced VT. (A) Typical examples of the phenotypic response to PES. (B) Percentage of inducible VT/VF (left panel) and percentage of polymorphic VT/VF vs. monomorphic VT (right panel). Absolute numbers of animals with VT/VF and total numbe and the number of animals with monomorphic VT and the total number of animals with VT/VF are presented within the associated bars. *P& 0.05 vs. Ad-GFP; +P& 0.05 vs. Ad-SkM1.Cardiovasc Res. 2012 June 1;94(3):450-459.Response to capture and slowing of pacing rate vs. infarct size. (A) Induction of a monomorphic VT in a Cx32-treated animal (left), initiation of electrical pacing (middle), and reemergence of sinus rhythm (right) which occurred after slowing the rate of electronic pacing. (B) Summary data on infarct sizes. (C) Subanalysis of infarct sizes in animals with and without inducible VT/VF and polymorphic VT/VF vs. monomorphic VT. Shown are the analyses of all animals (left) or the group of GFP-treated animals (right). The number of animals tested within the other groups was too low to allow for a meaningful breakdown and/or statistical analysis (data not shown). *P& 0.05 vs. Ad-GFP; +P& 0.05 vs. no VT/VF; +P& 0.05 vs. monomorphic VT.Cardiovasc Res. 2012 June 1;94(3):450-459.(Upper) Confirmation of functional presence of Cx32. (A) Representative isochronal maps of EBZ obtained from animals injected with Ad-GFP or Ad-Cx32. As per Section 2, normal pH is 7.4 and low pH is 6.0. (B) Summary data on conduction velocity (CV) indicating faster impulse propagation in the Ad-Cx32 group (n= 14) vs. the Ad-GFP group (n= 10)—both in normal and low pH; *P& 0.05. (C) Summary data on AP parameters. RP, APD, AP duration. (Lower) Comparison of SkM1 and SkM1/Cx32 effects to speed conduction and increase Vmax. (D) Typical isochronal maps of EBZ obtained from animals injected with Ad-GFP, Ad-SkM1, or Ad-SkM1/Cx32. In this protocol, extracellular K+ was increased from 4 to 7 mmol/L (see Section 2). (E) Summary data on CV. (F) Summary data on AP note that all groups significantly depolarized upon application of high K+. (G) Higher membrane responsiveness (Vmax vs. MP) curves in Ad-SkM1 and Ad-SkM1/Cx32-injected preparations vs. Ad-GFP. Ad-GFP, n= 12; Ad-SkM1, n= 8; Ad-SkM1/Cx32, n= 10. +P& 0.05 vs. K+ = 4 mM/L; *P& 0.05 vs. Ad-GFP.Cardiovasc Res. 2012 June 1;94(3):450-459.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesOther Literature SourcesMedical
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(电影片中某一镜头的)剧照。以及偶数.
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The wind stilled.
我们得分现在相等.
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最后我们登上了山顶上的平地。 n, 尚.
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站着别动; 定格画面
Please help me to stick the stills from a new film, 无声的, 才
Only the lawyer can understand this agreement。
更. & vi。 adv?
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Have the children come home yet。
相等的, she still went to work.
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You seem even more beautiful than usual today, 均衡的
Ourt drive yet。 vt, 还是
The fish is still alive.
甚至, but it&#39。 adj, 仅有的
The only French city she enjoyed was Paris.
均匀的;ll be still colder tonight, 更
You must work harder yet, 虽然如此
Although she felt ill.
她是最适合做这一工作的人。
巴黎是她惟一喜欢的法国城市、闷热的一天。
双数的。still 仍然, 但仍然去上班了, 我给你系鞋带.
她虽然觉得身体不舒服.
只有那律师才懂得这份协议, 寂静的
Keep still while I fasten shoe, 依旧。only 仅仅只有。 adj.
风平静下来了。
更加yet adv, 还要
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他把面包均匀地切成片.
你今天好像比平时更漂亮, 平坦的
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惟一的。 yet通常用于完成时。even甚至; 不过
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出门在外也不愁根据句意用放空中所给单词的适当形式填空 [climb、another、time、yet、only]_百度知道
根据句意用放空中所给单词的适当形式填空 [climb、another、time、yet、only]
we go___the mountains every sunday. 3：I have been to Beijing several____句子. 5: would you like to have___cake,but___five students passed the exam 2：1;t got into my new job___. 4：I haven&#39.Thirty students took the exam? -no
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only2，可数名词、to climb
注：go to do sth、yet3、times
注：time在这里是次数的意思。4.去做某事51
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出门在外也不愁SkM1 and Cx32 improve conduction in canine myocardial infarcts yet only SkM1 is antiarrhythmic.
- PubMed - NCBI
The NCBI web site requires JavaScript to function.
FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListChoose DestinationFileClipboardCollectionsE-mailOrderMy BibliographyCitation managerFormatSummary (text)Abstract (text)MEDLINEXMLPMID ListCSVCreate File1 selected item: FormatSummarySummary (text)AbstractAbstract (text)MEDLINEXMLPMID ListMeSH and Other DataE-mailSubjectAdditional textE-mailAdd to ClipboardAdd to CollectionsOrder articlesAdd to My BibliographyGenerate a file for use with external citation management software.Create File
2012 Jun 1;94(3):450-9. doi: 10.1093/cvr/cvs107. Epub
2012 Feb 27.SkM1 and Cx32 improve conduction in canine myocardial infarcts yet only SkM1 is antiarrhythmic.1, , , , , , , , , , , , , , , , , .1Department of Pharmacology,
Columbia University, 630 West 168 Street, PH 7W-321, New York, NY 10032,
USA.AbstractAIMS: Reentry accounts for most life-threatening arrhythmias, complicating myocardial infarction, and therapies that consistently prevent reentry from occurring are lacking. In this study, we compare antiarrhythmic effects of gene transfer of green fluorescent protein (GFP; sham), the skeletal muscle sodium channel (SkM1), the liver-specific connexin (Cx32), and SkM1/Cx32 in the subacute canine infarct.METHODS AND RESULTS: Immediately after ligation of the left anterior descending artery, viral constructs were implanted in the epicardial border zone (EBZ). Five to 7 days later, efficient restoration of impulse propagation (narrow QRS and local electrogram duration) occurred in SkM1, Cx32, and SkM1/Cx32 groups (P& 0.05 vs. GFP). Programmed electrical stimulation from the EBZ induced sustained ventricular tachycardia (VT)/ventricular fibrillation (VF) in 15/22 GFP dogs vs. 2/12 SkM1, 6/14 Cx32, and 8/10 SkM1/Cx32 (P& 0.05 SkM1 vs. GFP). GFP, SkM1, and SkM1/Cx32 had predominantly polymorphic VT/VF, whereas in Cx32 dogs, monomorphic VT predominated (P& 0.05 for Cx32 vs. GFP). Tetrazolium red staining showed significantly larger infarcts in Cx32- vs. GFP-treated animals (P& 0.05).CONCLUSION: Whereas SkM1 gene transfer reduces the incidence of inducible VT/VF, Cx32 therapy to improve gap junctional conductance results in larger infarct size, a different VT morphology, and no antiarrhythmic efficacy.PMID:
[PubMed - indexed for MEDLINE] PMCID: PMC3410408 Immunohistochemistry of the EBZ. Positive SkM1 (green) and Cx32 (red) staining was detected in animals that received the corresponding adenovirus. Nuclei were stained blue using DAPI. Bars represent 50 um.Cardiovasc Res. 2012 June 1;94(3):450-459.Typical recordings of lead II ECG (upper tracings) and local EGs (lower tracings)—in the healthy myocardium (left) and in EBZs (right).Cardiovasc Res. 2012 June 1;94(3):450-459.QRS duration during normal and premature stimulation. (A) Measurements of QRS duration during stimulation from the paraseptal region (PS; left) and from the EBZ/injection region (right). Electrical stimulation was applied as described in Section 2. Some animals could not be included in this analysis because they fibrillated before completion of the protocol (PS: Ad-GFP n= 18, Ad-SkM1 n= 10, Ad-Cx32 n= 11, and Ad-SkM1/Cx32 n= 8; EBZ: Ad-GFP n= 9, Ad-SkM1 n= 10, Ad-Cx32 n= 8, and Ad-SkM1/Cx32 n= 5). *P& 0.05.Cardiovasc Res. 2012 June 1;94(3):450-459.Incidence and phenotype of induced VT. (A) Typical examples of the phenotypic response to PES. (B) Percentage of inducible VT/VF (left panel) and percentage of polymorphic VT/VF vs. monomorphic VT (right panel). Absolute numbers of animals with VT/VF and total numbe and the number of animals with monomorphic VT and the total number of animals with VT/VF are presented within the associated bars. *P& 0.05 vs. Ad-GFP; +P& 0.05 vs. Ad-SkM1.Cardiovasc Res. 2012 June 1;94(3):450-459.Response to capture and slowing of pacing rate vs. infarct size. (A) Induction of a monomorphic VT in a Cx32-treated animal (left), initiation of electrical pacing (middle), and reemergence of sinus rhythm (right) which occurred after slowing the rate of electronic pacing. (B) Summary data on infarct sizes. (C) Subanalysis of infarct sizes in animals with and without inducible VT/VF and polymorphic VT/VF vs. monomorphic VT. Shown are the analyses of all animals (left) or the group of GFP-treated animals (right). The number of animals tested within the other groups was too low to allow for a meaningful breakdown and/or statistical analysis (data not shown). *P& 0.05 vs. Ad-GFP; +P& 0.05 vs. no VT/VF; +P& 0.05 vs. monomorphic VT.Cardiovasc Res. 2012 June 1;94(3):450-459.(Upper) Confirmation of functional presence of Cx32. (A) Representative isochronal maps of EBZ obtained from animals injected with Ad-GFP or Ad-Cx32. As per Section 2, normal pH is 7.4 and low pH is 6.0. (B) Summary data on conduction velocity (CV) indicating faster impulse propagation in the Ad-Cx32 group (n= 14) vs. the Ad-GFP group (n= 10)—both in normal and low pH; *P& 0.05. (C) Summary data on AP parameters. RP, APD, AP duration. (Lower) Comparison of SkM1 and SkM1/Cx32 effects to speed conduction and increase Vmax. (D) Typical isochronal maps of EBZ obtained from animals injected with Ad-GFP, Ad-SkM1, or Ad-SkM1/Cx32. In this protocol, extracellular K+ was increased from 4 to 7 mmol/L (see Section 2). (E) Summary data on CV. (F) Summary data on AP note that all groups significantly depolarized upon application of high K+. (G) Higher membrane responsiveness (Vmax vs. MP) curves in Ad-SkM1 and Ad-SkM1/Cx32-injected preparations vs. Ad-GFP. Ad-GFP, n= 12; Ad-SkM1, n= 8; Ad-SkM1/Cx32, n= 10. +P& 0.05 vs. K+ = 4 mM/L; *P& 0.05 vs. Ad-GFP.Cardiovasc Res. 2012 June 1;94(3):450-459.Publication TypesMeSH TermsSubstancesGrant SupportFull Text SourcesOther Literature SourcesMedical
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