Jove
Visualize
お問い合わせ
JoVE
x logofacebook logolinkedin logoyoutube logo
JoVEについて
概要リーダーシップブログJoVEヘルプセンター
著者向け
出版プロセス編集委員会範囲と方針査読よくある質問投稿
図書館員向け
推薦の声購読アクセスリソース図書館諮問委員会よくある質問
研究
JoVE JournalMethods CollectionsJoVE Encyclopedia of Experimentsアーカイブ
教育
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab Manual教員リソースセンター教員サイト
利用規約
プライバシーポリシー
ポリシー

関連する概念動画

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers01:22

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...
Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers01:24

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...
Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers01:12

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...
Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers01:20

Antiarrhythmic Drugs: Class IV Agents as Calcium Channel Blockers

Class IV antiarrhythmic drugs, such as verapamil and diltiazem, block calcium channels. They primarily affect the heart, slowing the conduction in calcium-dependent tissues like the SA and AV nodes. These drugs manage reentrant supraventricular tachycardia (SVT) and reduce ventricular rate in atrial flutter/fibrillation.
Verapamil, a calcium channel blocker, inhibits calcium movement across myocardial cell membranes and vascular smooth muscle. This results in the dilation of coronary and...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Mitral Stenosis I: Introduction01:22

Mitral Stenosis I: Introduction

Mitral Valve Stenosis (MVS) is a heart condition where the mitral valve narrows, impeding blood circulation from the left atrium to the left ventricle. The etiology and pathophysiology of this condition are multifaceted, leading to a cascade of cardiovascular complications.Causes of Mitral Valve StenosisRheumatic Heart Disease: It is the main cause of mitral valve stenosis, particularly in developing nations. This condition arises from rheumatic fever, an inflammatory illness resulting from...

こちらも読む

関連記事

共著者、ジャーナル、引用グラフによってこの研究に関連する記事。

並び替え
Same author

Mergers and migrations: drivers of population genetic structure in a captive rhesus macaque colony.

BMC genomics·2026
Same author

The genomic legacy of selectively breeding rhesus macaques for HIV/AIDS-related research.

bioRxiv : the preprint server for biology·2025
Same author

Canadian Surgery Forum: Abstracts of presentations to the Annual Meetings of the Canadian Association of Bariatric Physicians and Surgeons, Canadian Association of General Surgeons, Canadian Association of Thoracic Surgeons, Canadian Hepato-Pancreato-Biliary Society, Canadian Society of Surgical Oncology, Canadian Society of Colon and Rectal Surgeons, London, Ont. Sept. 15-18, 2011.

Canadian journal of surgery. Journal canadien de chirurgie·2022
Same author

Postmenopausal women's adherence to pelvic floor muscle exercises over 2 years.

Climacteric : the journal of the International Menopause Society·2021
Same author

Partnering with survivors & families to determine research priorities for adult out-of-hospital cardiac arrest: A James Lind Alliance Priority Setting Partnership.

Resuscitation plus·2021
Same author

Energy Flux Densities near the Electron Dissipation Region in Asymmetric Magnetopause Reconnection.

Physical review letters·2021
Same journal

Eugene Braunwald, MD, 1929-2026.

Circulation·2026
Same journal

AHA/ACC/ESC/WHF Expert Consensus Document: Second Universal Definition of Heart Failure (2026).

Circulation·2026
Same journal

Advancing Quality in the Evaluation, Surveillance, and Management of Aortic Stenosis: A Report From the AHA Target: AS Registry.

Circulation·2026
Same journal

Heart Failure Occurring in the Perinatal Period: A Scientific Statement From the American Heart Association.

Circulation·2026
Same journal

Correction to: 2026 ACC/AHA/AACVPR/ABC/ACPM/ADA/AGS/APhA/ASPC/NLA/PCNA Guideline on the Management of Dyslipidemia: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

Circulation·2026
Same journal

Correction to: The Natural History of Massive Left Ventricular Hypertrophy in Pediatric Hypertrophic Cardiomyopathy: A Multiregistry Analysis.

Circulation·2026
関連記事をすべて見る

関連する実験動画

Updated: Jun 23, 2026

Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure
07:41

Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure

Published on: February 8, 2022

ギャップ・ジャンクション・ブロッカーは,隔離されたウサギの心臓における心室屈折率の変化なしに除細動の値を下げる.

X Qi1, P Varma, D Newman

  • 1Department of Medicine, St Michael's Hospital, University of Toronto, Toronto, Ont, Canada.

Circulation
|September 26, 2001
PubMed
まとめ
この要約は機械生成です。

16-DSAと1-ヘプタノールのようなギャップ・ジャンクション・ブロッカーは,除細動の値 (DFT) と心房細動のサイクル長 (VFCL) の分散を著しく低下させます. 対照的に,リドカインは,伝導速度に同様の効果があるにもかかわらず,DFTを増加させます.

さらに関連する動画

Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence
10:52

Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence

Published on: December 23, 2022

Bidirectional Electrical and Optoelectronic Interfaces in Healthy and Ischemic Ex Vivo Rat Hearts
08:33

Bidirectional Electrical and Optoelectronic Interfaces in Healthy and Ischemic Ex Vivo Rat Hearts

Published on: July 18, 2025

関連する実験動画

Last Updated: Jun 23, 2026

Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure
07:41

Echocardiographic Evaluation of Atrial Communications before Transcatheter Closure

Published on: February 8, 2022

Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence
10:52

Closure of a Patent Foramen Ovale (PFO): An Intervention Sequence

Published on: December 23, 2022

Bidirectional Electrical and Optoelectronic Interfaces in Healthy and Ischemic Ex Vivo Rat Hearts
08:33

Bidirectional Electrical and Optoelectronic Interfaces in Healthy and Ischemic Ex Vivo Rat Hearts

Published on: July 18, 2025

科学分野:

  • 心血管電気生理学 心血管電気生理学
  • 薬理学 薬理学とは
  • 医学物理 医学物理学

背景:

  • リエントリー不律症は,屈折性や伝導速度などの組織特性に依存する.
  • 電気生理学と除細動値 (DFT) に対するNa(+) とK(+) チャンネルブロッカーの影響は知られていますが,ギャップジャンクションブロッカーの効果はあまり理解されていません.

研究 の 目的:

  • 隔離されたウサギの心臓における除細動値 (DFT) と電気生理学的特性に対するギャップ・ジャンクション・ブロッカー (16-ドキシルステアリック酸と1-ヘプタノール) とナトリウム・チャネル・ブロッカー (リドカイン) の影響を調査する.

主な方法:

  • 16ドキシルステアリック酸 (16-DSA),1ヘプタノール,またはリドカインを隔離された浸透されたウサギの心臓に投与する前に,および投与後に,除細動値 (DFT) を測定した.
  • 静脈動のサイクル長 (VFCL),QRSの持続時間,静脈動の有効耐火期を含む電気生理学的パラメータが評価されました.

主要な成果:

  • 16-DSAと1-heptanolは,それぞれ23%と21%のDFTを大幅に減少させました. リドカインはDFTを26%増加させた.
  • すべての薬剤はVFCLとQRSの持続時間を増加させ,VFCLの分散を減少させた. 屈折性はギャップ・ジャンクション・ブロッカーによって変化しなかったが,リドカインで増加した.
  • コントロールハートは,DFTまたは電気生理学的変数の有意な変化を示さなかった.

結論:

  • 16-DSAと1-ヘプタノールによる電気解離は,反射性に影響を与えることなく,DFTとVFCLの分散を減少させます.
  • リドカインは,同様に伝導を遅らせながら,DFTを増加させ,心臓の電気的安定性に対するチャネルブロッカーの差異的な効果を強調します.