Digoxin-Induced ventricular arrhythmias in the guinea pig heart in vivo: Evidence for a role of endogenous catecholamines in the genesis of delayed afterdepolarizations and triggered activity

1995 ◽  
Vol 10 (3) ◽  
pp. 119-127 ◽  
Author(s):  
Jiang Xu ◽  
Carl M. Hurt ◽  
Amir Pelleg
Keyword(s):  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Guinea Pig Heart ◽  
Triggered Activity ◽  
Endogenous Catecholamines ◽  
Delayed Afterdepolarizations

A novel guinea pig heart model for studying AV nodal conduction and triggered activity in vivo

1996 ◽  
Vol 270 (5) ◽  
pp. H1850-H1857 ◽  
Author(s):  
J. Xu ◽  
A. Pelleg
Keyword(s):  
Guinea Pig ◽  
Monophasic Action Potential ◽  
Guinea Pig Heart ◽  
Triggered Activity ◽  
His Bundle ◽  
Custom Made ◽  
Potential Map ◽  
Atrioventricular Nodal Conduction ◽  
First Time

A novel model is described that enables for the first time the recording of the His bundle electrogram (HBE), monophasic action potential (MAP), and early (EAD) and delayed (DAD) afterdepolarizations in the guinea pig heart in vivo. In this model, custom-made catheter electrodes have been used; their detailed design, a recipe for their construction, and the modes of their operation are given in detail. In addition, examples of experimental data obtained using this model are given. These include values of atrial-to-His bundle and His bundle-to-ventricle intervals, as well as DADs associated with digoxin-induced ventricular arrhythmias. The present model is a small and relatively inexpensive model in which studies of atrioventricular nodal conduction, as well as afterdepolarizations/triggered activity, can be performed in vivo.

Effects of pinacidil, verapamil, and heart rate on afterdepolarizations in the guinea-pig heart in vivo

1996 ◽  
Vol 11 (6) ◽  
pp. 289-302 ◽  
Author(s):  
Jiang Xu ◽  
Sina Zaim ◽  
Amir Pelleg
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Guinea Pig Heart

scholarly journals Effects of amiloride and an analogue on ventricular arrhythmias, contracture and cellular injury during reperfusion in isolated and perfused guinea pig heart.

1991 ◽  
Vol 55 (9) ◽  
pp. 845-856 ◽  
Author(s):  
HAJIME OTANI ◽  
YASUSHI KATO ◽  
TOKUMITSU KO ◽  
YOSHIYA SAKURAI ◽  
KIYOSHI KAGAWA ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ventricular Arrhythmias ◽  
Cellular Injury ◽  
Guinea Pig Heart

Human thrombocytes are able to induce a myocardial dysfunction in the ischemic and reperfused guinea pig heart mediated by free radicals-role of the GPIIb/IIIa-blocker tirofiban

Life Sciences ◽  
2002 ◽  
Vol 71 (19) ◽  
pp. 2319-2329 ◽  
Author(s):  
Christian Seligmann ◽  
Yusuf Simsek ◽  
Mike Schimmer ◽  
Tobias Leitsch ◽  
Andreas Bock ◽  
...  
Keyword(s):  
Free Radicals ◽  
Guinea Pig ◽  
Myocardial Dysfunction ◽  
Guinea Pig Heart

Effect of Acetaldehyde on the Isolated, Non-working Guinea-Pig Heart: Independence of the Coronary Flow Increase from Changes in Heart Rate and Oxygen Consumption

1974 ◽  
Vol 52 (3) ◽  
pp. 602-612 ◽  
Author(s):  
Minh-Hau Nguyen ◽  
L. Gailis
Keyword(s):  
Heart Rate ◽  
Oxygen Consumption ◽  
Guinea Pig ◽  
Gas Phase ◽  
Coronary Flow ◽  
Constant Pressure ◽  
Guinea Pig Heart ◽  
Bicarbonate Buffer

Guinea-pig hearts were perfused at constant pressure with Krehs–Henseleit bicarbonate buffer equilibrated with 95% O2 – 5% CO2. Acetaldehyde at 1 and 5 mM increased coronary flow, oxygen consumption, and heart rate. At 0.2 mM, it increased coronary flow and oxygen consumption only. In the rapidly paced heart, 1 mM acetaldehyde increased coronary flow, but not heart rate or oxygen consumption. Acetaldehyde increased coronary flow and oxygen consumption of the potassium-arrested heart. Acetaldehyde increased all parameters of the hypoxic heart (25% O2 gas phase), but the anoxic heart was not affected (coronary flow was already maximal).Reserpine (in vivo) and catecholamine β blockers (dichloroisoproterenol and propranolol) (in vitro) blocked the heart rate increases and moderated the rise in oxygen consumption. Dichloroisoproterenol plus phentolamine blocked the increases of both heart rate and oxygen consumption. None of the compounds affected the increase of coronary flow produced by acetaldehyde. Epinephrine, norepinephrine, and tyramine increased the heart rate and oxygen consumption, but not the coronary flow. Theophylline increased all three parameters. Neither tranylcypromine nor atropine modified the acetaldehyde effect. We conclude that the increase in heart rate is mediated by catecholamine β receptors. The increase in coronary flow is independent of the increase in heart rate or oxygen consumption and is not mediated by catecholamines.

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