ADAPTATION OF THE QT INTERVAL TO HEART RATE CHANGES IN ISOLATED PERFUSED GUINEA PIG HEART: INFLUENCE OF AMIODARONE ANDD-SOTALOL

1997 ◽  
Vol 35 (5) ◽  
pp. 409-416 ◽  
Author(s):  
ROBERTO PADRINI ◽  
GIORGIO SPERANZA ◽  
GIANDOMENICO NOLLO ◽  
SERGIO BOVA ◽  
DONATELLA PIOVAN ◽  
...  
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Qt Interval ◽  
Guinea Pig Heart

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

The effect of ATP-sensitive potassium channel modulation on heart rate in isolated muskrat and guinea pig hearts.

1994 ◽  
Vol 197 (1) ◽  
pp. 101-118
Author(s):  
D R Streeby ◽  
T A McKean
Keyword(s):  
Heart Rate ◽  
Guinea Pig ◽  
Potassium Channel ◽  
Extracellular Potassium ◽  
Guinea Pig Heart ◽  
Channel Activation ◽  
Extracellular Potassium Concentration ◽  
Local Factors ◽  
Hypoxic Conditions ◽  
Vagal Innervation

Muskrats (Ondontra zibethicus) are common freshwater diving mammals exhibiting a bradycardia with both forced and voluntary diving. This bradycardia is mediated by vagal innervation; however, if hypoxia is present there may be local factors that also decrease heart rate. Some of these local factors may include ATP-sensitive potassium channel activation and extracellular accumulation of potassium ions, hydrogen ions and lactate. The purpose of this study was to investigate the role of these factors in the isolated perfused hearts of muskrats and of a non-diving mammal, the guinea pig. Although lactate and proton administration reduced heart rate in isolated muskrat and guinea pig hearts, there was no difference in the response to lactate and proton infusion between the two species. Muskrat hearts were more sensitive to the heart-rate-lowering effects of exogenously applied potassium than were guinea pig hearts. Early increases in extracellular potassium concentration during hypoxia are thought to be mediated by the ATP-sensitive potassium channel. Activation of these channels under normoxic conditions had a mildly negative chronotropic effect in both species; however, activation of these channels with Lemakalim under hypoxic conditions caused the guinea pig heart to respond with an augmented bradycardia similar to that seen in the hypoxic muskrat heart in the absence of drugs. Inhibition of these channels by glibenclamide during hypoxia was partially successful in blocking the bradycardia in guinea pig hearts, but inhibition of the same channels in hypoxic muskrat hearts had a damaging effect as two of five hearts went into contracture during the hypoxia. Thus, although ATP-sensitive potassium channels appear to have a major role in the bradycardia of hypoxia in guinea pigs, the failure to prevent the bradycardia by inhibition of these channels in muskrat hearts suggests that multiple factors are involved in the hypoxia-induced bradycardia in this species.

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.

scholarly journals Electrocardiographic profile of guinea pig heart submitted to Ginkgo biloba extract and its terpenoids

2014 ◽  
Vol 16 (4) ◽  
pp. 819-825
Author(s):  
A.C.O. Santos ◽  
J.A.S. Souza ◽  
E.A. Conde-Garcia ◽  
A.A. Souza ◽  
J.E.R. Menezes-Filho ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Ginkgo Biloba ◽  
Qt Interval ◽  
Ginkgo Biloba Extract ◽  
Av Block ◽  
Channel Block ◽  
Guinea Pig Heart ◽  
Pr Interval ◽  
Arrhythmogenic Potential ◽  
Electrocardiographic Parameters

Electrocardiographic effects produced by Ginkgo biloba extract (EGb) and by ginkgolides A (GA) and B (GB), and bilobalide (BB) were investigated in guinea pig heart mounted in Langendorff apparatus (Tyrode, 34 ± 0.1 ºC, 95% O2, 5% CO2). Electrocardiographic parameters were evaluated in the conditions: 1) control with Tyrode and DMSO, 2) EGb (n=4), GA (n=5), GB (n=5) or BB (n=6), and 3) washout. The results showed that 0.1 and 1.0 mg/ml of EGb do not change the electrocardiographic parameters. However, 10 mg/ml of EGb increased the PR interval (PRi) at 21% (p<0.001). This increase was also observed for 50 mM GA (20%, p<0.001) and 70 mM BB (13%, p<0.001), which indicates Ca2+ channel block. However, the 50 mM GB reduced the PRi at 11 % (p<0.001). The GA (23%, p<0.001), GB (16%, p<0.001), and BB (40%, p<0.001) reduced the QT interval (QTi), which suggests the activation of the potassium channel. However, EGb increased QTi (6%, p<0.001). The EGb (28%, p<0.05) and GB (13%, p<0.05) reduced the heart rate. Atrioventricular (AV) block was observed with EGb, GA, and BB. We can conclude that EGb and its terpenoids alter the ECG parameters inducing AV block, which indicates possible arrhythmogenic potential.

Terfenadine Increases the QT Interval in Isolated Guinea Pig Heart

1995 ◽  
Vol 25 (1) ◽  
pp. 30-34 ◽  
Author(s):  
Sean P. Pinney ◽  
Bettina S. Koller ◽  
Michael R. Franz ◽  
Raymond L. Woosley
Keyword(s):  
Guinea Pig ◽  
Qt Interval ◽  
Guinea Pig Heart

scholarly journals Macrophage-Dependent Interleukin-6-Production and Inhibition of IK Contributes to Acquired QT Prolongation in Lipotoxic Guinea Pig Heart

2021 ◽  
Vol 22 (20) ◽  
pp. 11249
Author(s):  
Md. Kamrul Hasan Chowdhury ◽  
Laura Martinez-Mateu ◽  
Jenny Do ◽  
Kelly A. Aromolaran ◽  
Javier Saiz ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Action Potential ◽  
Interleukin 6 ◽  
Action Potential Duration ◽  
Guinea Pigs ◽  
Qt Interval ◽  
Torsade De Pointes ◽  
Delayed Rectifier ◽  
Guinea Pig Heart ◽  
Potent Inducer

In the heart, the delayed rectifier K current, IK, composed of the rapid (IKr) and slow (IKs) components contributes prominently to normal cardiac repolarization. In lipotoxicity, chronic elevation of pro-inflammatory cytokines may remodel IK, elevating the risk for ventricular arrythmias and sudden cardiac death. We investigated whether and how the pro-inflammatory interleukin-6 altered IK in the heart, using electrophysiology to evaluate changes in IK in adult guinea pig ventricular myocytes. We found that palmitic acid (a potent inducer of lipotoxicity), induced a rapid (~24 h) and significant increase in IL-6 in RAW264.7 cells. PA-diet fed guinea pigs displayed a severely prolonged QT interval when compared to low-fat diet fed controls. Exposure to isoproterenol induced torsade de pointes, and ventricular fibrillation in lipotoxic guinea pigs. Pre-exposure to IL-6 with the soluble IL-6 receptor produced a profound depression of IKr and IKs densities, prolonged action potential duration, and impaired mitochondrial ATP production. Only with the inhibition of IKr did a proarrhythmic phenotype of IKs depression emerge, manifested as a further prolongation of action potential duration and QT interval. Our data offer unique mechanistic insights with implications for pathological QT interval in patients and vulnerability to fatal arrhythmias.

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