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

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.

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.

Mechanism of the negative dromotrophic effect of adenosine 5?-triphosphate in the guinea pig heart in vivo

1993 ◽  
Vol 28 (3) ◽  
pp. 290-295 ◽  
Author(s):  
Jiang Xu ◽  
Li Wang ◽  
Carl Hurt ◽  
Amir Pelleg
Keyword(s):  
Guinea Pig ◽  
Guinea Pig Heart

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

An isolated guinea pig heart preparation with in vivo like features

1975 ◽  
Vol 353 (4) ◽  
pp. 317-326 ◽  
Author(s):  
Rolf B�nger ◽  
Francis J. Haddy ◽  
Axel Quereng�sser ◽  
Eckehart Gerlach
Keyword(s):  
Guinea Pig ◽  
Guinea Pig Heart ◽  
Heart Preparation

Effect of ouabain on potassium exchange in the mammalian heart

1961 ◽  
Vol 200 (5) ◽  
pp. 1055-1062 ◽  
Author(s):  
Sidney S. Schreiber ◽  
Murray Oratz ◽  
Marcus A. Rothschild
Keyword(s):  
Guinea Pig ◽  
Guinea Pig Heart ◽  
Intracellular Potassium ◽  
Ringer’S Solution ◽  
Mammalian Heart ◽  
Digitalis Glycoside ◽  
Ouabain Inhibition ◽  
Potassium Exchange

The effect of the digitalis glycoside, ouabain, on potassium exchange in the guinea pig heart in vitro was studied with the aid of K42. With modified Ringer's solution as a perfusate at 38 C, K was found to exchange at two rates in both washout and buildup studies. In vivo equilibration studies also suggested more than one rate of exchange. Ouabain, in vitro, effected inhibition of entrance of K into the slowly exchanging compartment, but did not affect influx into the fast compartment or efflux from the fast or slow compartments. The ouabain inhibition was seen at Ringer's K concentrations of 3.8–4.3 mEq/liter was equivocal at K concentrations of 5.0–5.5 mEq/ liter and absent at K concentrations of 7.0–7.5 mEq/liter. It was postulated that ouabain inhibition was directed toward the slowly exchanging fraction of intracellular potassium.

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