Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

Janse, Michiel J.; Kléber, André G.

doi:10.1161/01.res.49.5.1069

Cited by 297 publications

(138 citation statements)

References 113 publications

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“…Although simulated ischemia could not bring down muscle surface P02 to anoxic levels, it has been reported that it exerted larger effects on contractility, action potentials and intracellular pH than hypoxic superfusion (32). The depolarization in membrane potentials and shortening of APD induced by the present method were in agreement with previous results obtained in the global ischemia for guinea pig (38), porcine (39) and dog heart (40). However, in the present study, intracellular acidification induced by simulated ischemia was greater than that reported by previous authors (32).…”

Section: Simulated Ischemiasupporting

confidence: 91%

Effects of Stilbene Derivatives SITS and DIDS on Development of Intracellular Acidosis during Ischemia in Isolated Guinea Pig Ventricular Papillary Muscle In Vitro

Lai

Liu

Nishi

1996

Japanese Journal of Pharmacology

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ABSTRACT-Using ion-selective microelectrode techniques, we investigated the effects of 4-acetamido-4'-isothiocyanatostilbene-2,2 disulfonic acid (SITS) and 4,4' -diisothiocyanostilbene-2,2 disulfonic acid (DIDS), which are known as Cl--HCO3-exchange blockers, on action potentials and intracellular pH (pH;) in guinea pig ventricular papillary muscles subjected to simulated ischemia. Simulated ischemia was produced by stopping the flow of superfusing solution and then covering the preparations with mineral oil. Simulated ischemia induced a progressive decrease in the maximum upstroke rate and resting membrane potentials, shortened action potential duration, and resulted in cessation of action potentials within 10-12 min after the onset of simulated ischemia. The pH;-measurements revealed progressive intracellular acidosis during the period of simulated ischemia. SITS (0.5 mM) or DIDS (0.1 mM) delayed the onset of ischemiainduced deterioration of action potentials and prolonged the time to cessation of action potentials. SITS or DIDS (0.1-0.5 mM) induced an increase in pH, in HCO3--buffered solution and suppressed the development of intracellular acidosis during ischemia. Under the external Cl--free condition, the time to cessation of action potentials caused by ischemia was significantly delayed, and the development of intracellular acidosis during ischemia was attenuated. The present results indicate that activation of the Cl--HC03-exchange system would be involved, in part, in the development of intracellular acidosis during cardiac ischemia.

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Section: Simulated Ischemiasupporting

confidence: 91%

Effects of Stilbene Derivatives SITS and DIDS on Development of Intracellular Acidosis during Ischemia in Isolated Guinea Pig Ventricular Papillary Muscle In Vitro

Lai

Liu

Nishi

1996

Japanese Journal of Pharmacology

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“…The decrease in duration of the action potential which has been noted by the measurement of transmembrane potentials (Friedman, Steward, Fenoglio & Wit, 1973;Kleber, Janse, Van Capelle & Durrer, 1978) is due mainly to shortening of the plateau phase of repolarization (Janse & Kleber, 1981). The causes of the shortening are still unresolved.…”

Section: Discussionmentioning

confidence: 99%

“…During the early phases of regional ischaemia, ionic and electrical changes take place in a small area of the myocardium, leading to a decrease in the resting membrane potential and shortening in the duration of the action potential (producing disparate repolarization times); there is asynchronous activation due to differential conduction delay (Lazzara, El-Sherif & Scherlag, 1974;Downar, Janse & Durrer, 1977;Russell, Smith & Oliver, 1979;Janse & Kleber, 1981). The decrease in duration of the action potential which has been noted by the measurement of transmembrane potentials (Friedman, Steward, Fenoglio & Wit, 1973;Kleber, Janse, Van Capelle & Durrer, 1978) is due mainly to shortening of the plateau phase of repolarization (Janse & Kleber, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…Whatever the ionic mechanism, these electrical changes may influence the development of the ventricular arrhythmias of the early phase of ischaemia (Boineau & Cox, 1973;Lazzara, El-Sherif, Hope & Scherlag, 1978;Janse & Kleber, 1981); abnormally enhanced automaticity and diastolic depolarization may also play a role in this context. The changes in monophasic action potentials duration and conduction time, although crude estimations of refractoriness and conduction velocity, are relevant to the assessment of the electrophysiological alterations during ischaemia on the intact heart.…”

Section: Discussionmentioning

confidence: 99%

“…The duration of the paced endocardial evoked response and monophasic action potentials normally represent a measure of the local refractory period of the myocardium. Whether this ig true for ischaemic tissue, where postrepolarization refractoriness may cause a disparity between action potential duration and refractoriness (Janse & Kleber, 1981) is uncertain.…”

Section: Discussionmentioning

confidence: 99%

See 2 more Smart Citations

Differential effects of ischaemia and hyperkalaemia on myocardial repolarization and conduction times in the dog.

Donaldson¹,

Nashat²,

Noble³

et al. 1984

The Journal of Physiology

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SUMMARY1. The role of increased extracellular K+ concentration ([K+]O) in the production of the early electrophysiological changes induced by myocardial ischaemia, was evaluated by recordings of monophasic action potentials and the paced endocardial evoked response.2. Changes in the duration of local repolarization and conduction time were evaluated during ischaemia, K+ infusion and hypoxia. 7. Absolute reduction in repolarization time during K+ infusion was more marked at the apex than at the base in the epicardial recordings.8. The superimposition of hypoxia on hyperkalaemia resulted in marked slowing of repolarization and conduction time.9. Many but not all of the early electrophysiological abnormalities of acute ischaemia in the intact heart can be related to raised [K+]O.

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Overweight and Sudden Death

Messerli¹

1987

Arch Intern Med

199

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\s=b\Obesity has been documented to be an independent risk factor for sudden death and other cardiovascular mortality. The present study was designed to monitor and quantify cardiac arrhythmias in obese subjects with and without eccentric left ventricular hypertrophy, who were matched with regard to arterial pressure, age, sex, and height with lean subjects. Prevalence of premature ventricular (but not atrial) contractions was 30 times higher in obese patients with eccentric left ventricular hypertrophy compared with lean subjects. Similarly, obese patients with left ventricular hypertrophy scored higher with regard to the classification of Lown and Wolf than those without left ventricular hypertrophy and lean subjects having the same level of arterial pressure. Patients' class in the

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Electrophysiological changes and ventricular arrhythmias in the early phase of regional myocardial ischemia.

Cited by 297 publications

References 113 publications

Effects of Stilbene Derivatives SITS and DIDS on Development of Intracellular Acidosis during Ischemia in Isolated Guinea Pig Ventricular Papillary Muscle In Vitro

Effects of Stilbene Derivatives SITS and DIDS on Development of Intracellular Acidosis during Ischemia in Isolated Guinea Pig Ventricular Papillary Muscle In Vitro

Differential effects of ischaemia and hyperkalaemia on myocardial repolarization and conduction times in the dog.

Overweight and Sudden Death

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