Effects of Calcium Antagonists on the Alternation of the St‐t Complex and Associated Conduction Abnormalities During Coronary Occlusion in Dogs

Hashimoto, Hisakuni; Nakashima, Mitsuyoshi

doi:10.1111/j.1476-5381.1981.tb09981.x

Cited by 16 publications

(3 citation statements)

References 34 publications

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“…There have been a few animal studies conducted to examine the effect of anti-ischemic drugs on the occurrence of ST-T alternans during acute myocardial ischemia. Hashimoto, et al showed that calcium antagonists de-creased the incidence of ST-T alternans during acute myocardial ischemia, and Hayakawa, et al showed that diltiazem decreased the incidence of ST-T alternans and ventricular tachycardia/fibrillation during acute myocardial ischemia [8][9][10]20) . We have shown, by measuring extracellular K + , pH, and intramyocardial conduction time in an animal model, the anti-ischemic effect of verapamil [5][6][7] .…”

Section: Discussionmentioning

confidence: 99%

“…We have reported that calcium antagonists decrease both the rise in extracellular K + [K + ] e , and the fall in extracellular pH (pH e ), and previous studies have shown that calcium antagonists reduce the incidence of ST-T alternans during acute myocardial ischemia and decrease the incidence of ventricular fibrillation during ischemia [6][7][8][9][10] . We also have shown that ATP-sensitive K + channel opener pinacidil decreases the rise in [K + ] e and the fall in pH e that occur during acute myocardial ischemia 11) .…”

Section: Introductionmentioning

confidence: 99%

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Effects of Pinacidil on ST-T Wave Alternans During Acute Myocardial Ischemia in the In-situ Pig Heart

Watanabe

Gettes

2017

Nichidai Igaku Zasshi

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ST-T alternans during ischemia is associated with ventricular arrhythmias and reflects primary changes in repolarization, and changes secondary to 2:1 conduction block. We studied the effect of pinacidil, an ATP-sensitive K + channel activator, on the incidence of ST-T alternans during ischemia. K +-and pH-sensitive electrodes and unipolar and bipolar electrodes were inserted into the midmyocardium in 9 open-chested pigs. Transmembrane action potentials were recorded from the epicardial surface. The carotid artery was shunted to the left anterior descending artery via a roller pump, and 25 μM pinacidil was infused. Prior to pinacidil administration, ST-T alternans occurred in all 9 pigs during control ischemia, at a mean onset time of 4 minutes 23 seconds ± 22 seconds. After pinacidil infusion, no ST-T alternans occurred during the 8-minute ischemic period. Furthermore, after pinacidil infusion, the final rise in extracellular K + ([K + ] e) and the fall in extracellular pH (pH e) were similar to the those at the onset of ST-T alternans under control conditions ([K + ] e : 7.6 ± 0.9 vs. 6.9 ± 0.9 mM; pH e : 7.08 ± 0.78 vs. 7.05 ± 0.18). Activation delay was also similar with pinacidil administration compared with that at the onset of ST-T alternans, under the control condition (27 ± 18 ms vs. 34 ± 24 ms). With pinacidil, the action potential duration after 8 minutes of ischemia was decreased by 50% (from 250 ± 36 ms to 127 ± 15 ms). The complete suppression of ST-T alternans by pinacidil may reflect an increase in the diastolic interval.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Pinacidil on ST-T Wave Alternans During Acute Myocardial Ischemia in the In-situ Pig Heart

Watanabe

Gettes

2017

Nichidai Igaku Zasshi

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“…Ischaemic action potential duration alternans, reflecting cellular repolarization abnormalities, is probably the major cause of ischaemic T-wave alternans [17]. In one experimental study, severe conduction delay occurred concomitantly with episodes of alternans of action potential or ST segment elevation preceding ventricular arrhythmias, suggesting that re-entry is the mechanism of arrhythmia [18]. In another study that examined the role of ST alternans in the occurence of ventricular fibrillation after reperfusion in dogs, the magnitude of ST alternans increased progressively until ventricular fibrillation occurred.…”

Section: Discussionmentioning

confidence: 98%

Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs

et al. 2002

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We showed previously a direct arrhythmogenic effect of the intracoronary infusion of endothelin-1 (ET-1). We aimed to examine the electrophysiological effects of intracoronary bolus administration of ET-1 using monophasic action potential (MAP) recordings. Eight mongrel dogs received boli of ET-1 (1 and 2 nmol) into the left anterior descending coronary artery. These intracoronary ET-1 boli rapidly caused a marked decrease in coronary blood flow (1 nmol, 78+/-7%; 2 nmol, 89+/-7%). Ischaemic changes of MAP morphology, a decrease in upstroke velocity (baseline, 1.78+/-0.2 V/s; 1 nmol, 0.95+/-0.18 V/s; 2 nmol, 0.45+/-0.21 V/s; P<0.01) and a decrease in MAP duration at 90% repolarization (MAPD(90)) [1 nmol, from 191+/-3 to 176+/-5 ms (P<0.05); 2 nmol, from 212+/-4 to 180+/-8 ms (P<0.05)] occurred after ET-1 bolus administration. However, at 7-10 min after the 1 nmol bolus, a significant increase in MAPD(90) was observed (10 min, in the left ventricular anterior epicardial region: from 191+/-3 to 206+/-6 ms; P<0.05). The incidence of ventricular arrhythmias was as follows: after the 1 nmol ET-1 bolus: ventricular tachycardia, 3/8 animals; ventricular fibrillation, 1/8; after the 2 nmol ET-1 bolus: ventricular tachycardia, 5/7; ventricular fibrillation, 5/7. MAP alternans was present in each animal (1 nmol, 18.2+/-5.8%; 2 nmol, 10.8+/-2.5%). Thus electrophysiological and coronary blood flow changes indicate the predominance of an ischaemic arrhythmogenic effect of the bolus administration of ET-1 (shortening of action potential duration; appearance of MAP alternans), whereas the observed delayed prolongation of MAPD(90) suggests a direct arrhythmogenic effect of ET-1. The expressed MAP alternans could have a pathogenic role in the onset of ventricular arrhythmias induced by an intracoronary bolus of ET-1.

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Effects of bepridil and lidocaine on the intravenctricular conduction in acutely ischaemic and infarcted canine myocardium

Hashimoto

Satoh

Nakashima

1990

Naunyn-Schmiedeberg's Arch Pharmacol

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Effects of bepridil, an antiarrhythmic and antianginal drug, on intraventricular conduction in acutely ischaemic and infarcted myocardium were examined in anaesthetized dogs, and compared with those of lidocaine. Bepridil at doses of 2 and 5 mg/kg markedly prolonged the conduction time of a premature excitation induced by a ventricular stimulation in the infarcted zone. The effect of bepridil was dependent on a coupling time of the stimulation. Bepridil showed a marked effect at a coupling time of 150 ms, while it showed no significant effect at a prolonged coupling time of 1 s. In other words, the effect of bepridil was interval-dependent. Lidocaine showed a similar interval-dependent effect, but the effect of lidocaine at a longer coupling time was less than that of bepridil. The premature stimulation produced severely delayed conduction which resulted in reentrant beats. Bepridil blocked these conductions, thereby preventing reentrant beats. In contrast to the depressant effect of bepridil in the infarcted myocardium, bepridil prevented the prolongation of conduction time during acute ischaemia. The alternation of the ST-T complex during acute ischaemia which is also an important arrhythmogenic factor was also attenuated by bepridil. Contrary to bepridil, lidocaine significantly enhanced the conduction delay and the alternation in the ST-T complex. In conclusion, bepridil as well as lidocaine showed an interval-dependent depression of the conduction in the infarcted zone of the heart, whereas during acute ischaemia bepridil in contrast to lidocaine attenuated the conduction delay and ST-T alternans.

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Effects of Calcium Antagonists on the Alternation of the St‐t Complex and Associated Conduction Abnormalities During Coronary Occlusion in Dogs

Cited by 16 publications

References 34 publications

Effects of Pinacidil on ST-T Wave Alternans During Acute Myocardial Ischemia in the In-situ Pig Heart

Effects of Pinacidil on ST-T Wave Alternans During Acute Myocardial Ischemia in the In-situ Pig Heart

Expressed monophasic action potential alternans before the onset of ventricular arrhythmias induced by intracoronary bolus administration of endothelin-1 in dogs

Effects of bepridil and lidocaine on the intravenctricular conduction in acutely ischaemic and infarcted canine myocardium

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