Acceleration of Recovery of Mitochondrial Function after Coronary Reperfusion by Various Coronary Dilating Drugs in Canine Hearts

Hanaki, Yoshihiro; Sugiyama, Satoru; Ajioka, Masayoshi; Kondo, Taizo; Fukushima, Akihiko; Ozawa, Takayuki

doi:10.1097/00005344-198902000-00025

Cited by 7 publications

(1 citation statement)

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“…Studies on regional myocardial stunning and show slight increases in the end diastolic presing. sure (LVPed) and in the unstressed diastolic segment length during early reperfusion.9 32 Comparably, circumferential length was Ltrac-increased at constant LVPed in our globally IVo2stunned myocardium as indicated by intravennned tricular diameter. LVPed in this study was lo; fig decreased, however, if comparison was made iency at constant end diastolic volumes.…”

Section: Systolic Propertiessupporting

confidence: 49%

Haemodynamic and energetic properties of stunned myocardium in rabbit hearts.

Schipke

Korbmacher

Dorszewski

et al. 1996

Heart

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Objective-To amplify the description of myocardial stunning. Design-Control versus 30 min after a 20 min no flow ischaemia. Experimental animals-i 5 isolated rabbit hearts perfused with erythrocyte suspension. Main outcome measures-Left ventricular systolic function in terms of aortic flow, peak systolic pressure (LVPmax), dP/dtmax, and the end systolic pressurevolume relation (ESPVR); early relaxation from dP/dtmin and rate of left ventricular pressure decay (T). Passive properties: ventricular and myocardial stiffness. Coronary resistance from coronary blood flow and perfusion pressure. Total myocardial oxygen consumption (MVo,tot). Total mechanical energy via pressure-volume area (PVA). Contractile efficiency (Econ) and MVo, of the unloaded contracting heart (MVo2unl).External mechanical efficiency (Eext) from stroke work and MVo2tot.Results-Systolic variables in stunned myocardium were significantly decreased (mean (SD)): aortic flow: 38 (13) v 9 (11) mllmin; LVPmax: 112 (19) 138 (73) v 125 (58) mm Hg/ml, but the volume axis intercept was shifted rightward: 0 30 (0.37) v 0*65 (0.25) ml. Likewise, early relaxation was impaired: dP/dtmin (-1275 (250) v -975 (250) mm Hg/s) and T (37 (7) v 46 (10) ms). LVPed was significantly decreased at 19 (12) v 12 (7) mm Hg, and both the ventricular (end diastolic pressure-volume relation) and the myocardial stiffness (constant k) were increased by 75% and 31%, respectively. Coronary resistance increased non-significantly from 0-83 (0.31) to 1.04 (0.41) mm HgI(mlnmin/100 g). Decreases in PVA (570 (280) v 270 (200) mm Hgnml/100 g), MVo2tot (40 (9) v 34 (8) ulIbeat/100 g), and MVo,unl (26 (9) v 22 (6),uIIbeat/100 g) did not reach significance, in contrast to significant decreases in Econ (31 (18) Conclusions-Ventricular systolic function is decreased after brief episodes of ischaemia. The decrease in diastolic function probably amplifies the systolic deterioration during myocardial stunning. Passive diastolic properties are also changed, shown by increases in both ventricular and myocardial stiffness. The increase in coronary resistance indicates stunning at the vascular level which could limit oxygen supply. With maintained MVo,tot during stunning, external efficiency is decreased. Possible candidates for this metabolic stunning are inadequate excitation-contraction coupling and disturbed 02 utilisation by the contractile apparatus. (Heart 1996;75:55-61) Keywords: stunning; coronary resistance; efficiency; isolated heart After brief periods of ischaemia, myocardial function remains depressed for hours or even days. This is known as myocardial stunning.1 2 Although there are many published reports on myocardial stunning,3-5 the phenomenon is far from completely understood. Many of the studies focus only on systolic properties6-8 as one aspect of that particular myocardial state.Depending on the duration and severity of the ischaemic insult, postischaemic myocardium can become entirely2 or almost entirely akinetic.910 In the present study, we reve...

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Section: Systolic Propertiessupporting

confidence: 49%

Haemodynamic and energetic properties of stunned myocardium in rabbit hearts.

Schipke

Korbmacher

Dorszewski

et al. 1996

Heart

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Electrophysiologic effects of potassium channel openers

Haverkamp

Borggrefe

Breithardt

1995

Cardiovasc Drug Ther

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Potassium-channel openers or activators have been introduced as a new class of antihypertensive and antianginal agents that act by increasing membrane conductance to potassium, mainly through augmentation of the ATP-sensitive potassium current. Recent in vitro studies have shown that K(+)-channel openers exert concentration-dependent effects on cardiac electrophysiology. A shortening of the cardiac action potential by acceleration of repolarization has been reported in multicellular preparations as well as in isolated myocytes. However, drug concentrations that affect the action potential duration of myocardial cells are considerably higher (10- to 100-fold) than those needed for effects on vascular smooth muscle cells. Studies in which mostly high concentrations of K(+)-channel openers were used have demonstrated that these drugs may accelerate automaticity and may promote reentrant activity. Particular interest has focused on the question whether opening of potassium channels may be potentially arrhythmogenic in the setting of acute myocardial ischemia. On the other hand, recent studies have shown that K(+)-channel openers are effective in suppressing polymorphic ventricular tachyarrhythmias induced by early afterdepolarizations and triggered activity in vivo. The clinical relevance of these experimental studies to the clinical situation is still unclear. Some K(+)-channel openers have been shown to produce electrocardiographic T-wave changes in patients in whom their effectiveness as antihypertensives was tested. However, this effect was not associated with adverse effects and has not been demonstrated for all compounds.(ABSTRACT TRUNCATED AT 250 WORDS)

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