Effect of regional ischemia on the left ventricular end-systolic pressure-volume relationship of isolated canine hearts.

Sunagawa, Kenji; Maughan, W L; Sagawa, Kiichi

doi:10.1161/01.res.52.2.170

Cited by 148 publications

(77 citation statements)

References 29 publications

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“…Also, the present results differ from those of Sunagawa et al (1983), in which a parallel rightward shift of the end-systolic pressure-volume relationship in the physiological end-systolic pressure range and a lower slope of the line in the subphysiological end-systolic pressure range were found. Although the reason why the present data seemed to differ from theirs is unclear, it should be noted that there are important methodological differences.…”

Section: Slope Changes In the End-ejection Pressure-ejected Volume Recontrasting

confidence: 99%

Effects of coronary artery stenosis on left ventricular end-ejection pressure-ejected volume relationships in isolated perfused canine hearts.

Maruyama

Shimizu

Watanabe

et al. 1985

Tohoku J. Exp. Med.

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We investigated the behavior of the left ventricular end-ejection pressure-ejected volume relation with and without left circumflex coronary stenosis in isolated perfused canine hearts. To change ventricular afterload pressure, the peripheral resistance of the hydraulic model attached to the aortic root of the excised hearts was changed in a stepwise fashion to five different levels. The end-ejection pressure-ejected volume relationship was nearly linear in both preischemic and ischemic states. The slope changes following left circumflex coronary stenosis differed among the hearts used in the present study, and there was no significant difference in average slope (n =10) between the pre-ischemic and ischemic states (i,e., -7.4+1.0 and -8.4+1.2 mmHg/ml, respectively). Therefore, the slope of the relation was not useful in judging the presence of depressed ventricular function induced by coronary stenosis. In contrast, the ejected volume axis intercept decreased significantly from 16.5+1.1 ml to 13.6+1.1 ml (p<0.05) with regional ischemic.

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Section: Slope Changes In the End-ejection Pressure-ejected Volume Recontrasting

confidence: 99%

Effects of coronary artery stenosis on left ventricular end-ejection pressure-ejected volume relationships in isolated perfused canine hearts.

Maruyama

Shimizu

Watanabe

et al. 1985

Tohoku J. Exp. Med.

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“…Furthermore, LCx region AT and %AT fell significantly with both low-and highdose intracoronary propranolol. However, LAD region AT and %AT did not change significantly from control, as shown in table 4. Changes in segment 946 length after propranolol in the LAD and LCx regions were analogous to changes in wall thickness.…”

Section: Resultsmentioning

confidence: 74%

“…The end-systolic pressurevolume relationship (ESPVR) has been suggested as a relatively load-independent measure of global ventricular function.1-' The variables used to define the ESPVR, the slope Ees, and volume-axis intercept VO have been shown to be functions of cardiac contractile state,2 to be relatively independent of preload and afterload,3 and to be altered by ischemia. 4 Osakada et al 5 were the first to suggest that endsystolic measures of ventricular performance could be applied regionally. In their preliminary study, the endsystolic pressure-thickness relationship (ESPTR) was constructed by changing ventricular loading conditions pharmacologically.…”

mentioning

confidence: 99%

End-systolic measures of regional ventricular performance.

Aversano¹,

Maughan²,

Kass³

et al. 1986

Circulation

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“…The shift of the ESPVR in a nearly parallel manner with heart rate increase above 180 beats/min is very similar to the change previously shown in regional ischemia. 22 We have no evidence, however, that regional ischemia was present, nor is there an a priori reason to believe so. An alternative explanation would be that the shape of the heart has changed at the higher heart rate, leading to the ESPVR shift.…”

Section: Espvr De-mentioning

confidence: 84%

Effect of heart rate on the canine end-systolic pressure-volume relationship.

et al. 1985

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Although the rate dependence of isolated muscle contractility is well known, the ventricular end-systolic pressure-volume relationship (ESPVR) has been reported to be insensitive to heart rate. To resolve this contradiction, we used an isolated, ejecting canine heart preparation perfused at a constant coronary arterial pressure. Heart rate was changed from 60 to 200 beats/min in steps of 20 beats/min. At least 10 pressure-volume loops under different filling pressures were obtained at each heart rate in each of six hearts. Over a heart rate range from 60 to 120 beats/min, the slope of the ESPVR (Ees) increased significantly from 3.5 ± 0.4 (SE) to 5.3 0.6 mm Hg/ml. In the range between 120 and 180 beats/min there was little change in Bes (5.3 + 0.6 to 5.4 + 0.6 mm Hg/ml), but at 200 beats/min Ees increased slightly to 5.7 0.5 mm Hg/ml. The volume axis intercept (V0) of the ESPVR changed little over the range of heart rate from 60 to 160 beats/min (10.2 ± 2 ml to 9.4 ± 1.3 ml) but increased to 15.2 + 1.2 ml at a rate of 200 beats/min. The change in ESPVR with increase in heart rate from 60 to 120 beats/min (i.e., increase in Ees without change in V0) is the same as those seen with a positive inotropic intervention with calcium or cathecholamines, whereas the V0 changes over the range from 160 to 200 beats/min is similar to those seen with regional ischemia. The insensitivity of ESPVR in the midrange may be the result of a balance of positive and negative influences on ventricular contraction or a restricted range for the increase in inotropic state with higher rate. Circulation 72, No. 3, 654-659, 1985. PHYSIOLOGISTS have long been aware that frequency of contraction influences the contractile state of myocardium. The earliest description of this phenomenon has been credited to Bowditch'; many investigators have since shown that in isolated muscle preparations24 and in isovolumically contracting hearts,5-' peak systolic tension or pressure is increased as the frequency of contraction increases.However, several investigators have questioned the importance of the frequency effect on contractility in vivo. 14 For example, Kavaler et al.9 showed that the effect was far less marked or absent in unexcised canine papillary muscles beating in situ. Suga et al.14 showed that changing heart rate over the midrange caused very little change in the end-systolic pressurevolume relationship (ESPVR).The purpose of this investigation was to reinvesti- 654 gate in excised, ejecting canine hearts the effects of extensive change in heart rate on the ESPVR under strictly controlled ejecting conditions, free of reflex stimulation, and over a wider range of heart rates than previously tested. MethodsSurgical preparation. The supported isolated canine heart preparation used in this study has been previously described.8 Briefly, we used two dogs (20 to 25 kg) per experiment. Both dogs were anesthetized with sodium pentobarbital (25 mg/kg iv bolus) and placed on respirators. One dog supplied oxygenated blood to the heart excise...

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Effect of regional ischemia on the left ventricular end-systolic pressure-volume relationship of isolated canine hearts.

Cited by 148 publications

References 29 publications

Effects of coronary artery stenosis on left ventricular end-ejection pressure-ejected volume relationships in isolated perfused canine hearts.

Effects of coronary artery stenosis on left ventricular end-ejection pressure-ejected volume relationships in isolated perfused canine hearts.

End-systolic measures of regional ventricular performance.

Effect of heart rate on the canine end-systolic pressure-volume relationship.

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