Maximum exercise heart rate reduction with maturation in the rat

Corre, Kenneth A; Cho, H.; Barnard, R. James

doi:10.1152/jappl.1976.40.5.741

Cited by 12 publications

(9 citation statements)

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“…We have chosen the right atrial pacing model to increase heart rate in vivo as a tool to investigate processes that may occur in response to alteration of the local environment, in the absence of systemic metabolic changes such as sympathetic activation in response to physical workload exposure [13]. By this method, we obtained almost a twofold increase in the heart rate, from about 330-350 beats/min under resting conditions to about 600 beats/min, which was comparable with that (580 ± 9 beats/min) observed in rats subjected to maximum exercise [28]. Measurements of activities of antioxidant enzymes and concentrations of non-enzymatic antioxidants or biomarkers of oxidative stress were obtained both under basal conditions and after short-term rapid cardiac pacing to determine whether hypertrophy compromises the ability of the heart to tolerate the stress of tachycardia.…”

Section: Introductionsupporting

confidence: 61%

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Kłapcińska¹,

Sadowska-Krępa²,

Jagsz³

et al. 2009

J Physiol Sci

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Increased oxidative stress resulting from enhanced production of reactive oxygen species and/or inadequate mechanisms of antioxidant defenses has been recognized as an important factor contributing to the initiation and progression of cardiac dysfunction under a wide variety of pathophysiological conditions. The main objective of this study was to examine the effect of electrically induced tachycardia on oxidative stress and the capacity of antioxidant defenses in the normal and hypertrophied left ventricle (LV) in the rat. Left ventricular hypertrophy (LVH) was produced by banding the descending abdominal aorta. The activities of antioxidant enzymes, concentrations of non-enzymatic antioxidants, and biomarkers of oxidative stress were measured in the LV of aortic-banded animals (LVH), untreated or banded rats subjected to short-term (45 min) atrial pacing [(CTR + S) and (LVH + S), respectively], and untreated (CTR) or sham-operated (SHAM) controls. The results indicate that the increase in heart rate in vivo as a result of atrial pacing to a maximum level, independent of sympathetic nerve activity, leads to a substantial increase in oxidative stress and a marked decline in the activities of antioxidant enzymes in both the normal and hypertrophied left ventricle of the rat. The accompanying increase in tissue content of alpha- and gamma-tocopherols seem to contribute to attenuation of the oxidant stress-related loss of thiol stores in the LV. Stable left ventricular hypertrophy induced by aortic banding for six weeks has a minor impact on the capacity of the endogenous antioxidant defense system in the LV, but significantly and negatively affects the ability of the heart LV to tolerate the stress of tachycardia.

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Section: Introductionsupporting

confidence: 61%

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Kłapcińska¹,

Sadowska-Krępa²,

Jagsz³

et al. 2009

J Physiol Sci

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“…Nevertheless, rapid relaxation would be an important adaptive mechanism for a rat heart, forced by exercise to increase its heart rate to values as high as 600 beats/min 13 so that adequate diastolic time would be available for filling of the ventricle and perfusion of the coronary arteries. The improved relaxation that was found in CH may be related to the greater calcium uptake and binding found by Penpargkul et al 14 in sarcoplasmic reticulum isolated from" CH compared to SH.…”

Section: Studies On Hearts Of Conditioned Ratsmentioning

confidence: 99%

Effects of physical training on end-diastolic volume and myocardial performance of isolated rat hearts.

Bersohn¹,

Scheuer²

1977

Circulation Research

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SUMMARY We studied the performance of ventricular muscle and cardiac function of hearts from rats conditioned by swimming (CH) and from sedentary rats (SH) in an isolated working heart apparatus modified to measure end-diastolic volume by dye dilution. Instantaneous aortic flow, left ventricular (LV) pressure and oxygen consumption were measured. Heart rate and mean aortic pressure were kept constant, and atrial filling pressure was varied from 5 to 20 cm H 2 O. Heart weights of SH and CH were equal and end-diastolic pressures and volumes were similar at all atrial pressures. However, ejection fraction, calculated circumferential fiber velocity, peak systolic pressure, peak aortic flow, cardiac output, and stroke work were all greater in CH than in SH, and the differences increased as atrial pressure was increased. Maximal negative dP/dt was greater in CH than SH at all preloads (P < 0.001). Oxygen consumption of CH was increased in proportion to the increase in work. These results indicate that the improved pumping performance of CH is due to a change in ventricular muscle function. Faster relaxation is a prominent effect of physical training on the rat heart and may foster more complete filling at high heart rates.THE ISOLATED working rat heart apparatus was originally developed by Neely et al. 1 to study cardiac metabolism in a heart performing external work. Performance could be assessed from measurements of left ventricular (LV) and aortic pressures and cardiac output. 1 and from these approximate values for external work could be obtained. However, more precise measurement of the pumping characteristics of the heart (instantaneous flow as well as pressure) was not possible, and the inability to measure ventricular volume precluded making extrapolations to muscle function.The contractile performance of the heart is determined in part by the amount of stretch applied prior to contraction, as governed by the end-diastolic volume. Although end-diastolic pressure could be measured in the isolated working rat heart apparatus, the relation between enddiastolic pressure and volume might vary in different experimental conditions, and a change in this relationship would make alterations in cardiac performance impossible to interpret in terms of muscle function. For instance. Penpargkul and Scheuer 2 showed that cardiac performance was enhanced in hearts from rats subjected to moderate physical conditioning but. in the absence of information about ventricular volumes, it was not known whether the enhanced pumping performance resulted from greater muscle fiber-shortening from the same end-diastolic volume (increased contractility) or from an increased enddiastolic volume due to a change in compliance.This paper reports modifications of the rat heart apparatus so that end-diastolic volume can be determined by a dye-dilution technique and aortic flow can be measured with an electromagnetic flowmeter. From these data, ejection fraction, ventricular volume, peak values and first derivatives of pressure and flow, external ...

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“…The infarct border zone was more prone to alternans, as demonstrated by the ratio of alternans magnitude in border zone versus non-infarcted zone (Figure 4A, example in Figure 3C), with the difference statistically significant for bcls of 100–120 ( p < 0.05; Wilcoxon signed rank test) and near-significant at 95, 130, and 140 ms ( p = 0.078, 0.055, 0.078, respectively; Wilcoxon signed rank test). Medium pacing intervals (bcl 100–120 ms) led to the largest increase of alternans in border zone compared to non-infarcted zone; these bcls correspond to the heart rates seen during exercise in rats (Corre et al, 1976). During slower pacing (bcl 130–140 ms) the increase was smaller (Figure 4A), which can be explained by low levels of alternans throughout the tissue (Figure 3A).…”

Section: Resultsmentioning

confidence: 64%

β-Adrenergic Receptor Stimulation and Alternans in the Border Zone of a Healed Infarct: An ex vivo Study and Computational Investigation of Arrhythmogenesis

et al. 2019

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Background: Following myocardial infarction (MI), the myocardium is prone to calcium-driven alternans, which typically precedes ventricular tachycardia and fibrillation. MI is also associated with remodeling of the sympathetic innervation in the infarct border zone, although how this influences arrhythmogenesis is controversial. We hypothesize that the border zone is most vulnerable to alternans, that β-adrenergic receptor stimulation can suppresses this, and investigate the consequences in terms of arrhythmogenic mechanisms. Methods and Results: Anterior MI was induced in Sprague-Dawley rats ( n = 8) and allowed to heal over 2 months. This resulted in scar formation, significant ( p < 0.05) dilation of the left ventricle, and reduction in ejection fraction compared to sham operated rats ( n = 4) on 7 T cardiac magnetic resonance imaging. Dual voltage/calcium optical mapping of post-MI Langendorff perfused hearts (using RH-237 and Rhod2) demonstrated that the border zone was significantly more prone to alternans than the surrounding myocardium at longer cycle lengths, predisposing to spatially heterogeneous alternans. β-Adrenergic receptor stimulation with norepinephrine (1 μmol/L) attenuated alternans by 60 [52–65]% [interquartile range] and this was reversed with metoprolol (10 μmol/L, p = 0.008). These results could be reproduced by computer modeling of the border zone based on our knowledge of β-adrenergic receptor signaling pathways and their influence on intracellular calcium handling and ion channels. Simulations also demonstrated that β-adrenergic receptor stimulation in this specific region reduced the formation of conduction block and the probability of premature ventricular activation propagation. Conclusion: While high levels of overall cardiac sympathetic drive are a negative prognostic indicator of mortality following MI and during heart failure, β-adrenergic receptor stimulation in the infarct border zone reduced spatially heterogeneous alternans, and prevented conduction block and propagation of extrasystoles. This may help explain recent clinical imaging studies using meta-iodobenzylguanidine (MIBG) and 11C-meta-hydroxyephedrine positron emission tomography (PET) which demonstrate that border zone denervation is strongly associated with a high risk of future arrhythmia.

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Maximum exercise heart rate reduction with maturation in the rat

Cited by 12 publications

References 0 publications

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Short-term effects of electrically induced tachycardia on antioxidant defenses in the normal and hypertrophied rat left ventricle

Effects of physical training on end-diastolic volume and myocardial performance of isolated rat hearts.

β-Adrenergic Receptor Stimulation and Alternans in the Border Zone of a Healed Infarct: An ex vivo Study and Computational Investigation of Arrhythmogenesis

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