Normalization of depressed heart function in rats by ribose

Zimmer, Heinz‐Gerd; Ibel, H.

doi:10.1007/bf02580628

Cited by 15 publications

(24 citation statements)

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“…Due to the influence of ADP on the creatine kinase equilibrium (Lawson and Veech, 1979;McGilvery and Murray, 1974), the low ADP value may have prevented exhaustion of phosphocreatine. The low ADP level helped to partially preserve the free energy of ATP hydrolysis, and indicated a general overall deficiency in the nucleotide pool as observed in other heart failure models (Zimmer, 1983). Whether ADP is calculated from the creatine kinase equilibrium or from direct measurements, including assumptions for compartmentalization and binding, based on published values as described by Kammermeier et al (1982), the free energy of ATP hydrolysis is considerably lower in hearts of the Syrian hamster, compared with normal hearts.…”

Section: Discussionmentioning

confidence: 91%

“…Since other heart failure models are characterized by a decrease in high energy phosphates (WikmanCoffelt et al, 1979), a depressed nucleotide pool (Zimmer, 1983), and a decrease in the free energy of ATP hydrolysis (Kammermeier et al, 1982), energy metabolites were analyzed. Hearts were examined in an isolated perfused state during both normal and maximum work performance.…”

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confidence: 99%

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Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

Sievers¹,

Parmley²,

James³

et al. 1983

Circulation Research

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SUMMARY. The following studies were carried out to examine energy metabolites and cardiac performance of the failing heart (hereditary cardiomyopathy) of the Syrian hamster (strain UM-X7.1) perfused either by normal or stress conditions, and to determine whether cyclical changes in energy-related metabolites occurred in the glucose-perfused hearts of both normal and heart failure animals. Hamster hearts from 250-day-old animals with moderate heart failure were removed and perfused either as nonworking hearts (Langendorff method, an afterload pressure of 90 mm Hg and 2.5 rriM calcium in the perfusate) or as working hearts with stress conditions [an afterload of 110 mm Hg, high calcium concentrations in the perfusate (3.5 ITIM), and 10~8 M isoproterenol]. Mechanical parameters (developed pressure and max dP/dt) and measurements of oxygen consumption indicated that both contractility and oxygen consumption had fallen 50% in myopathic hearts, compared with those of normal hamsters perfused with either of the two conditions. By means of a specially designed stimulator-triggered freeze clamp, hearts were terminated at systole and diastole, and tissue content of ATP, ADP, AMP, adenosine, phosphocreatine, creatine, pyruvate, lactate, and inorganic phosphate were analyzed. A 50% reduction in cardiac performance of the cardiomyopathic hamster hearts was associated with a corresponding reduction in systolic ATP, adenosine, and phosphocreatine values, while inorganic phosphate and lactate increased. With glucose as the sole substrate, the high energy phosphates, ATP and phosphocreatine, reached maximum values during diastole and minimum values during systole. The phase alternate was observed with creatine, ADP, AMP, and inorganic phosphate. Cyclical changes were less obvious in the cardiomyopathic hearts due to less ATP utilization per cycle. A decrease in high energy phosphates, a low level in the free energy of ATP hydrolysis, augmented levels of lactate, increased inorganic phosphate, and a depressed purine nucleotide pool all of which occur concurrently, may cause the decrease in cardiac performance in the failing heart of the cardiomyopathic Syrian hamster. (Circ Res 53: 759-766, 1983)

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Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

Sievers¹,

Parmley²,

James³

et al. 1983

Circulation Research

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“…After the myocardial carnitine levels were restored to normal in these myopathic hamsters, the second purpose of this study was then to determine whether cardiac performance would improve during isolated-heart perfusion with maintenance of high-energy phosphate stores comparable to normal control hearts. Decreased high-energy phosphate stores are associated with the Syrian hamster model of cardiomyopathy 1 *- 29 -"' 32 and other models of heart failure, along with depressed adenosine nucleotide pools 18 - 34 and a reduction in the release of free energy by ATP hydrolysis. 35 Therefore, high-energy phosphate levels were assayed and used, along with hemodynamic parameters of cardiac function, to indicate functional integrity of the myocardium.…”

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confidence: 99%

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

Whitmer

1987

Circulation Research

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Hamsters with either the dilated (BIO 53.58) or hypertrophic (BIO 14.6) form of cardiomyopathy and an inbred control strain of hamster (FIB) were treated for 6 months with high-dose L-carnitine (1 g/kg/day i.p.). After treatment, the animals were killed and their hearts perfused by the isolated working technique. Mechanical performance (as indicated by the double product of heart rate and left ventricular [LV] peak systolic pressure) of both carnitine-treated cardiomyopathic groups was increased significantly above their respective sham-treated groups. Associated with these increases in mechanical performance were significant increases in both peak-positive LV dP/dt (index of contractility) and peak negative dP/dt (index of relaxation) in both carnitine-treated myopathic groups. Serum carnitine levels were increased 10-15 times within 2 hours after injection of L-carnitine in all 3 groups. Myocardial free-carnitine levels were increased twofold in both control and dilated myopathic hearts above their respective sham-treated groups, restoring the level in the dilated hearts comparable to those of controls. Myocardial carnitine levels in the hypertrophic group were not significantly affected by treatment. Total high-energy phosphate stores, i.e., ATP plus creatine phosphate, were restored to control levels by L-carnitine treatment in both cardiomyopathic groups. Levels of the breakdown products of ATP were maintained primarily in the more readily convertible adenosine diphosphate and adenosine monophosphate forms in all three treated groups. These changes resulted in significantly higher ratios of (ATP)/(ADP + AMP + adenosine) and (creatine phosphate)/ (creatine) in the treated hearts. This is the first study demonstrating that high-dose L-carnitine treatment results in improved cardiac performance and increased myocardial total high-energy phosphate stores in the Syrian hamster model with one of two distinct forms of cardiomyopathy, i.e., dilated or hypertrophic. The mechanisms for these effects of exogenous L-carnitine treatment cannot be totally explained by changes in oxidative energy metabolism. (Circulation Research 1987; 61:396-408)

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“…It is, however, a characteristic metabolic feature of the myocyte to very slowly restore their adenine nucleotide pool after it has been depleted [29]. It has been shown that myocytes find two alternative pathways for ATP production under these conditions that would allow them reversing the ventricular dysfunction [14]. The first one would involve adenosine, inosine, and adenine (salvage pathway); and the second would be by stimulating adenine nucleotide biosynthesis.…”

Section: Discussionmentioning

confidence: 99%

“…Furthermore, ribose has no influence on coronary blood flow, myocardial oxygen consumption, and hemodynamics in the normal heart. Therefore, ribose has been suggested to be an attractive nutraceutical supplement for the metabolic support of the heart in numerous cardiac disorders [14][15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

Ribose Treatment Reduced the Infarct Size and Improved Heart Function after Myocardial Infarction in Rats

Gónzalez¹,

Rabald

Briest

et al. 2009

Cell Physiol Biochem

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Objective: In this study the effect of ribose on heart function and infarct-size was analyzed 6 h after myocardial infarction (MI) in rats. Methods: Continuous i.v.-infusion of NaCl or ribose (200 mg/kg/h) was started one day prior to induction of MI in female Sprague-Dawley rats which was done by ligation of the left coronary artery. Six hours after MI heart function was measured with 3F tip catheter, cardiac output by thermodilution method. Thereafter the ischemic area was delineated by Evans Blue infusion, and the infarct area was visualized by triphenyltetrazolium chloride staining. The mRNA expression of interleukin (IL)-1β, IL-6, matrix-metalloproteinase (MMP)-8, and -9 was measured by ribonuclease protection assay. Results: Heart function was severely depressed 6 hours after coronary artery occlusion, but recovered significantly under the influence of ribose. Left ventricular (LV) systolic pressure (LVSP) and contractility (LVdP/dt_max) were restored to the normal levels of sham-operated animals, while parameters of LV relaxation (LVdP/dt_min and time constant of relaxation τ) were impaired compared to sham-operated animals, but significantly improved by ribose treatment compared to sham-treated MI-rats. Moreover, the infarct size was significantly smaller in the ribose treated animals despite a comparable ischemic area at risk in all MI-rats. The cytokine mRNA expression after MI was significantly reduced after ribose treatment, while there were no differences regarding MMP expression. Conclusion: MI size was significantly reduced and LV function significantly improved by ribose treatment at 6 h after MI. This seemed to be based on slowing the velocity of the necrotic wave front across the LV wall after MI resulting in smaller infarcts.

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Normalization of depressed heart function in rats by ribose

Cited by 15 publications

References 0 publications

Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

Energy levels at systole vs. diastole in normal hamster hearts vs. myopathic hamster hearts.

L-carnitine treatment improves cardiac performance and restores high-energy phosphate pools in cardiomyopathic Syrian hamster.

Ribose Treatment Reduced the Infarct Size and Improved Heart Function after Myocardial Infarction in Rats

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