The Role of Certain Electrolytes and Hormones in Disseminated Myocardial Necrosis*

Lehr, David

doi:10.1159/000388563

Cited by 11 publications

(12 citation statements)

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“…Our observations arc in agreement with results of Selye [11] and Lehr [12] dem onstrating a role for PTH in cardiac disease of experi mental uremia. Our results further suggest that total abla tion of the parathyroid glands in states of CRF is not the treatment of choice for the prevention of myocardiopathy.…”

Section: Discussionsupporting

confidence: 93%

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Effect of Chronic Renal Failure on Heart

El-Belbessi¹,

Brautbar²,

Anderson³

et al. 1986

Am J Nephrol

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This study examined the effects of chronic renal failure in rats with and without parathyroid glands on myocardial energy production, transfer and utilization as well as on cardiac index. Chronic renal failure was produced by 7/8 nephrectomy in rats weighing between 240 and 350 g with intact parathyroid glands (CRF-control) and in parathyroidectomized (CRF-PTX) rats maintained normocalcemic. The data were compared to results obtained in intact rats and in normocalcemic parathyroidectomized rats with normal renal function. There were significant (p < 0.01) decrements in myocardial content of ATP and creatine phosphate, mitochondrial oxygen consumption, and in the activity of both mitochondrial and myofibrillar creatine phosphokinase in CRF-control rats as compared to normal animals. The myocardial calcium content and the ⁴⁵Ca uptake in CRF-control rats were significantly (p < 0.01) higher than in normal rats. In CRF-PTX animals, the myocardial content of ATP, mitochondrial oxygen consumption, ⁴⁵Ca uptake and calcium content were normal, but PTX did not normalize the activity of mitochondrial and myofibrillar creatine phosphokinase. Parathyroidectomy in rats with normal renal function was associated with a significant reduction in the activity of creatine phosphokinase of myocardial mitochondria and myofibrils. There was a significant (p < 0.01) decrease in cardiac index in CRF-control rats as compared to normal animals, and cardiac index did not return to normal in CRF-PTX rats. The data indicate that (1) chronic renal failure in the presence of intact parathyroid glands is associated with impaired energy production, transfer and utilization by the myocardium and with a decrease in cardiac index; (2) the decrease in energy production (ATP content and mitochondrial oxygen consumption) is due to excess PTH and not to other consequences of chronic renal failure; (3) the impairment in energy transfer (mitochondrial creatine phosphokinase) and energy utilization (myofibrillar creatine phosphokinase) is most likely due to excess PTH, but complete lack of PTH did not correct these abnormalities, since absence of the hormone even in rats with normal renal function is associated with reduced activities of these enzymes; (4) the effects of PTH on the heart in a state of chronic renal failure is, at least partly, mediated by enhanced entry of calcium into the myocardium; (5) the optimal activity of creatine phosphokinase of the myocardial mitochondria and myofibrils requires physiological amounts of PTH and both excess of the hormone or its lack are deleterious to these enzymes and, hence, to energy transfer and utilization, and (6) total parathyroidectomy is not the procedure of choice for the prevention of uremic myocardiopathy.

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Section: Discussionsupporting

confidence: 93%

“…First. Seyle [11] and Lehr [12] found that cardiac lesions predictably occurred in uremic rats; ad ministration of PTH enhanced these lesions and parathy roidectomy either inhibited or completely prevented their development. Second.…”

mentioning

confidence: 99%

Effect of Chronic Renal Failure on Heart

El-Belbessi¹,

Brautbar²,

Anderson³

et al. 1986

Am J Nephrol

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“…The maximum increments in beating rate induced by 1-34 PTH were 53±3.8% (SE) and was achieved with 5 U/ml medium while the maximum increments with 1-84 bPTH were obtained with 40-60 U/ml medium. The carboxy-terminal (53-84) PTH in concentration of [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] gg/ml did not stimulate the beating of the heart cells (Table II). Inactivation of 1-34 and 1-84 bPTH abolished their effects (Table II).…”

Section: Resultsmentioning

confidence: 99%

“…First, either a-or B3-adrenergic agents (phenylephrine or isoproterenol, respectively) were added to the medium to provide a concentration of [10][11][12][13][14][15][16][17][18][19][20] AM and the beating rates were measured at 0.5, 1, 2, 3, and 5 min thereafter. Preliminary studies showed that these concentrations of the agonists produced maximum stimulation of the beating rate of the heart cells.…”

Section: Effect Of Catecholamines and Their Interaction With Pthmentioning

confidence: 99%

Effect of parathyroid hormone on rat heart cells.

Bogin¹,

Massry²,

Harary³

1981

J. Clin. Invest.

324

134

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A B S T R A C T Myocardiopathy is commion in uremia, but its cause is unknown. Excessive entry of calcium in heart cells by catecholamines has been shown to cause necrosis of myocardium. The high blood levels of parathyroid hormone (PTH) in uremia may also enhance entry of calcium into heart cells and exert deleterious effects on the heart. We examined the effect of PTH on rat heart cells grown in culture. Both amino-terminal (1-34) PTH and intact (1-84) PTH, but not the carboxy-terminal (53-84) PTH produced immediate and sustained significant rise in beats per minute and the cells died earlier than control. The effect was reversed if PTH was removed from medium, and was abolished by inactivation of the hormone. There was a dose-reponse relationship between both moieties of PTH and the rise in heart beats, but the effect of 1-84 PTH was significantly greater than that of 1-34 moiety. PTH stimulated cyclic AMP production within 1 min, and cyclic AMP remained significantly elevated thereafter. The effect of PTH required calcium, was mimicked by calcium ionophore, was prevented by verapamil and was not abolished by a-or ,8-adrenergic blockers. PTH action was additive to phenylephrine and synergistic with isoproterenol. Sera from uremic parathyroidectomized rats did not affect heart beats, but sera from uremic rats with intact parathyroid glands or from uremic-parathyroidectomized rats treated with PTH had effects similar to PTH. Data indicate that (a) heart cell is a target organ for PTH and may have receptors for the hormone; (b) PTH increases beating rate of heart cells and causes early death of cells; (c) PTH effect appears to be due to calcitum entry into heart cells; (d) the locus of action through which PTH induces calcium entry is different from that for catecholamines;

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“…Thus, it seems probable that the resulting ne crosis is a consequence of biochemical alterations affecting myocardial cell metabolism [Kahn et al. 1969], Although an unfavorable balance between oxygen demand and sup ply is an important factor in the pathogenesis of ISOinduced myocardial ischemic injury (Mil), the degree of myocardial damage can be modified by complex interac tions between catecholamines, mineralocorticoids and electrolytes [Lehr. 1966].…”

Section: Introductionmentioning

confidence: 99%

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

Bhimji¹,

Godin

McNeill³

1986

Cells Tissues Organs

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The functional and ultrastructural changes observed during myocardial ischemic injury (Mil) in the rabbit are described. Mil was induced by repeated subcutaneous injections of increasing doses of isoproterenol (ISO; 0.5 mg/kg on day 1, to 15.5 mg/kg on day 15). Measurement of cardiovascular changes revealed a significant decrease in the mean arterial pressure and an increase in heart rate of the ISO-treated animals. ISO treatment also initiated a variety of atrial and ventricular arrhythmias, including ventricular fibrillation, as well as significant ST segment elevations and the appearance of Q waves. Electron-microscopic analysis of hearts from ISO-treated animals showed accumulation of lipid and depletion of glycogen. The myofibrils had poorly defined Z bands and appeared as a homogenous mass. The most marked effects of ISO treatment were on the mitochondria, which appeared swollen and fragmented. The mitochondrial cristae were also disrupted and fragmented. A few amorphous electron-dense bodies were observed in and around the mitochondria. The changes observed in this study are qualitatively similar to those observed in the rabbit following coronary artery ligation.

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The Role of Certain Electrolytes and Hormones in Disseminated Myocardial Necrosis*

Cited by 11 publications

References 0 publications

Effect of Chronic Renal Failure on Heart

Effect of Chronic Renal Failure on Heart

Effect of parathyroid hormone on rat heart cells.

Isoproterenol-Induced Myocardial Ischemic Injury in the Rabbit: Functional and Ultrastructural Alterations

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