The effect of hypothermia on the occurrence of the calcium paradox

Boink, A. B. T. J.; Ruigrok, T. J. C.; Moes, Danièle; Maas, A. H. J.; Zimmerman, A. N. E.

doi:10.1007/bf00588688

Cited by 41 publications

(15 citation statements)

References 17 publications

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“…Whereas we used intact adult rat hearts at 37°C, Goshima et al (1980) used isolated myocytes prepared from fetal mouse hearts, and they carried out their experiments at 25°C. The Ca ++ paradox is age-(Chizzonite and Zak, 1981;Frank and Rich, 1983) and temperature-sensitive (Holland and Olson, 1975;Alto and Dhalla, 1979;Boink et al, 1980;Langer, 1982, Baker et al, 1983). The use of isolated myocytes must also be taken into account, because some of the damage that occurs upon repletion results in physical disruption of the weakened intercalated discs, an event which will create abnormal routes of Ca ++ entry (Ganote et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

Calcium, sodium, and the calcium paradox.

Nayler¹,

Perry²,

Elz³

et al. 1984

Circulation Research

115

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SUMMARY. The effect of "sodium loading,' of verapamil and of nifedipine on the gain in calcium and sodium, and on the loss of myoglobin, during the calcium paradox in adult rat hearts was examined. Raising cell sodium from 56.5 ± 2.6 to 129.5 ± 10.2 jtmol sodium/gram dry weight did not alter the degree or rate of calcium gain or myoglobin release during calcium repletion after long periods (>2 minutes) of calcium-free perfusion; under these conditions, and in the presence of 10 ng/\Her verapamil, calcium gain was enhanced. However, after shorter periods (0.5-1.5 minutes), of calcium-free perfusion, calcium gain was enhanced in "sodium-loaded" hearts, even in the absence of verapamil, and particularly during the early stages of repletion. The presence of 1 and 10 j/mol/liter dl-verapamil and 1 //mol/liter nifedipine before, during, and after 10 minutes of calcium-free perfusion significantly (P < 0.01) slowed the early (up to 1 minute for verapamil and 2 minutes for nifedipine) but not the late gain in calcium. When verapamil was present, the late gain in calcium was actually enhanced. These agents also abolished the early (45 seconds) but not the late (>2 minutes) gain in sodium that occurs during repletion. We propose that the gain in calcium that occurs during calcium repletion after a period of calciumfree perfusion can be divided into at least two phases (early and late), and that the early phase contains a verapamil/nifedipine-sensitive component and a verapamil/nifedipine-insensitive component, the latter probably involving sodium-calcium exchange. (Circ Res 55: 227-237, 1984)

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Section: Discussionmentioning

confidence: 99%

Calcium, sodium, and the calcium paradox.

Nayler¹,

Perry²,

Elz³

et al. 1984

Circulation Research

115

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“…Mansier and Lelievre (1982) perfused rat heart for 1 minute at room temperature with Ca ++ -free buffer and demonstrated a conversion of heart Na + ,K + -ATPase into a form highly sensitive to ouabain. Although other laboratories have shown that hypothermic Ca ++ -free perfusion does not lead to a complete Ca ++ paradox (Holland and Olson, 1975;Boink et al, 1980;Rich and Langer, 1982), the observation of Mansier and Lelievre (1982) indicates that the operation of Na The depression of Na + ,K + -ATPase after Ca ++ depletion cannot be attributed to gross changes in the protein pattern of SL membranes. It is important to emphasize here that the employed SDS-PAGE separation technique detects changes only in the molecular weight of SDS-denatured proteins.…”

Section: Sl Function After Ca ++ Depletionmentioning

confidence: 95%

Biochemical properties of membranes isolated from calcium-depleted rabbit hearts.

Lamers¹,

Stinis²,

Ruigrok³

1984

Circulation Research

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SUMMARY. The purpose of this study was to define the biochemical properties of sarcolemma from the caldum-depleted rabbit heart. Caldum repletion after caldum-free perfusion results in irreversible damage to the heart (caldum paradox). No difference was found in specific activity of the Na + -Ca ++ antiporter in a crude preparation of sarcolemmal vesicles that was isolated from caldum-depleted hearts, compared with control perfused hearts. Likewise, the passive caldum efflux from sarcolemmal vesicles, preloaded with caldum via the Na + -Ca ++ antiporter, showed rates that were identical with control values. This indicates that the sarcolemma caldum permeability is not affected by caldum-free perfusion of the heart. Na + ,K + -ATPase activity in sarcolemma isolated from caldum-depleted hearts was reduced by 75% (P < 0.005) compared with the control activity. Sarcolemmal phosphoproteins, whether produced by endogenous cyclic AMP-or caldum-calmodulin-dependent protein kinase, were not altered by caldum-free perfusion of the heart. The content of an important caldum-binding site in the myocardial cell, the sialic add residues, was also estimated. Only a long period (60 minutes) of caldum-free perfusion resulted in a significant decrease (by 68%, P < 0.025) of sialic add content in the homogenate but not in the sarcolemma preparation. In hearts that were reperfused for 15 minutes with a normal caldum concentration (1.3 mM), sarcolemmal Na + ,K + -ATPase remained depressed and caldum permeability was still unchanged. It is possible that the sarcolemma isolation method selected a distinct part of the sarcolemma from the caldum-depleted and repleted heart that had no modified glycocalyx and permeability barriers to caldum ions, and that another part of the sarcolemma with altered properties was lost during the isolation procedure. Another possibility is that reconstitution processes during isolation affected membrane permeability properties. The results of the Na + ,K + -ATPase measurements provide evidence that the net caldum gain of the cells after caldum repletion may be associated, in part, with a loss in ability of the sarcolemma to remove caldum from the cytosol. (Circ Res 54: 217-226, 1984)

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“…The dependence of a calcium paradox induction on the perfusion temperature and the time of calcium depletion had been previously described by several investigators in the heart of both mammals and ectotherms [12,20]. It has been reported that depriving rat hearts of calcium for periods longer than 10 min predisposes them to the calcium paradox, even when the perfusion temperature is 20°C [12], whereas in the frog heart the induction of this phenomenon depends on the temperature (37°C) and the duration of calcium deprivation (30 min) [20].…”

Section: Discussionmentioning

confidence: 99%

“…It is generally accepted that the induction of the calcium paradox in rat depends on the perfusion temperature and the duration of calcium depletion [12][13]. This phenomenon has been studied in the heart of various other mammalian species than rat such as dog, cat, rabbit, guinea pig, and mouse [10,[14][15] as well as in isolated cardiac myocytes of neonatal mouse, adult rat and in human myocardial strips [16][17].…”

Section: Introductionmentioning

confidence: 99%

Characterisation of the Calcium Paradox in the Isolated Perfused Pigeon Heart: Protection by Hypothermia, Acidosis and Alkalosis

Gaitanaki¹,

Anezaki²,

Margieti³

et al. 2002

Cell Physiol Biochem

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The aim of the present investigation was to examine the conditions inducing a calcium paradox in the isolated perfused pigeon heart. Loss of mechanical and electrical activity, creatine phosphokinase and total protein release were used to define cell damage. Perfusion was performed at 36, 38, 40 and 42°C and calcium deprivation lasted 5, 10, 20 or 40 min. At low temperatures even prolonged calcium depletion failed to induce a calcium paradox. After a 40 min calcium depletion at normal body temperature (42°C) ventricular activity ceased and a major contraction occurred followed by an increase in resting tension. During the 20-min reperfusion period the release of creatine phosphokinase was 267.18 ± 0.8 IU/g of dry wt and the total amount of protein loss was 109.3 ± 1.0 mg/g of dry wt, while lower temperatures resulted in a decreased loss of protein and creatine phosphokinase. Using two different Tyrode''s perfusion buffers instead of normal bicarbonate ones, a protection of the pigeon heart against the induction of this phenomenon was observed. Furthermore, acidosis as well as alkalosis protected the heart as estimated by the significant recovery of electromechanical activity, and the quite low total protein and creatine phosphokinase losses. The results of this study suggest that the basic mechanisms and damaging effects of calcium overloading are common in mammalian and pigeon hearts.

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The effect of hypothermia on the occurrence of the calcium paradox

Cited by 41 publications

References 17 publications

Calcium, sodium, and the calcium paradox.

Calcium, sodium, and the calcium paradox.

Biochemical properties of membranes isolated from calcium-depleted rabbit hearts.

Characterisation of the Calcium Paradox in the Isolated Perfused Pigeon Heart: Protection by Hypothermia, Acidosis and Alkalosis

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