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  • 1
    Electronic Resource
    Electronic Resource
    Prevention by 7-oxo-prostacyclin of the calcium paradox in rat heart: Role of the sarcolemmal (Na,K)-ATPase (1996)
    Springer
    Molecular and cellular biochemistry 160-161 (1996), S. 257-263 
    Details
    ISSN: 1573-4919
    Keywords: 7-oxo-prostacyclin ; calcium paradox ; sarcolemmal (Na,K)-ATPase ; subsarcolemmal sodium ; subsarcolemmal Na/Ca ratio ; calcium overload of the heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract It is demonstrated a fast and significant depression in the sarcolemmal (Na,K)-ATPase activity that occurs as early as 25 sec after the onset of Ca2+ depletion, and participates in the development of Ca2+-paradox in the rat heart. Pretreatment of the animals with 7-oxo-prostacyclin (PG12) 24–48 h prior to the experiment prevented fairly the Ca2+-depletion-induced depression in (Na,K)ATPase activity and the accompanying structural and functional damage to the heart and sarcolemma during Ca2+-depletion as well as the development of Ca2+-paradox during the subsequent Ca2+-repletion. Pretreatment with PGI, was chosen intentionally because previous experiments revealed, that in its late effect the drug is acting via stabilizing the membranes due induction of high activity of (Na,K)-ATPase that has increased affinity to ATP. From results obtained the following may be concluded: If during the phase of Ca2+-deprivation, the capability of heart sarcolemma to maintain sodium extrusion remains preserved, the expected aggravation of Ca2+-overload injury to Ca2+-paradox that would develop during Ca2+-repletion, may be definitely prevented. Sufficiently preserved (Na,K)-ATPase activity, hand in hand with stabilized sarcolemmal structure, may prevent an accumulation of sodium beneath the sarcolemma and consequently also an overexcessive entry of Ca2+ into the myocytes.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00240057
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  • 2
    Electronic Resource
    Electronic Resource
    Release of 6-KETO-PGF1α and thromboxane B2 in late appearing cardioprotection induced by the stable PGI analogue: 7-OXO-PGI (1993)
    Springer
    Molecular and cellular biochemistry 119 (1993), S. 129-132 
    Details
    ISSN: 1573-4919
    Keywords: late appearing cardioprotection ; PGI2 ; TXA2 ; ischaemia ; reperfusion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract We have shown earlier that prostacylin (PGI2) and its stable analogue: 7-oxo-prostacyclin(7-OXO) may induce a prolonged, late appearing (24–48 h after drug administration), dose dependent protection of the heart from harmful consequences of a subsequent severe ischaemic stress, such as myocardial ischaemia, life-threatening ventricular arrhythmias and early ischaemic morphological changes. In an other study we observed that a similar but shortlived (less than 1 h) cardioprotection, induced by ‘preconditioning’ brief coronary artery occlusions, is greatly reduced by blockade of the cyclooxygenase pathway, suggesting that prostanoids might play a role in this shortlasting protection. Objective of our present study was to elucidate the importance of some arachidonic acid (AA) metabolites, such as PGI2 and thromboxane A2 (TXA2) in the mechanism of the late appearing, prolonged cardioprotection. Estimation of the metabolites: 6-keto-PGF1α (6-KETO) and thromboxane B2 (TXB2) was made from the perfusate of isolated Langendorff hearts of guinea-pigs pretreated with 50 μg/kg 7-OXO, 24 and 48 h before preparation. Pretreatment alone produced a slight, but significant elevation of 6-KETO (from 206±11 to 284±19 pg/ml/min after 24 h, and to 261±18 pg/ml/min after 48 h). No change was seen in TXB2 production. Global ischaemia for 25 min (followed by 25 min reperfusion) markedly increased the release of both AA metabolites; maximal values were observed in the third min of reperfusion (6-KETO from 206±11 to 1275±55 pg/ml/min and TXB2 from 29±4 to 172±12 pg/ml/min). All values returned to the preischaemic level by the 25th min of reperfusion. Ischaemic increase in 6-KETO level was significantly higher in the perfusate of hearts from pretreated animals (1507±73 pg/ml/min after 24 h, and 1398±54 pg/ml/min after 48 h) that in those of untreated controls. There was no difference in TXB2 values. Thus both basal and ischaemic release of PGI2 increased 24 and 48 h after pretreatment with 7-OXO but not TXA2 production. Results suggest that endogenous prostanoids might play a role in late appearing cardioprotection.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00926863
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