Effect of α-tocopherol on hypoxic-perfused and reoxygenated rabbit heart muscle

Guarnieri, Chiara; Ferrari, Roberto; Visioli, O; Caldarera, C. M.; Nayler, Winifred G.

doi:10.1016/0022-2828(78)90336-x

Cited by 99 publications

(13 citation statements)

References 26 publications

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“…Under each of these conditions, drugs which either preserve membrane ultrastructure (e.g. corticosteroids, a tocopherol (25,26) and phospholipase inhibitors) or maintain the tissue stores of ATP above the critical level needed for maintaining intracellular Ca 2 § homeostasis (24) could be effective in preventing Ca 2 § overload, irrespective of whether they have a direct inhibitory effect on Ca 2+ influx through the slow channels.…”

Section: Other Methods For Defining "Calcium Antagonists"mentioning

confidence: 99%

Calcium antagonists: definition and mode of action

1981

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The term "calcium antagonist" has been used for more than a decade to describe a group of drugs whose negative inotropism is overcome by calcium. Because this term lacks specificity with respect to a precise mode of action, and implies a classical receptor-agonist-antagonist relationship, its continued use should be questioned. Drugs belonging to this group are verapamil, D600, nifedipine and diltiazem. They inhibit the slow inward current of the action potential and would more appropriately be called "slow channel inhibitors". The group is heterogenous and may have to be subclassified. The negative inotropism of these drugs can be attributed to a reduction of the slow calcium current. The function of most intracellular organelles is unaffected. Studies with radioactively labelled verapamil show tight binding to glycolipids or glycoproteins in the sarcolemma. Consequent change in the conformational state of the cell membrane could inhibit the slow calcium current. The ability of these drugs to protect heart muscle against the deleterious effects of ischaemia and reperfusion may reflect their negative inotropism, with consequent maintenance of tissue ATP above the levels needed to maintain intracellular Ca2+ homeostasis, rather than a direct inhibitory effect on calcium influx during ischaemia or on reperfusion.

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Section: Other Methods For Defining "Calcium Antagonists"mentioning

confidence: 99%

Calcium antagonists: definition and mode of action

1981

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“…During hypoxia, the levels of CP, NADH, NAD, pyruvate, and G6P decreased significantly, as compared to the control condition (normoxia). The decrease in CP level seemed less marked than that reported by REIBEL and ROVETTO (1978) and GAUDUEL et al (1979), while it was comparable to the decrease reported in the case of the rabbit heart perfused using the Langendorff technique (GUARNIERI et al, 1978). The levels of IMP, Pi, and lactate remained unchanged during the hypoxia.…”

Section: Resultsmentioning

confidence: 41%

“…(FEUVRAY and DE LEIRIS, 1975). The depletion of tissue ATP and CP during hypoxia has been demonstrated by many investigators (KUBLER and SPIECKERMANN, 1970 ;NAYLER et al, 1976 ;GUARNIERI et al, 1978 ;REIBEL and ROVETTO, 1978;GAUDUEL et al, 1979). They found that decrease in the total tissue ATP seemed to develop relatively slowly, but that in the tissue CP levels proceeded rather rapidly.…”

Section: Resultsmentioning

confidence: 97%

Surface layer ATP-related contraction in isolated,superfused canine ventricular papillary muscle: An isotachophoretic analysis.

et al. 1982

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“…In various pathological conditions involving the myocardium (hyp oxia, ischemia) this antioxidant is inhibited due to excessive utilization in antioxidant reactions linked with activation of lipid per oxidation [23]. Tocopherol, an effective means for prevention of ischemia [10], is capable of improving energy processes and contractility in isolated ischemic hearts [8]. As seen in table VII, a-tocopherol in the model of epinephrine-induced arrhythmia facilitated the normalization of activity of glutathione's antioxidant system, signifi cantly decreased glutathione reductase activ ity, and increased the content of SH-groups, which are essential for the biological activity of SH-containing enzymes such as creatine phosphokinase and succinate dehydroge nase.…”

Section: Resultsmentioning

confidence: 99%

Antioxidants as Antiarrhythmic Drugs

Frolkis¹,

Frol'kis²,

Dubur

et al. 1987

Cardiology

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Experiments on rats and rabbits using models of arrhythmias induced by vasopressin, epinephrine, strophanthin, and CaCl₂ showed that antioxidants derived from 1,4-dihydropyridines, dibunol, and α-tocopherol possessed antiarrhythmic effects. Administration of these antioxidants decreased the occurrence of extrasystoles, disturbances of atrioventricular conductivity and ventricular fibrillation. These drugs also prevented changes in membrane phospholipid composition, inhibited activation of peroxidation, decreased phospholipase activity, prevented a decrease of Ca²⁺ ATPase and Ca²⁺ binding and uptake by sarcoplasmic reticulum, and increased sarcolemmal Na⁺, K⁺-ATPase, sarcoplasmic reticulum creatine phosphokinase.

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Effect of α-tocopherol on hypoxic-perfused and reoxygenated rabbit heart muscle

Cited by 99 publications

References 26 publications

Calcium antagonists: definition and mode of action

Calcium antagonists: definition and mode of action

Surface layer ATP-related contraction in isolated,superfused canine ventricular papillary muscle: An isotachophoretic analysis.

Antioxidants as Antiarrhythmic Drugs

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