Disturbance of Ca++-transport function and lipid component of sarcoplasmic reticulum membranes during total ischemia of the rat myocardium

Brovkovich, V. M.; Nikitchenko, Yu. V.; Lemeshko, Victor V.

doi:10.1007/bf00845069

Cited by 2 publications

(1 citation statement)

References 4 publications

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“…LPC also activated a nonselective leak channel via its detergent action (11). LPC has been reported to suppress function of various iontransport proteins, including the Na+-K+ pump (8) and Na+-Ca2+ exchanger (9), and to depress Ca2+ uptake by the sarcoplasmic reticulum (27,28). Although several of the processes affected by LPC are important in K+ regulation, to our knowledge this is the first study to characterize directly the effects of LPC on cellular K+ balance in the heart.…”

Section: Discussionmentioning

confidence: 96%

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

Goldhaber

Deutsch

Alexander

et al. 1998

J Cardiovasc Pharmacol Ther

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BACKGROUND: Lysophospholipids such as lysophosphatidylcholine (LPC) have many direct electrophysiological effects on cardiac muscle and have been implicated as a cause of lethal ventricular arrhythmias during acute myocardial ischemia. Because extracellular K(+) accumulation is also a key arrhythmogenic factor during acute ischemia, we examined the effects of LPC on cellular K(+) balance, including its interaction with adenosine triphosphate-sensitive K(+) (K(ATP)) channels. METHODS AND RESULTS: Isolated rabbit interventricular septa paced at 75 beats/min were loaded with (42)K(+) to measure unidirectional K(+) efflux rate (in (42)K(+) washout experiments) or tissue K(+) content ((42)K(+) uptake experiments) and action potential duration (APD) during exposure to 20 µM LPC for 30 minutes. LPC caused tissue K(+) content to decrease by 15 +/- 2% (n = 4) at a steady rate over 30 minutes, associated with gradual APD shortening and a delayed increase in unidirectional K(+) efflux rate. Pretreatment with 12 µM cromakalim to selectively activate K(ATP) channels shortened APD by 44 +/- 66% and had no effect on net tissue K(+) content during control aerobic perfusion. However, cromakalim increased net K(+) loss during exposure to LPC to 22 +/- 4%, a 47% increase. CONCLUSIONS: LPC induced net K(+) loss in heart, which was potentiated by the K(ATP) channel agonist cromakalim. This ATP finding suggests that if LPC accumulates to similar levels during myocardial ischemia and hypoxia, it may be an important mechanism in net K(+) loss.

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Section: Discussionmentioning

confidence: 96%

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

Goldhaber

Deutsch

Alexander

et al. 1998

J Cardiovasc Pharmacol Ther

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Free radicals and cell chemiluminescence

Vladimirov

Проскурнина

2009

Biochemistry Moscow

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Application of chemiluminescence (CL) for study of free-radical reactions in human and animal cells and tissues is considered in this review. Historically, the study of intrinsic (ultraweak) luminescence gave place to the measurement of CL in the presence of chemical activators (CL probes) and physical activators (sensitizers) of luminescence, which made the method much more sensitive and specific. The methods of CL and EPR are direct methods of radical investigation, though the advantage of the CL method consists in the fact that CL intensity is directly proportional to a steady-state concentration of the radicals responsible for luminescence (first of all, lipid and oxygen radicals) irrespective the activity of these radicals. The mechanisms of CL reactions in the absence of activators and in the presence of luminol and lucigenin are considered. Examples of various applications of the CL method in medical, biological, and clinical investigations are given including those for estimation of the phagocytic activity of cells, antioxidant activity, determination of toxicity, and other purposes.

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Disturbance of Ca++-transport function and lipid component of sarcoplasmic reticulum membranes during total ischemia of the rat myocardium

Cited by 2 publications

References 4 publications

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

Free radicals and cell chemiluminescence

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