The inhibition of Na+ and K+ stimulated ATPase activity of rabbit and dog heart sarcolemma by lysophosphatidyl choline

Karli, J; Karikas, George A.; Hatzipavlou, P.K.; Levis, Gabriel M.; Moulopoulos, Spyridon

doi:10.1016/0024-3205(79)90238-8

Cited by 83 publications

(18 citation statements)

References 18 publications

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“…A similar in hibitory effect has been reported with lyso phosphatidylcholine (LPC) from dog and rabbit heart sarcolemma (41,42). It has been shown that several lysophospholipids have some detergent-like properties.…”

Section: Discussionsupporting

confidence: 69%

Inhibition of synaptosomal (Na++K+)-ATPase activity by lysophosphatidic acid: Its possible role in membrane depolarization.

et al. 1988

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Section: Discussionsupporting

confidence: 69%

Inhibition of synaptosomal (Na++K+)-ATPase activity by lysophosphatidic acid: Its possible role in membrane depolarization.

et al. 1988

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“…The slow inward current carried by calcium appears to be reduced in magnitude by LPC (12) although intracellular calcium appears to increase with an associated increase in contractility (12,37). This effect of LPC may be secondary to inhibition of sarcolemmal Na+-K+ ATPase (38,39) with accumulation of intracellular sodium and enhanced Na'-Ca2' exchange. Thus, the electrophysiologic effects of LPC delivered from the extracellular compartment appear to be secondary to a reduction in the membrane conductances to Na+, K+, and Ca2+.…”

Section: Methodsmentioning

confidence: 99%

Electrophysiologic effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs.

Akita

Creer²,

Yamada

et al. 1986

J. Clin. Invest.

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Lysophosphatidylcholine (LPC) accumulates in ischemic tissue, and exogenous LPC (20-100 MM) induces electrophysiologic alterations in vitro. However, to determine whether compartmentalization is critical, intracellular pressure microinjection of LPC was performed with simultaneous recording of the transmembrane action potential. Intracellular LPC in concentrations as high as 500 AM (n = 18), calculated based on calibration of injectate volume and cellular volume, did not induce electrophysiologic alterations. The concentrations and efflux of phospholipids and lysophospholipids were assessed in lymph obtained from the supracardiac lymph vessel in anesthetized dogs to assess the extent of extracellular accumulation. Prior to ischemia, phosphatidylcholine (PC) was the major phospholipid in lymph (79±2%) with substantial quantities of sphingomyelin (11±2%) and LPC (6±1%). With ischemia, the concentration of LPC increased by 18%, and net efflux of LPC increased by 24% (P < 0.01) with no net efflux of PC or other assayed phospholipids. The calculated concentration of LPC increased from 84 to 197 MM in lymph within the ischemic region, a concentration sufficient to induce electrophysiologic derangements.

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“…Accumulation of intracellular calcium can lead to the activation of phospholipase A 2 (13) and phosphatidyl choline. This lysophosphoglyceride has detergent properties and can alter electrophysiological properties and induce arrhythmias (5), contracture (3), delayed afterdepolarizations (39), and inhibit Na-K APTase activity (15). Elevation of calcium levels can also result in an increase in intracellular oxygen free radicals and mitochondrial damage (28) and impair sarcoplasmic reticulum Ca 2ϩ transport (43) and abnormal contractile function after recovery from ischemia (41).…”

mentioning

confidence: 99%

Cardioprotection by HO-4038, a novel verapamil derivative, targeted against ischemia and reperfusion-mediated acute myocardial infarction

Mohan¹,

Khan²,

Wisel³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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protection by HO-4038, a novel verapamil derivative, targeted against ischemia and reperfusion-mediated acute myocardial infarction. Am J Physiol Heart Circ Physiol 296: H140 -H151, 2009. First published October 31, 2008 doi:10.1152/ajpheart.00687.2008.-Many cardiac interventional procedures, such as coronary angioplasty, stenting, and thrombolysis, attempt to reintroduce blood flow (reperfusion) to an ischemic region of myocardium. However, the reperfusion is accompanied by a complex cascade of cellular and molecular events resulting in oxidative damage, termed myocardial ischemia-reperfusion (I/R) injury. In this study, we evaluated the ability of HO-4038, an N-hydroxypiperidine derivative of verapamil, on the modulation of myocardial tissue oxygenation (PO2), I/R injury, and key signaling molecules involved in cardioprotection in an in vivo rat model of acute myocardial infarction (MI). MI was created in rats by ligating the left anterior descending coronary artery (LAD) for 30 min followed by 24 h of reperfusion. Verapamil or HO-4038 was infused through the jugular vein 10 min before the induction of ischemia. Myocardial PO 2 and the free-radical scavenging ability of HO-4038 were measured using electron paramagnetic resonance spectroscopy. HO-4038 showed a significantly better scavenging ability of reactive oxygen radicals compared with verapamil. The cardiac contractile functions in the I/R hearts were significantly higher recovery in HO-4038 compared with the verapamil group. A significant decrease in the plasma levels of creatine kinase and lactate dehydrogenase was observed in the HO-4038 group compared with the verapamil or untreated I/R groups. The left ventricular infarct size was significantly less in the HO-4038 (23 Ϯ 2%) compared with the untreated I/R (36 Ϯ 4%) group. HO-4038 significantly attenuated the hyperoxygenation (36 Ϯ 1 mmHg) during reperfusion compared with the untreated

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The inhibition of Na+ and K+ stimulated ATPase activity of rabbit and dog heart sarcolemma by lysophosphatidyl choline

Cited by 83 publications

References 18 publications

Inhibition of synaptosomal (Na++K+)-ATPase activity by lysophosphatidic acid: Its possible role in membrane depolarization.

Inhibition of synaptosomal (Na++K+)-ATPase activity by lysophosphatidic acid: Its possible role in membrane depolarization.

Electrophysiologic effects of intracellular lysophosphoglycerides and their accumulation in cardiac lymph with myocardial ischemia in dogs.

Cardioprotection by HO-4038, a novel verapamil derivative, targeted against ischemia and reperfusion-mediated acute myocardial infarction

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