Accumulation of lysophosphoglycerides with arrhythmogenic properties in ischemic myocardium.

Sobel, Burton E.; Corr, Peter B.; Robison, Alice K.; Goldstein, Richard A.; Witkowski, Francis X.; Klein, Milton S.

doi:10.1172/jci109159

Cited by 292 publications

(86 citation statements)

References 17 publications

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“…More recently there has been interest that the lysophospholipids, lvsophosphatyl choline (LPC) and lysophosphatyl ethanolamine (LPE) might be these unidentified factors (43,44 Because the mechanisms of the "instantaneous" and "delayed"…”

Section: Early Phase Arrhythmiasmentioning

confidence: 99%

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

Murdock¹,

Loeb²,

Euler³

et al. 1980

Circulation

110

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Section: Early Phase Arrhythmiasmentioning

confidence: 99%

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

Murdock¹,

Loeb²,

Euler³

et al. 1980

Circulation

110

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“…33,34 Lyso-PAF, the precursor of PAF, can increase by as much as 50% within 20 minutes of myocardial ischemia. 35 Developing collateral vessels may have even greater potential to produce PAF because the monocytes, neutrophils, and platelets adherent to the collateral endothelial surfaces are capable of producing PAF.…”

Section: Discussionmentioning

confidence: 99%

Effect of Platelet Activation on Coronary Collateral Blood Flow

Kinn

Bache

1998

Circulation

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Background-The platelet products thromboxane A 2 and serotonin have been shown to cause constriction of welldeveloped coronary collateral vessels. This study was performed to determine whether intravascular platelet activation produced with platelet activating factor (PAF) can cause a decrease in coronary collateral blood flow. Methods and Results-Collateral vessel growth was induced by embolization of a hollow stainless steel plug into the left anterior descending coronary artery (LAD) of adult dogs. The animals were returned to the laboratory 3 to 6 weeks later for surgical instrumentation and measurement of collateral blood flow. Collateral flow was assessed by measuring retrograde blood flow from the cannulated collateral-dependent artery. PAF (10 nmol) was injected into the left main coronary artery to allow products of platelet activation to reach collateral vessels arising from the left coronary system. PAF caused a vasoconstrictor response, which became maximal 3 minutes after injection and resulted in a 40.3Ϯ7.4% decrease in retrograde blood flow (32.1Ϯ2.1 to 19.6Ϯ3.2 mL/min; PϽ0.05). By 15 minutes after the PAF injection, both retrograde blood flow and transcollateral resistance had returned to normal. After pretreatment with the thromboxane A 2 receptor antagonist SQ30,741, the vasoconstrictor response to PAF was abolished and, in contrast to the decrease in retrograde blood flow from PAF alone, a weak vasodilator effect was unmasked. Conclusions-PAF caused a decrease in coronary collateral blood flow. This vasoconstrictor response required the participation of thromboxane A 2 .

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“…The present stud;r demonstrates that the decreased intracellular phospholipids under anoxic conditions was not accompanied by an increase in the corresponding lysophospholipids, and thus cannot bL attributed to phospholipase Al activity. Phospholipase Al was ruled out by other investigators [8,10], however, the mechanism of phospholipid degradation under anoxic conditions remained unresolved.…”

Section: Discussionmentioning

confidence: 99%

Anoxic injury accelerates phosphatidylcholine degradation in cultured cardiac myocytes by phospholipase C

Nachas¹,

Pinson²

1992

FEBS Letters

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ln neonatal cultured cardiac myosytes under normoxic conditions, 3zP, incorporation pattern into various phospholipids. and double-labeling experiments with 32Pi and ['Hlmethyl choline, suggest that phosphatidylcholine and phosphaLidylinosifo1 are turned over rapidly, whereas the turnover of phosphatidylethanolamine is probably much slower. While increased levels of the corresponding lysophospbolipids were not found under anoxia, release of diacylgycerol and phosphorylcholine was observed. That data strongly suggest that phospholipase C. and not phospholipase A?, is involved in phospholipid degradation in cultured cardiomyocytes under anoric conditions.

show abstract

Accumulation of lysophosphoglycerides with arrhythmogenic properties in ischemic myocardium.

Cited by 292 publications

References 17 publications

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

Electrophysiology of coronary reperfusion. A mechanism for reperfusion arrhythmias.

Effect of Platelet Activation on Coronary Collateral Blood Flow

Anoxic injury accelerates phosphatidylcholine degradation in cultured cardiac myocytes by phospholipase C

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