Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Kawaguchi, Hideaki; Yasuda, Hisakazu

doi:10.1161/01.res.62.6.1175

Cited by 28 publications

(8 citation statements)

References 34 publications

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“…One explanation could be the activation of phospholipases by hypoxia, resulting in an increased degradation of phospholipids (23,24). During the first 3 h of hypoxia more prostaglandin I 2 was released than in the following 21 h. Similar results were obtained by Palluy et al (25) and also by Farber et al (26), who suggest a transient activation of cyclooxygenase by hypoxia.…”

Section: Discussionsupporting

confidence: 77%

In Vitro Effects of Hypoxia and Reoxygenation on Human Umbilical Endothelial Cells

Windischbauer

Griesmacher²,

Müller³

1994

CCLM

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Summary:We investigated metabolic changes in human umbilical venous endothelial cells, when these were incubated under hypoxic followed by hyperoxic conditions, thus simulating hypoxia and reoxygenation..The human umbilical venous endothelial cells were incubated with a degassed buffer (oxygen content: 0-0.5%) for either 3 h or 24h, followed by a 60min incubation with oxygen-perfused buffer (oxygen content: 100%). Three hours of hypoxia led to a slight decrease in the ATP and creatine phosphate content (-16% ± 5%), while a pronounced decrease of high energy phosphates (-54% ± 4%) was observed after 24 h of hypoxia. Reoxygenating the cells after 3 h of hypoxia led to restoration of the content of high energy phosphates, while reoxygenation after 24 h resulted in a strong decrease (-66% ± 4%). The prostaglandin I 2 release during the first 3 h of hypoxia exceeded the release in the following 21 h. In all cases, reoxygenation increased the prostaglandin I 2 release. Under normoxic conditions the ratio between oxidised glutathione and reduced glutathione shifted from l : 100 to l : 4.5 after 3 h of hypoxia. The content of lipid peroxidation products was almost unaffected during hypoxia, whereas reoxygenation resulted in a pronounced increase (+ 380% ± 60%). The results of this in vitro study suggest that relatively long periods of hypoxia lead to a deficiency of high energy phosphates in the cell. Reoxygenation leads to the formation of oxygen-derived radicals, irrespectively of a prior hypoxia.

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Section: Discussionsupporting

confidence: 77%

In Vitro Effects of Hypoxia and Reoxygenation on Human Umbilical Endothelial Cells

Windischbauer

Griesmacher²,

Müller³

1994

CCLM

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“…In patients with acute myocardial infarction, elevation of the serum FFA level and increased catecholamine secretion have been reported [1]. We have also reported that FFA and PGI 2 are released by hypoxic perfused rat hearts [2] and have demonstrated that increased FFA and PGI2 are caused by enhanced phospholipase A 2 [3]. Kurien and Oliver first reported the existence of a relationship between high serum FFA concentrations and serious arrhythmias and/or death in patients with acute myocardial infarction [4].…”

Section: Introductionmentioning

confidence: 76%

Effect of palmitic acid and fatty acid binding protein on ventricular fibrillation threshold in the perfused rat heart

Makiguchi

Kawaguchi

Tamura

et al. 1991

Cardiovasc Drug Ther

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The effects of increased free fatty acid (FFA) levels on ventricular arrhythmias remain controversial. Using ventricular fibrillation threshold (VFT), we examined the relationship between FFA levels and ventricular arrhythmias. Isolated rat hearts were perfused with palmitate bound to either albumin or fatty acid binding protein (FABP) by Langendorf's method. The VFT was determined by electrical stimulation. Perfusion with 0.12 mM albumin alone, 0.12 mM palmitate bound to 0.12 mM albumin, and 0.36 mM palmitate bound to 0.12 mM albumin did not lower the VFT significantly. However, 0.60 mM palmitate bound to 0.12 mM albumin lowered VFT from 2.19 +/- 0.20 mA to 1.56 +/- 0.13 mA. The perfusion of 0.36 mM palmitate bound to 0.12 mM FABP lowered the VFT from 2.05 +/- to 0.19 mA to 1.47 +/- 0.23 mA, but 0.12 mM FABP alone did not affect the VFT. Perfusion with 0.36 mM palmitate bound to 0.12 mM FABP caused the VFT to fall more than perfusion with 0.36 mM palmitate bound to 0.12 mM albumin. Then the effects of verapamil perfusion or a low concentration of perfusate Ca2+ on VFT were examined. VFT was determined by electrical stimulation. Palmitate (0.6 mM) bound to 0.12 mM albumin lowered VFT. Verapamil 10(-7) M perfusion and a low concentration of Ca2+ (Ca2+ 1.67 mM) suppressed the FFA-induced fall of VFT. These results suggested that the arrhythmogenic action of FFA was related to Ca2+ overload in myocardial cells.

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“…PLA2 activity was increased in homogenates of small intestinal mucosal cells after ischemia and reperfusion (34). Kawaguchi and Yasuda (39) reported increases of mitochondrial and microsomal PLA2 activity in hypoxic myocardium. This PLA2 activity had a substrate specificity for PE, but the mechanism of activation was not clarified and the enzymatic activity was not further characterized.…”

Section: Introductionmentioning

confidence: 98%

Subcellular characteristics of phospholipase A2 activity in the rat kidney. Enhanced cytosolic, mitochondrial, and microsomal phospholipase A2 enzymatic activity after renal ischemia and reperfusion.

Nakamura¹,

Nemenoff²,

Gronich³

et al. 1991

J. Clin. Invest.

111

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Phospholipase A2 (PLA2) activities in cytosolic, mitochondrial, and microsomal fractions of rat kidneys were characterized under control conditions, after ischemia, and subsequent to ischemia and reperfusion. Two forms of PLA2 activity were present in the cytosolic fraction: a high molecular weight form, active against phosphatidyicholine (PC), and phosphatidylethanolamine (PE), which upon purification has a molecular mass of 110 kD', and a smaller form (M, 14 kD), active against PE.In mitochondrial and microsomal fractions a single form (Mr 14 kD), active against both PC and PE, was dominant. Activities in each fraction were optimal at pH 8.5-9.5. Cytosolic PLA2 activity was enhanced when Ca2' concentration (ICa2+I) was increased over the range of iO' to 106 M. Mitochondrial PLA2 activity required higher ICa2+I for activation (> 10' M).After 45 min of ischemia cytosolic PLA2 activity was decreased, whereas mitochondrial and microsomal activities were increased. When ischemia was followed by 1 h of reperfusion, cytosolic, mitochondrial, and microsomal activities were enhanced. Ischemia alone did not change the gel filtration chromatography patterns of PLA2 activity, but ischemia and reperfusion resulted in the appearance of a new peak of activity in cytosolic and mitochondrial fractions (M, 2-3 kD).Thus, the rat kidney has multiple forms of PLA2 activity, likely representing distinct enzymes, with Ca2+ dependencies suggesting regulation by Ca2+ in vivo. Ischemia and reperfusion result in stable increases of PLA2 activity in each subcellular fraction, perhaps related to covalent modifications of PLA2's, which likely account for membrane phospholipid degradation, and increased tissue levels of unsaturated free fatty acids. (J.

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Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Cited by 28 publications

References 34 publications

In Vitro Effects of Hypoxia and Reoxygenation on Human Umbilical Endothelial Cells

In Vitro Effects of Hypoxia and Reoxygenation on Human Umbilical Endothelial Cells

Effect of palmitic acid and fatty acid binding protein on ventricular fibrillation threshold in the perfused rat heart

Subcellular characteristics of phospholipase A2 activity in the rat kidney. Enhanced cytosolic, mitochondrial, and microsomal phospholipase A2 enzymatic activity after renal ischemia and reperfusion.

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