Thromboxane B<sub>2</sub> biosynthesis and phospholipids hydrolysis in platelets from hypercholesterolemic rabbits

Kawaguchi, Hideaki; Ishibashi, Teruo; Imai, Yoh

doi:10.1007/bf02534919

Cited by 27 publications

(6 citation statements)

References 30 publications

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“…In particular, cholesterol:phospholipid ratio has been reported to be increased. 3,4,6,[11][12][13] Changes in platelet phospholipid fatty acid composition have also been reported in several studies. These, however, are not always in accordance because in some studies the experimental diets contained, in addition to cholesterol, saturated fat as coconut or peanut oil, which may influence per se this parameter.…”

Section: Studies In Experimental Animalsmentioning

confidence: 59%

Hypercholesterolemia and Platelets

Tremoli¹,

Colli²,

Maderna³

et al. 1993

Semin Thromb Hemost

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Section: Studies In Experimental Animalsmentioning

confidence: 59%

Hypercholesterolemia and Platelets

Tremoli¹,

Colli²,

Maderna³

et al. 1993

Semin Thromb Hemost

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“…27 Fatty acid methyl esters were prepared by a borontrifluoridemethanol reagent, according to previous methods 28 and analyzed by gas liquid chromatography with a column (0.3 X 200 cm) of 3% ethylene glycol succinate silicone-X on Chromosorb W (80-100 mesh) according to previous methods. 25 - 29 Myocardial lactate concentration was determined by the method of Gutmann and Wahlefeld. …”

Section: Other Methodsmentioning

confidence: 99%

Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Kawaguchi

Yasuda

1988

Circulation Research

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Phospholipid metabolism was studied in rat myocardial slices that were incubated under normoxia or hypoxia for up to 24 hours. Phospholipid degradation was prominent in hypoxic myocardium, particularly phosphatidylcholine, which markedly decreased after 24 hours of hypoxia. In contrast, lysophosphatidjlcholine increased. The mechanism of phospholipid degradation in hypoxic myocardium was studied. The highest activity for phospholipase A 2 among subcellular fractions was found in microsomal fraction. In hypoxic myocardium, this phospholipase A 2 activity markedly increased and had substrate specificity toward phosphatidylcholine and phosphatidylethanolamine. Phosphatidylcholine was slightly hydrolyzed in control myocardium, but it was markedly hydrolyzed in hypoxic myocardium. Phospholipase C activity was found in cytosol and had a high substrate specificity toward phosphatidylinositol. In hypoxic myocardium, its activity gradually decreased during hypoxic incubation. Prostacyclin biosynthesis was also determined. The synthesis of prostacyclin in hypoxic myocardial microsomes did not increase. These results suggest that hypoxia causes phospholipid degradation and activates phospholipase A 2 activity. {Circulation Research 1988;62:1175-1181) H igh levels of circulating free fatty acids have been observed in patients after myocardial infarction, 1 " 4 and elevated free fatty acid levels have been correlated with the appearance of ventricular arrhythmias.3 Many aspects of the changes associated with myocardial ischemia have been intensively studied.67 Abnormal lipid metabolism alters cardiac function by changing the cardiac cell membrane properties. These functional changes may contribute to decreased myocardial contractility, arrhythmia, and cell death that follow coronary artery occlusion.8 Despite early functional changes in membrane properties that are responsible for the electrophysiological manifestation of ischemia, little is known about myocardial phospholipid metabolism. The possibility that lysophospholipids contribute to ischemic heart damage was first suggested by Hajidu et al. Lysophospholipid accumulation is caused by decreased lysophospholipase a c t i v i t y " ; however, the extent of the lysophosphatide increase in the ischemic heart is a matter of controversy.Recently, we showed that free fatty acid and prostacyclin [prostaglandin (PG)I14 2 ] are released from isolated heart during hypoxia; phospholipid degradation in canine ischemic myocardium has been also reported by Chien et al. But the mechanisms of phospholipid degradation and fatty acid release remain unclear.This study was performed to determine the early and delayed effects of hypoxia on phospholipase activity and prostaglandin synthesis. We attempt to clarify the enzymatic mechanisms of phospholipid degradation Received December 12, 1986; accepted January 15, 1988. leading to free fatty acid and PGI 2 releases in hypoxic myocardium. Materials and Methods Experimental ProtocolExperiments were carried out on male Wistar rats (200-300 g)...

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“…Phospholipids in renal homogenates were separated by TLC, which was developed in chloroform/methanol/ acetic acid/water (50:30:8:4, vol/vol/vol/vol), then determined as described earlier. 22 Fatty acids in renal homogenates were determined by gas-liquid chromatography, as described earlier. 22 Triplicate samples were analyzed in all experiments.…”

Section: Other Methodsmentioning

confidence: 99%

“…22 Fatty acids in renal homogenates were determined by gas-liquid chromatography, as described earlier. 22 Triplicate samples were analyzed in all experiments. Student's / test was used to analyze the results.…”

Section: Other Methodsmentioning

confidence: 99%

Renal phospholipase C and diglyceride lipase activity in spontaneously hypertensive rats.

Kawaguchi¹,

Okamoto²,

Saitô³

et al. 1987

Hypertension

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SUMMARY Phospholipase C activity and diglyceride lipase activity were studied in the renal cortex and medulla of 10-and 40-week-old stroke-prone spontaneously hypertensive rats (SHRSP) and agematched normotensive Wistar-Kyoto rats (WKY). Enhanced phospholipase C activity was found in the cortical and medullary cytosol of kidney from SHRSP, and microsomal diglyceride lipase in SHRSP also increased. In SHRSP, phospholipase C and diglyceride lipase activities increased with age, but this increase was not evident in WKY. Phospholipase C had high substrate specificity for phosphatidylinositol in renal cytosol of both WKY and SHRSP. The increased activities were accompanied by prostaglandin E 2 synthesis in renal medullary microsomes of 10-week-old SHRSP and were also present in the kidney of 40-week-old SHRSP. Total phospholipid and arachidonic acid contents in kidney were markedly high in the medulla of 10-week-old SHRSP, but these lipids were decreased in 40-week-old SHRSP. These results suggest that phospholipids and arachidonic acid in SHRSP may be genetically high and that the activated phospholipase C and diglyceride lipase hydrolyze phospholipids, providing arachidonic acid for prostaglandin synthesis, which results in a decrease of phospholipids and arachidonic acid in the kidney of 40-week-old SHRSP. These studies demonstrate that a phosphatidylinositol-specific phospholipase C-prostaglandin synthetic system may play an important role in the course of hypertension in SHRSP. (Hypertension 10: 100-106, 1987) KEY WORDS • phospholipase C • phosphatidylinositol * prostaglandin E 2 * arachidonic acid • diglyceride lipase • phospholipids P ROSTAGLANDINS participate in blood pressure regulation in hypertensive states.

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Thromboxane B₂ biosynthesis and phospholipids hydrolysis in platelets from hypercholesterolemic rabbits

Cited by 27 publications

References 30 publications

Hypercholesterolemia and Platelets

Hypercholesterolemia and Platelets

Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Renal phospholipase C and diglyceride lipase activity in spontaneously hypertensive rats.

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Thromboxane B2 biosynthesis and phospholipids hydrolysis in platelets from hypercholesterolemic rabbits

Cited by 27 publications

References 30 publications

Hypercholesterolemia and Platelets

Hypercholesterolemia and Platelets

Prostacyclin biosynthesis and phospholipase activity in hypoxic rat myocardium.

Renal phospholipase C and diglyceride lipase activity in spontaneously hypertensive rats.

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Thromboxane B₂ biosynthesis and phospholipids hydrolysis in platelets from hypercholesterolemic rabbits