Serum prostacyclin binding defects in thrombotic thrombocytopenic purpura.

Wu, Kenneth K.; Hall, Elizabeth R.; Rossi, Ennio C.; Papp, Audrey C.

doi:10.1172/jci111670

Cited by 77 publications

(13 citation statements)

References 20 publications

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“…This the addition of HDL, the half-life was prolonged from 4.8 min (o) to 22.3 min (.). Albumin has been reported to bind PGI2 and to prolong PGI2 activity (3)(4)(5)(6)(7). Indeed, the PSF activity was found in human albumin (Cohn fraction V albumin, Sigma).…”

Section: Resultsmentioning

confidence: 99%

“…However, it binds to PSF resulting in a more stable substance. Recently, decreased PSF activity has been reported in thrombotic disorders (acute myocardial infarction (2), thrombotic thrombocytopenic purpura (3) and ischemic stroke) (4) and PSF is suspected to play an important role in the pathogenesis of the thrombus formation in these diseases. Albumin has been considered as a candidate for the stabilizing factor (5-7).…”

Section: Introductionmentioning

confidence: 99%

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Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Yui¹,

Aoyama²,

Morishita³

et al. 1988

J. Clin. Invest.

189

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Yui¹,

Aoyama²,

Morishita³

et al. 1988

J. Clin. Invest.

189

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“…21 The crossreactivity rate for anti-6kPGF la was <7.7%, with a sensitivity of 15 pg/200 ^1 (B/B 0 =80%). 22 Data were calculated and are presented as mean ± standard errors of the mean (SEM) picograms of metabolite per milligram of brain protein and underwent two-way analysis of variance (ANOVA), treating metabolite concentration as a repeated measure to identify significant interactions between subgroups and metabolite levels. A separate two-way ANOVA comparing metabolite concentrations in Subgroups A3 and A4 showed no significant differences, permitting values from the two subgroups to be combined for all other statistical analyses.…”

Section: Methodsmentioning

confidence: 99%

Effect of thromboxane synthase inhibition on eicosanoid levels and blood flow in ischemic rat brain.

Pettigrew

Grotta

Rhoades

et al. 1989

Stroke

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Reperfusion of ischemic brain is associated with production of thromboxane A 2 (TXAJ, a proaggregatory vasoconstrictor. We used an animal model of transient forebrain ischemia to study the effects of 1-benzylimidazole (1-BI), a selective inhibitor of thromboxane synthase, upon cerebral eicosanoid levels and cerebral blood flow. Male Wistar rats were subjected to 30 minutes of four-vessel occlusion. The mean±SEM brain level of TXB 2 , the stable metabolite of TXA 2 , determined after 60 minutes of reperfusion was 101 ±20 pg/mg brain protein in five ischemic control rats. Infusion of 10 figlg 1-BI reduced mean±SEM cerebral TXB 2 concentration to 11±3 pg/mg brain protein in five rats (p^0.002). Mean±SEM hemispheric cerebral blood flow measured in four ischemic control rats after 60 minutes of reperfusion was 42 ±9 ml/ 100 g brain/min compared with 104±13 ml/100 g brain/min in three 1-BI-treated rats (p:£0.001). Mean±SEM hippocampal blood flow in four ischemic control rats after 60 minutes of reperfusion was 51±14 ml/100 g brain/min compared with 125±25 ml/100 g brain/min in three 1-BI-treated rats (p^O.04). We conclude that selective inhibition of thromboxane synthase may alleviate ischemic brain damage by reducing cerebral TXA 2 concentrations and elevating cerebral blood flow. (Stroke 1989;20:627-632) T hromboxane A 2 (TXA2), an enzymic product of arachidonic acid (AA), has been implicated in causing platelet aggregation and vasoconstriction leading to the reduction of microcirculatory blood flow in various organ systems. The synthesis and release of TXA 2 from activated platelets may promote secondary aggregation by interacting with TXA 2 /prostaglandin H 2 (PGHJ receptors on platelet membranes. 12 The vasoconstrictive properties of TXA 2 have been demonstrated in bioassay experiments showing contraction of vascular smooth muscle and reduction of renal and coronary blood flow. 34Cerebral ischemia causes a massive release of AA, stearic acid, and other free fatty acids cleaved by phospholipases from phospholipid membranes in damaged cells.5 - 8 The release of AA is considered to be the rate-limiting step in eicosanoid metabolism within ischemic brain. The cyclooxygenase and peroxidase Received June 6, 1988; accepted November 23, 1988. activities of prostaglandin endoperoxide synthase convert AA to the proaggregatory endoperoxide PGH 2 . Thromboxane synthase (TX synthase) in activated platelets converts PGH 2 to TXA 2 , thereby promoting secondary platelet aggregation, arterial thrombosis, and vasoconstriction in brain subjected to ischemia or subarachnoid hemorrhage. 9 - 11Selective inhibition of TX synthase during early reperfusion of ischemic brain may augment recovery of microcirculatory blood flow. We tested this hypothesis by studying the effects of 1-benzylimidazole (1-BI), a selective inhibitor of TX synthase, 12 in an animal model of transient forebrain ischemia. Materials and MethodsWe divided 33 male Wistar rats into two groups for the determination of eicosanoid levels in brain (n=20, Group A) and m...

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“…Plasma of patients with TTP depresses the synthesis of PGI, in the vessel wall (28) and PGI, is degraded more rapidly in TTP plasma (29). Furthermore, it has been found that PGI, serum binding capacity is reduced during the acute phase of TTP and returns to normal after disease recovery (30). A recent study showed that in vivo PGI, synthesis is also reduced in children with HUS, as indicated by lower than normal urinary excretion of renal PG12 metabolites in the acute phase of the disease that normalizes in remission (31).…”

Section: Endothelial Cell Injurymentioning

confidence: 99%

The pathophysiology and management of thrombotic thrombocytopenic purpura

Ruggenenti

Remuzzi

1996

European J of Haematology

111

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Serum prostacyclin binding defects in thrombotic thrombocytopenic purpura.

Abstract: To understand the pathophysiologic significance of abnormal serum prostacyclin (PGI2) binding activities in thrombotic thrombocytopenic purpura (TTP), we

Cited by 77 publications

References 20 publications

Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Serum prostacyclin stabilizing factor is identical to apolipoprotein A-I (Apo A-I). A novel function of Apo A-I.

Effect of thromboxane synthase inhibition on eicosanoid levels and blood flow in ischemic rat brain.

The pathophysiology and management of thrombotic thrombocytopenic purpura

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