1968
DOI: 10.1016/s0368-1319(68)80044-4
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Inhibitors of the plasminogen-activation in patients with primary “Carbohydrate-induced” hypertriglyceridemia

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1969
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Cited by 9 publications
(5 citation statements)
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“…These findings are consistent with the previous studies in Chinese adults [25, 26] and other ethnic populations [2729]. TG increase may promote hypertension by the development of atherosclerotic changes in blood vessels [30]. Moreover, the pre-3-lipoprotein fraction rich in endogenous triglycerides inhibits the plasminogen activator secretion in the blood vessel wall and its deficiency may cause inhibition of fibrinolysis.…”
Section: Discussionsupporting
confidence: 92%
See 1 more Smart Citation
“…These findings are consistent with the previous studies in Chinese adults [25, 26] and other ethnic populations [2729]. TG increase may promote hypertension by the development of atherosclerotic changes in blood vessels [30]. Moreover, the pre-3-lipoprotein fraction rich in endogenous triglycerides inhibits the plasminogen activator secretion in the blood vessel wall and its deficiency may cause inhibition of fibrinolysis.…”
Section: Discussionsupporting
confidence: 92%
“…Moreover, the pre-3-lipoprotein fraction rich in endogenous triglycerides inhibits the plasminogen activator secretion in the blood vessel wall and its deficiency may cause inhibition of fibrinolysis. The fibrinolysis inhibition also can promote hypertension by the development of atherosclerotic changes in blood vessels [30]. Hyperglycemia can alter intracellular signaling pathway leading to endothelial dysfunction, which was associated with increased blood pressure [31, 32].…”
Section: Discussionmentioning
confidence: 99%
“…It is known that the pre-3-lipoprotein fraction rich in endogenous triglycerides inhibits the plasminogen activator secretion in the blood vessel wall and its deficiency may cause inhibition of fibrinolysis (Spottl et al, 1968). Both triglyceride increase and fibrinolysis inhibition may promote the development of atherosclerotic changes in blood vessels.…”
Section: Discussionmentioning
confidence: 99%
“…[24,28,31]. In previous papers concerning the fibrinolytic system in patients with PCH we have reported on an increase of fibrinogen, proactivator-plasminogen, slow-reacting antiplasmin and in the in hibitors of plasminogen activation by urokinase, whereas PA activity was found to be decreased [28,29,30], The inhibition of PA release from the vessel wall is supposed by H ow ell [18] to be one of the points, where the plasminogen activation sequence is blocked by lipids. The purpose of the present study was to investigate the PA release following venous occlusion in patients with PCH.…”
Section: Enhancement Of the Fibrinolytic Activity By Venous Occlusionmentioning
confidence: 90%
“…The PA released by venous occlusion was found to be inversely correlated with the triglyceride and phospholipid level, indicating that these lipids inter fere with the stasis induced activator or its release from the vessel wall. This finding was surprising, since we had evidence that triglycerides or chylomicrons do not inhibit the direct plasminogen activation by urokinase, whether in PCH [30], nor in alimentary hypertriglyceri demia [5,26], nor after infusion of a triglyceride emulsion [10], nor after in vitro addition1. These findings can be explained by means of 2 theories:…”
Section: Prc-occlusion Activator Level : Normal Persons (N-24)mentioning
confidence: 95%