1980
DOI: 10.1016/0049-3848(80)90263-7
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The effect of hirudin on endotoxin induced disseminated intravascular coagulation (DIC)

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1986
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Cited by 28 publications
(20 citation statements)
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“…* P < 0·05, ** P < 0·01 and ***P < 0·001 as compared to the LPS group; ‡ P < 0·05, ‡ ‡ P < 0·01 as compared to the r-hirudin þ t-PA group. r-Hirudin given alone, in agreement with previous reports (Ishikawa et al, 1980;Hoffmann et al, 1990;Hermida et al, 1998), reduced the consumption of platelets, fibrinogen, AT III and protein C but also attenuated the increase of PAI-1 at 2 h, which could be due to a lower stimulation of its thrombin-mediated release from the endothelium (Gelerther & Sznycer-Laszuk, 1986;Bevilacqua et al, 1986;Van Hinsberg et al, 1988). PAI-1 was not reduced at 6 h which was probably due to the action of tumour necrosis factor-a (TNF-a) which would induce a retarded, sustained PAI-1 increase, although some controversy about the relationship between TNF-a and PAI-1 exists (Emeis et al, 1995).…”
Section: Discussionsupporting
confidence: 93%
“…* P < 0·05, ** P < 0·01 and ***P < 0·001 as compared to the LPS group; ‡ P < 0·05, ‡ ‡ P < 0·01 as compared to the r-hirudin þ t-PA group. r-Hirudin given alone, in agreement with previous reports (Ishikawa et al, 1980;Hoffmann et al, 1990;Hermida et al, 1998), reduced the consumption of platelets, fibrinogen, AT III and protein C but also attenuated the increase of PAI-1 at 2 h, which could be due to a lower stimulation of its thrombin-mediated release from the endothelium (Gelerther & Sznycer-Laszuk, 1986;Bevilacqua et al, 1986;Van Hinsberg et al, 1988). PAI-1 was not reduced at 6 h which was probably due to the action of tumour necrosis factor-a (TNF-a) which would induce a retarded, sustained PAI-1 increase, although some controversy about the relationship between TNF-a and PAI-1 exists (Emeis et al, 1995).…”
Section: Discussionsupporting
confidence: 93%
“…These results are in accord with those in previous studies showing that r-hirudin can decrease the consumption of platelets, fibrhaogen, and ATIII, as well as diminishing increases in fibrin monomers, thrombin-antithrombin complexes, fibrinogen-fibrin degradation products, and fibrin deposition in different animal models of endotoxininduced DIC. [22][23][24] Furthermore, a prior study with rabbits infused with gram-negative bacteria showed that mortality in animals treated with r-hirudin and antibiotic was lower than in animals treated with heparin and antibiotic. 25 The improvement in protein C concentration with r-hirudin treatment was remarkable among the changes observed in coagulation parameters.…”
Section: Discussionmentioning
confidence: 99%
“…17-2° However, human and animal studies have shown that r-hirudin may be useful in the treatment of venous and arterial thrombosis, 21 and experimental models suggest that it may be an attractive agent for treating endotoxin-induced DIC. [22][23][24][25][26] The goal of the present study was to evaluate the effect of different doses of r-hirudin on mortality and kidney fibrin deposition in a rabbit model of endotoxin-induced DIC. As a secondary endpoint, we analyzed the changes in several coagulation-related and fibrinolytic parameters.…”
mentioning
confidence: 99%
“…The antithrombitic action of hirudin is dependent on its blood levels. The efficacy of hirudin in preventing venous and arterial thrombosis and disseminated intravascular coagulation (DIC) has been demonstrated in various animal models (12,40,45,55,67,83,89,103,139).…”
Section: Pharmacologymentioning
confidence: 99%