Anticoagulant Properties of Rabbit Lungs in Tissue Thromboplastin-induced Intravascular Coagulation

Vad, Henrik; Tvedskov, Tove F; Hansen, Knud Bendix; Albrechtsen, Ole K.; Jespersen, Jørgen; Gram, Jørgen Brodersen

doi:10.1055/s-0038-1656033

Cited by 3 publications

(4 citation statements)

References 17 publications

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“…In our DIC model, induced by bolus injection of bovine lung thromboplastin, the 4‐h test showed that both DHPC and warfarin significantly inhibited a prolonged PT and APTT, increased fibrinogen levels, decreased FDP and increased platelet count. These findings are consistent with other animal models of DIC studies (Imanishi et al , 1991; Yamazaki et al , 1994; Vad et al , 1997). Gitel and Wessler (1979) reported that warfarin decreased FVII, which inhibited FXa generation, within 6 h in thromboplastin‐induced DIC rats.…”

Section: Discussionsupporting

confidence: 93%

“…The combination of a prolonged PT and APTT, low platelet count, decreased fibrinogen and increased FDPs appears to be an adequate indicator of DIC (Baglin, 1996; Vad et al , 1997; Bick, 1998; Levi & Ten Cate, 1999). The PT and APTT are measures of thrombin formation, fibrinogen indicates the efficiency of the fibrinolytic system and the presence of FDP indicates fibrin polymerisation.…”

Section: Discussionmentioning

confidence: 99%

“…The PT and APTT are measures of thrombin formation, fibrinogen indicates the efficiency of the fibrinolytic system and the presence of FDP indicates fibrin polymerisation. These parameters have been investigated in several experimental DIC studies (Wada et al , 1984; Yamazaki et al , 1994; Vad et al , 1997; Tanabe et al , 1999). It is true that certain other parameters commonly used to diagnose DIC, e.g.…”

Section: Discussionmentioning

confidence: 99%

“…It may also cause bleeding as a result of both the consumption of platelets and coagulation factors and the anticoagulant effect of secondary fibrinolytic products (Selighsohn, 2001). DIC‐like symptoms are usually induced in experimental animals by intravenous infusion of endotoxin (Uchiba et al , 1997), carrageenan (Wada et al , 1984) or thromboplastin (Vad et al , 1997).…”

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confidence: 99%

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6,7‐Dihydroxy‐3‐phenylcoumarin inhibits thromboplastin induced disseminated intravascular coagulation

et al. 2004

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Summary 6,7‐Dihydroxy‐3‐phenylcoumarin (DHPC) was tested to determine whether it had any effect on vitamin K inhibition, by investigating the prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen level and platelet count. The anticoagulant and antithrombotic effects of DHPC were compared with those of warfarin by conducting a 4 h acute trial on thromboplastin‐induced disseminated intravascular coagulation (DIC), investigating various haemostatic and antioxidant system parameters and performing a haemogram. Of most significance was that in the 5‐d DHPC trial on healthy controls, PT, APTT, fibrinogen, platelet count remained within normal levels. In the 4‐h DIC trial, both DHPC (0·025 mg/kg, i.v.) and warfarin (0·25 mg/kg, i.v.) significantly inhibited DIC, by reducing the PT, APTT, and fibrin degradation products and increasing fibrinogen levels and platelet count. In the DIC drug groups, lipid peroxidation significantly increased only in the warfarin group and glutathione significantly increased only in the DHPC group. However leucocyte count was significantly higher in the DHPC than the warfarin group. Further investigation is required for why DHPC is effective on the parameters investigated, at doses one‐tenth of those of warfarin.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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6,7‐Dihydroxy‐3‐phenylcoumarin inhibits thromboplastin induced disseminated intravascular coagulation

et al. 2004

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Activation of blood coagulation in pigs following lower limb gunshot trauma

Münster

Jensen²,

Bech³

et al. 2001

Blood Coagulation and Fibrinolysis

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A standardized, quantifiable gunshot trauma to one hind leg of fourteen anaesthetized and sedated pigs was used to investigate the extent to which an isolated gunshot trauma causes activation of blood coagulation. The traumatized pigs were mechanically ventilated in intensive care for 48 h before they were euthanized. Blood samples were drawn at baseline (t = 0), 24, 27 and 48 h after trauma to examine the late effects on haemostasis. The median energy absorption in the pigs was 27.57 (22.6-31.7) J/kg. This gunshot injury caused increased creatine kinase and body temperature and led to a combined metabolic and respiratory alkalosis; the pigs remained circulatory stable. Within the haemostatic system the trauma caused increased activated partial thromboplastin time at 48 h (P < 0.05), prothrombin time at 24 and 27 h (P < 0.05), fibrinogen and soluble fibrin concentration at 48 h (P < 0.05), and 24 h (P < 0.05), respectively. The platelet count, protein C activity, tissue factor concentration and trombin-antithrombin concentration decreased throughout the experiment (P < 0.05); the changes of antithrombin activity did not reach statistical significance. In conclusion, this study in pigs demonstrates that a standardized gunshot trauma to a hind leg activates blood coagulation without signs of organ failure or disseminated intravascular coagulation within 48 h.

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Protein C Activation during the Initial Phase of Experimental Acute Pancreatitis in the Rabbit

et al. 1999

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Background: Disturbances of coagulation and fibrinolysis are well-known systemic effects of acute necrotising pancreatitis (ANP). The purpose of this experimental study was to evaluate the initial events in the haemostatic activation during ANP in an animal model with relevance to the human situation. Methods: ANP was introduced in 7 rabbits by infusion of chenodeoxycholic acid in the pancreatic duct. Seven rabbits served as sham-operated controls. Serial measurements of coagulation variables (prothrombin time, activated partial thromboplastin time, FVII activity, fibrinogen, tissue factor activity), anticoagulant proteins (protein C, antithrombin) and fibrinolytic factors (tissue plasminogen activator, plasminogen activator inhibitor-1) were performed for 5 h. Results: ANP was confirmed by elevated serum amylase, development of ascites, and histological changes of the pancreas. A moderate activation of the coagulation system was found in both study groups. A significant decrease in protein C concentration from 1 h after the induction of ANP was found, whereas the response of antithrombin and the inhibition of the fibrinolytic system were similar in the 2 study groups. Microthrombosis of the lungs or kidneys was found in 2 rabbits with ANP. Conclusion: An immediate activation of protein C is a specific characteristic of the haemostatic activation in ANP in rabbits. This activation has not been described previously and the possible therapeutic implications ought to be studied.

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Anticoagulant Properties of Rabbit Lungs in Tissue Thromboplastin-induced Intravascular Coagulation

Cited by 3 publications

References 17 publications

6,7‐Dihydroxy‐3‐phenylcoumarin inhibits thromboplastin induced disseminated intravascular coagulation

6,7‐Dihydroxy‐3‐phenylcoumarin inhibits thromboplastin induced disseminated intravascular coagulation

Activation of blood coagulation in pigs following lower limb gunshot trauma

Protein C Activation during the Initial Phase of Experimental Acute Pancreatitis in the Rabbit

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