Arteriovenous shunt thrombosis

A method for the direct observation of extracorporal thrombus formation has been introduced by Rowntree and Shionoya (1927). These first studies could provide evidence that anticoagulants like heparin and hirudin do inhibit thrombus development in arteriovenous shunts. Since today, the A-V-shunt thrombosis models have been often used to evaluate the antithrombotic potential of new compounds in different species including rabbits (Knabb et al. 1992), rats (Hara et al. 1995), pigs (Scott et al. 1994), dogs and cats (Best et al. 1938), and non-human primates (Yokoyama et al. 1995). 

Rats are anaesthetized and fixed in supine position on a temperature-controlled heating plate to maintain body temperature. The left carotid artery and the right jugular vein are catheterized with short polyethylene catheters. The catheters are filled with isotonic saline solution and clamped. The two ends of the catheters are 

The measurement of the patency of the shunt is performed indirectly with a NiCrNi-thermocouple which is fixed distal to the glass capillary. If blood is flowing the temperature rises from room temperature to body temperature. In contrast, decreases of temperature indicates the formation of an occluding thrombus. The temperature is measured continuously over 30 min after opening of the shunt. 

It has been shown by Best et al. (1938) that the thrombi formed in the AV-shunt are to a greater part white arterial thrombi. This might be due to the high pressure and shear rate inside the shunts the thrombi tend to be more arterial in character (Chi et al. 1999). 

Best CH, Cowan C, MacLean DL (1938) Heparin and the formation of white thrombi. J Physiol 92 20-31 Chi L, Rebello S, Lucchesi BR (1999) In vivo models of thrombosis. In U Prichard ACG and Gallagher KP (eds) Anti-thrombotics. Springer-Verlag, Berlin Heidelberg, pp 101-127 

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Recombinant human erythropoietin (rHuEpo) may increase the risk of thrombosis (201). It has been reported that patients with carcinoma of the cervix who received chemotherapy and rHuEpo have an increased risk of symptomatic venous thrombosis (201). In clinical trials where the maintenance hematocrit was 3% on PROCRIT clotting of the arteriovenous shunts occurred at an annual rate of about 0.25 events per patient per year. However, other thrombotic conditions such as cerebrovascular events, transient ischemic attacks, myocardial infarction, or pulmonary embolism occurred at a rate of 0,04 events per patient per year (202). In a separate study of I, I I I untreated patients on hemodialysis, clotting of arteriovenous shunts occurred at a rate of 0.5 events per patient per year. In patients with chronic renal failure on hemodialysis who also had congestive heart failure, ischemic heart disease and venous thrombosis were increased in patients who were treated with PROCRIT targeted to a hematocrit level of 42 3% compared to those targeted to 30 3% (202). It has also been reported... 

Thrombosis of the cavernous sinus is characterized by proptosis, chemosis, impaired vision and ophthalmoplegia. If it is not septic, prognosis is good because of collateral drainage and spontaneous recanalization. The same symptoms, with the exception of a possible bruit, may result from arteriovenous shunting in carotid-cavernous fistulae. The treatment of choice in this case is endovascular occlusion (thrombosis ) of the cavernous sinus. 

Thrombolysis may also be considered for ocular thrombosis (urokinase) and for thrombosed arteriovenous shunts (streptokinase). 

Arteriovenous shunts, arterioportal fistula Portal vein thrombosis... 

Using an arteriovenous shunt model of thrombosis in the rat, compounds 4 and 7 were evaluated for their ability to maintain patency of the extracorporeal circuit which serves as a thrombogenic surface [76]. Table 2 shows that on a gravimetric basis r-hirudin and inhibitor 4, were equipotent [r-hirudin EDis = 1.4 mg/kg 4 EDi5= 1.2 mg/kg i.v. bolus]. The thrombin inhibitor 7 was less effective in this assay having an EDi5= 6.3 mg/kg. 

Fast and/or turbulent arterial flow within the sinus due to existing DAVM may result in intimal injury, secondary hyperplasia, and sinus stenosis or occlusion. In some cases the two mechanisms may be involved simultaneously. In a case reported by Wakamoto et al (1999), angiographically proven sinus thrombosis resulted in venous infarction without an arteriovenous shunt. A DAVM developed 4 months later (presumably as a result of sinus thrombosis), at which time the sinus has already recanalized. The DAVM persisted and resulted in rethromhosis of the sinus within another year (Wakamoto et al. 1999). 

The events that ensue freezing and nonfreezing cold injury are similar and include (1) arterial and arteriolar vasoconstriction, (2) excessive venular and capillary vasodilatation, (3) increased endothelial leakage, (4) erythrostasis, (5) arteriovenous shunting, (6) segmental vascular necrosis, and (7) massive thrombosis (Heller Page and Shear 1993). 

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