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Query: UMLS:C0012739 (disseminated intravascular coagulation)
 8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifteen patients with severe intermittent claudication were treated by therapeutic defibrination with subcutaneous injections of ancrod for 5 weeks. Mean plasma-fibrinogen was maintained below 50% of the initial value throughout the treatment period. This reduction in plasma-fibrinogen was accompanied by a parallel fall in whole-blood viscosity and a pronounced clinical improvement. Objective measurements showed maximum benefit on the 21st day of treatment, when the mean resting ankle/arm pressure index had increased by 37%, the post-exercise pressure index had increased by 50%, and the time taken for the pressure index to return to a resting value after a constant exercise had decreased by 33%. (The claudication-count had increased by 59%).
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PMID:Treatment of severe intermittent claudication by controlled defibrination. 6 29

Forty-two patients, mean age 68 years, with severe leg ischaemia were randomly treated with placebo or by controlled defibrination with ancrod for 3 weeks. Plasma fibrinogen concentration was kept at about 20% of normal in the ancrod treated group. The two groups proved to be well matched regarding factors which could affect the degree of ischaemia. Objective measurements showed a significant rise in ankle and toe systolic blood pressure in the ancrod group lasting for 3 months. There was no rise in distal blood pressure in the control group. In the ancrod treated group the toe and ankle systolic pressures rose about 8 mmHg, but this was not accompanied by an improvement in the clinical course.
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PMID:Treatment of severe foot ischaemia by defibrination with ancrod: a randomized blind study. 36 Mar 66

Recent studies in experimental crescentic glomerulonephritis, using the technique of glomerular culture, have shown that the macrophage is a major cell type present within the glomeruli and developing crescents. It has been suggested that their accumulation is a consequence of glomerular fibrin deposition. The effect of defibrination with ancrod on the cellular events occurring in experimental crescentic glomerulonephritis in the rabbit was therefore assessed in this disease using the techniques of culture of isolated glomeruli, electronmicroscopy or renal tissue, and light microscopy. Defibrinated animals developed only minimal renal impairment, virtually no fibrin deposition in Bowman's Space and only a mild degree of crescent formation, in contrast to the severe renal failure, fibrin deposition and crescent formation that occurred in the untreated animals. The culture of isolated glomeruli and electronmicroscopy of intact renal tissue demonstrated large numbers of macrophages within and emerging from glomeruli of both defibrinated and untreated animals. However, only in untreated animals were macrophages seen to migrate into Bowman's Space, phagocytose fibrin, transform into epithelioid cells and accumulate to form crescents. These studies suggest that fibrin deposition in Bowman's Space is the major stimulus to the macrophage migration from capillary loops and accumulation in Bowman's Space. However, fibrin deposition does not appear to be the stimulus to macrophage accumulation within capillary loops as this event was not affected by defibrination.
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PMID:The effect of defibrination on macrophage participation in rabbit nephrotoxic nephritis: studies using glomerular culture and electronmicroscopy. 48 57

44 patients were treated with subcutaneous ancrod (Arwin) for peripheral arterial occlusive disease (Fontaine stage III). An acute fulminating arterial occlusion occurred in two patients on the 10th and 23rd days respectively, and in a third patient a deep venous thrombosis developed in the leg on the 45th day after beginning treatment. Accordingly, vascular occlusion must be expected during defibrination in the presence of poor peripheral drainage conditions and if the serum fibrinogen can no longer be maintained below 1.0 g/1 in spite of increasing the ancrod dosage. Under these circumstances the treatment must be terminated.
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PMID:[Thrombotic arterial and venous obstructions under ancrod (Arwin) therapy (author's transl)]. 65 69

Defibrination with ancrod in nephrotoxic nephritis in rabbits. In rabbits with nephrotoxic nephritis, defibrination with ancrod provided protection when administered during the autologous phase, after extensive glomerular fibrin deposition had occurred and crescents and renal failure were developing. When further glomerular fibrin deposition was prevented by defibrination, deposited fibrin was rapidly removed, indicating that glomerular fibrin-clearing mechanisms are retained in crescentic nephritis. Defibrination had no effect on the extent of glomerular C3 deposition or on the amount of proteinuria.
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PMID:Defibrination with ancrod in nephrotoxic nephritis in rabbits. 79 57

An experimental model of surgically-induced arterial thrombosis was devised using the femoral arteries of dogs. Within 7 days, 67% of the arteries became completely thrombosed and only 12% remained compeletly patent. In the group of dogs that received low-dose heparin, 69% of the vessels were completely thrombosed and 6% remained completely patent. In the group of dogs treated with low-dose Ancrod to induce partial defibrination, 75% remained completely patent while only 19% of their femoral arteries were completely thrombosed. Although the ancrod was effective in preventing arterial thrombosis, 88% of the wounds showed moderate to severe separations. Most likely the absence of a fibrin lattice, necessary for the securement and growth of fibroblasts as the wound heals, explains this latter effect. Thus while Ancrod may become useful as an anticoagulant in certain clinical situations, it should not be used in proximity to surgery. Finally, in these studies of acute arterial thromboses, low-dose heparin therapy offered no protective effect.
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PMID:Comparison of ancrod and heparin as anticoagulants following endarterectomy in the dog. 95 68

The protective effects of anticoagulants in nephrotoxic nephritis in rabbits have been studied, using various doses of heparin and defibrination with ancrod. Massive doses of heparin (2000 units/kg/day) were required before significant reduction in glomerular fibrin deposition, extracepillary cell proliferation and urea retention occurred. Doses of 300 and 1000 units/kg/day were insufficient to modify fibrin deposition and cell proliferation. Defibrination with ancrod provided protection, judged by histological and functional criteria, comparable to 2000 units of heparin/kg/day; but fibrin could still be demonstrated in the glomeruli of animals treated with 2000 units of heparin/kg/day, contrasting with the virtual absence of fibrin in animals given ancrod.
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PMID:A quantitative evaluation of anticoagulants in experimental nephrotoxic nephritis. 121 1

Quantitative studies of the effects of defibrination (with ancrod) have been undertaken in two forms of allergic glomerular damage, nephrotoxic serum nephritis and acute serum sickness in rabbits. No differences in intrarenal fixation of nephrotoxic antibody, complement activation or host antibody response were detected between defibrinated and untreated rabbits with nephrotoxic serum nephritis. Defibrination prevented intraglomerular fibrin deposition in this disease; but some glomerular damage as shown by a rise in blood urea and endothelial proliferation still occurred in defibrinated animals. No differences in immune elimination of BSA, circulating immune complex formation or intrarenal localization of immune complexes were noted in defibrinated animals with acute serum sickness. No intraglomerular fibrin deposition was detected in treated or untreated animals in this disease model. It is concluded that the protective effects of ancrod are directly related to defibrination, and not to any other modification of allergic events.
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PMID:The effects of defibrination with ancrod in experimental allergic glomerular injury. 121 11

Using electromagnetic flow probes, cardiac output and hind limb blood flow were measured in dogs in which one hind limb had been rendered ischemic. Four dogs served as controls; seven were defibrinated by intravenous infusion of ancrod, 1 unit/kg, over a 30-minute period. In both groups, hematocrit readings remained constant, but cardiac output fell (this was attributed to barbiturate anesthesia), as did flow in the normal hind limb. In the controls after three hours, flow in the ischemic hind limb had decreased by 34%, but in the treated animals it had increased by 20%. The difference was statistically significant (P less than .001). The selective increase in blood flow in the ischemic limb may be explained by the greater reduction in blood viscosity at low shear rates achieved by defibrination.
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PMID:Improvement in blood flow through a critical arterial stenosis by defibrination with ancrod. 126 5

We have compared the effects of ancrod and recombinant tissue plasminogen activator (rtPA) on nephrotoxic nephritis induced in pre-immunized rabbits by the administration of nephrotoxic globulin (NTG; sheep anti-rabbit glomerular basement membrane). We used three different doses of NTG: in each experiment three groups of six rabbits were preimmunized with normal sheep globulin and given NTG: group A received no further treatment; group B received rtPA, 2 mg/kg 12 hourly; group C received ancrod 2 U/kg 12 hourly. Animals were bled daily for estimation of plasma fibrinogen and serum creatinine, then killed on day 5 and kidneys removed for histology. 1 ml/kg of NTG caused massive glomerular necrosis, all three groups having severe renal failure. With 0.5 ml/kg of NTG, ancrod and rtPA both effectively prevented fibrin deposition in Bowman's space, but all animals had severe proliferative glomerulonephritis and marked renal failure. With 0.25 ml/kg of NTG, control animals developed severe proliferative nephritis and advanced renal failure, ancrod provided almost complete protection, and the rtPA group had renal injury and functional impairment intermediate between the other two groups. We conclude that renal failure in severe nephrotoxic nephritis is fibrin-independent, but in less fulminant nephritis renal function can be protected by defibrination with ancrod. rtPA is capable of reducing glomerular fibrin accumulation as effectively as ancrod, but provides inferior protection of renal function.
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PMID:Effects of ancrod and rtPA on fibrin accumulation, glomerular inflammation and renal function in nephrotoxic nephritis. 176 13


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