In vivo effects of Agkistrodon rhodostoma venom: studies with fibrinogen-131I.

Regoeczi, E.; Gergely, J.; McFarlane, A. S.

doi:10.1172/jci105426

Cited by 81 publications

(27 citation statements)

References 21 publications

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“…2 h after intravenous administration of 1'5I fibrinogen to normal rabbits, 87% ofplasma radioactivity was clottable by the addition of thrombin. 1251 radioactivity disappeared from the plasma with an initial half-life of 15.5 h, and then maintained a half-life of 40 h. These results are consistent with previous studies employing labeled fibrinogen (27). 125I fibrinogen was injected intravenously as a tracer dose to each rabbit 15 h before the conclusion ofeach experiment, when the animals were killed.…”

Section: Quantitation Ofglomerularfibrinsupporting

confidence: 88%

Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit.

Holdsworth¹,

Tipping²

1985

J. Clin. Invest.

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Glomerular fibrin deposition is important in the pathogenesis of renal failure and crescent formation in glomerulonephritis. The mechanisms of glomerular fibrin deposition are unknown. The current studies explored the role of macrophages in this process. Methods were developed for measuring glomerular fibrin de-position and glomerular procoagulant activity in a passive model of the autologous phase of antiglomerular basement membrane antibody-induced glomerulonephritis in rabbits. Significant fibrin deposition was observed to be associated with glomerular macrophage accumulation. Leukocyte ablation with mustine hydrochloride prevented both glomerular macrophage accumulation and fibrin deposition without affecting the coagulation system or the deposition ofdisease-inducing antibodies and complement. Repletion with mononuclear inflammatory cells produced significant fibrin deposition. To examine the role of tissue injury per se in glomerular fibrin deposition, a macrophage-independent model of glomerular injury (heterologous phase glomerulonephritis) was also studied. Although a similar degree of glomerular injury occurred, there was no significant fibrin deposition. This suggests that macrophages, rather than injury alone, are responsible for fibrin deposition. Lysates of isolated glomeruli containing macrophages demonstrated greatly enhanced procoagulant activity compared with lysates of glomeruli without macrophages. Thus macrophages appear to be directly responsible for glomerular fibrin deposition in antiglomerular basement membrane antibody-induced glomerulonephritis, and this appears to be due to their ability to express procoagulant activity rather than their propensity to cause glomerular injury.

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Section: Quantitation Ofglomerularfibrinsupporting

confidence: 88%

Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit.

Holdsworth¹,

Tipping²

1985

J. Clin. Invest.

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“…During defibrination therapy with Arvin or Reptilase, there is a decrease of fibrinogen and plasminogen levels and presence of fibrinogen-fibrin de gradation products (FDP), but no increase of plasma fibrinolytic activity [19,9,10], The activation of the endogenous fibrinolytic system as a se condary effect of the intravascular coagulation [24,22,21,25] is not pre vented by EACA [5,22,16,3,9], whereas in Reptilase-treated dogs, Trasylol was able to delay but not to prevent the fibrinolytic response [19,9,10]. On the other hand, the presence of soluble unclottable complexes during defi brination with Ancrod or Defibrase would indicate that FDP is derived from proteolysis of soluble fibrin [2,11,17].…”

Section: Introductionmentioning

confidence: 99%

Experimental Defibrination with Bothropase

Kelen¹,

Rosenfeld²,

Vainzof³

et al. 1978

Pathophysiol Haemos Thromb

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Fibrinogen was depleted in dogs injected with a single dose of bothropase even if pretreatment followed by a continuous infusion of antifibrinolytic drugs was performed during defibrination. The activation of the fibrinolytic system as a secondary effect of the defibrination syndrome induced by bothropase injection was blocked completely by aprotinin (Trasylol) but not by EACA. Plasmin activity in spite of the inhibition of plasminogen activator suggests that, either an excess of activator is released in circulation, or a plasmin-antiplasmin complex is dissociated by the circulating fibrin, according to the hypothesis of Ambrus and Markus [1], and Back et al. [4] for the mechanism of fibrinolysis in vivo. An experimental model is suggested for the study of the fibrinolytic mechanism in vivo, by the association of defibrinating agents, antivenom and antifibrinolytic drugs.

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“…The CE produces progressive depletion of the fibrinogen pool, probably through the formation of an atypical fibrin monomer differing from that produced by thrombin (1)(2)(3)(4)(5). Kinetic data obtained from animal experiments employing labeled fibrinogen indicate that fibrinogen depletion can, under optimal circumstances, proceed at exceptionally rapid rates, corresponding to half-times of 5-15 min (3,6,7). However, these values were obtained using large amounts of CE in radiated animals and are not representative of the therapeutic doses employed in man by Bell, Pitney, and Goodwin (8) and Sharp, Warren, Paxton, and Allington (9).…”

Section: Introductionmentioning

confidence: 99%

Isotopic studies of therapeutic anticoagulation with a coagulating enzyme

Bell¹,

Regoeczi²

1970

J. Clin. Invest.

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A BSTRA CT The kinetics of the depletion of plasma fibrinogen were studied in seven patients who received fibrinogen-"3'I 1 hr before an intravenous injection of the coagulating enzyme (CE) derived from the venom of the pit viper, Agkistrodon rhodostoma. Disappearance of the clottable radioactively labeled fibrinogen from the circulation conformed to an exponential decay with an average half-life of 0.85 hr. The mean clearance rate for protein-bound radioactivity, composed of fibrinogen and it's split products, was 12% of the intravascular pool per hour. The breakdown products of fibrin produced by CE inhibited polymerization of fibrin in vitro.Studies in five patients performed between the 3rd and 10th day following the administration of CE revealed that the absolute catabolic rates of fibrinogen were subnormal initially, but gradually increased as the fibrinogen concentration returned to normal.In rabbits, after the administration of CE, regeneration of the fibrinogen pool was markedly prolonged. This delayed regeneration time was not influenced by an excess of antivenene, but rapid regeneration to pretreatment values of plasma fibrinogen was immediately initiated by stimulating fibrinogen synthesis with subcutaneous turpentine.

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In vivo effects of Agkistrodon rhodostoma venom: studies with fibrinogen-131I.

Cited by 81 publications

References 21 publications

Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit.

Macrophage-induced glomerular fibrin deposition in experimental glomerulonephritis in the rabbit.

Experimental Defibrination with Bothropase

Isotopic studies of therapeutic anticoagulation with a coagulating enzyme

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