Purified Cobra Venom Factor: Effect on Blood Platelets

Wj, Dodds; Rj, Pickering

doi:10.3181/00379727-140-36473

Cited by 13 publications

(2 citation statements)

References 4 publications

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“…Human platelets and platelets of other mammalian species may respond with the release reaction and/or lysis after activation of the classical complement pathway with anti-platelet antibody (1,2), immune aggregates (3)(4)(5), or activation of the alternative pathway with immune aggregates, endotoxin, inulin, cobra venom factor (CVF),I or zymosan (6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Description of a coagulation abnormality in the blood of rabbits congenitally deficient in C6 (18) and demonstration of the role of platelets in this coagulation defect (2,(19)(20)(21) has suggested that complement-platelet interaction may proceed in the absence of known complement activators.…”

Section: Introductionmentioning

confidence: 99%

Human platelet-initiated formation and uptake of the C5-9 complex of human complement.

Zimmerman¹,

Kolb²

1976

J. Clin. Invest.

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A B S T R A C T We have studied the interaction of radiolabeled complement components with normal human platelets, platelets from a patient with paroxysmal nocturnal hemoglobinuria, and rabbit platelets in the absence of known complement activators or in the presence of coba venon factor (CVF). When unwashed platelets in platelet-rich plasma, or washed platelets suspended in serum or autologous plasma, were incubated for 30 min, C3 and terminal components (C5, C8, and C9) were found to bind to them. The terminal components were shown to be bound as the C5-9 complex, rather than as individual proteins, by eluting them from the platelet membrane and examining their behavior on ultracentrifugation. They cosedimented at a rate characteristic of the stable C5-9 complex (22S). As many as 370-1,380 C5-9 complexes/platelet were calculated to have been bound during the incubation period. The complex so formed did not differ by ultracentrifugational criteria from that binding to rabbit platelets after CVF activation of complement. Though C3 was not included in the complex, it did not appear to be bound by nonspecific absorption. It could not be removed by washing but rather was eluted by the freeze-thaw technique used to elute the C5-9 complex. Incubation of radiolabeled components in platelet-free plasma did not result in C5-9 complex formation, indicating an initiating role for platelets in this reaction. In contrast to platelets, erythrocytes incubated in analogous plasma did not induce detectable C5-9 formation. Neither EDTA, phenylmethylsulfonylfluoride, nor epsilon-amino-N-caproic acid prevented platelet-initiated formation of C5-9, suggesting that the reaction may involve mechanisms of complement activation not previously described.

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Section: Introductionmentioning

confidence: 99%

Human platelet-initiated formation and uptake of the C5-9 complex of human complement.

Zimmerman¹,

Kolb²

1976

J. Clin. Invest.

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“…Besides complement activation, CVF effects included an alteration of both extrinsic and intrinsic coagulation activities, a striking eleva tion of fibrinogen, an increase in plasma platelet fac tor 3 activity, and a pronounced leukocytosis. CVF also has been shown to cause aggregation and release of intracellular constituents of guinea pig platelets [29]. The exact requirement of complement for these effects of CVF has not been rigorously examined, but in view of the known interrelationships between com plement and coagulation systems, a complement re quirement cannot be ruled out.…”

Section: Discussionmentioning

confidence: 99%

Enhancement of Antigen-Induced Bronchoconstriction in the Guinea Pig after Intravascular Complement Activation with Cobra Venom Factor

Regal¹

1990

Int Arch Allergy Immunol

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The purpose of the present studies was to begin to test the hypothesis that the complement system is important for antigen-induced bronchoconstriction in the guinea pig. The effect of the complement-depleting agent cobra venom factor (CVF) on antigen-induced bronchoconstriction in guinea pigs passively sensitized with IgG or IgE antibody to ovalbumin was determined. Intravenous injection of CVF significantly reduced total hemolytic complement activity (CH₅₀), caused a transient decrease in dynamic lung compliance, an increase in pulmonary resistance, and a decrease in circulating white blood cells with a sustained decrease in platelets. Antigen-induced bronchoconstriction was not inhibited in either IgG- or IgE-sensitized guinea pigs depleted of complement. Thus, a role for the complement system as a contributing factor in antigen-induced bronchoconstriction was not supported. On the contrary, our studies revealed an enhanced antigen-induced bronchoconstriction in guinea pigs depleted of complement with CVF. Our studies were then directed towards characterizing the enhanced response to begin to determine the mechanism responsible. The enhanced antigen-induced bronchoconstriction occurred in both IgG- and IgE-sensitized guinea pigs and was most apparent at lower antigen doses. The enhanced response still occurred in animals treated for 5 min with a dose of CVF (10 U) which caused no demonstrable decrease in CH₅₀, a 30% level of conversion of C3, and a normal response to C5a. These data suggested that the enhanced response was not related to the level of C5a responsiveness of the animal. In addition, CVF-treated animals were normally responsive to various purported mediators of antigen-induced bronchoconstriction: histamine, leukotriene C₄, platelet activating factor, the thromboxane-mimetic U-46,619, and prostaglandin F_2α. The response to prostaglandin D₂ was slightly enhanced. Thus, CVF treatment did not result in a generalized airway hyperreactivity. Since antigen-induced bronchoconstriction was not inhibited in animals depleted of complement, these studies suggest that an intact complement system is not necessary for this antigen-induced event. However, the enhanced antigen-induced bronchoconstriction seen after CVF treatment suggests that complement depletion and/or activation in vivo may be an important modulator or determinant of the severity of a subsequent antigen-induced bronchoconstriction.

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Microcirculatory Disturbances Induced by Generalized Intravascular Coagulation

Müller‐Berghaus¹,

Lasch²

1975

Experimental Production of Diseases: Heart and Circulation

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Purified Cobra Venom Factor: Effect on Blood Platelets

Cited by 13 publications

References 4 publications

Human platelet-initiated formation and uptake of the C5-9 complex of human complement.

Human platelet-initiated formation and uptake of the C5-9 complex of human complement.

Enhancement of Antigen-Induced Bronchoconstriction in the Guinea Pig after Intravascular Complement Activation with Cobra Venom Factor

Microcirculatory Disturbances Induced by Generalized Intravascular Coagulation

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