Interactions of the Classical and Alternate Complement Pathway with Endotoxin Lipopolysaccharide EFFECT ON PLATELETS AND BLOOD COAGULATION

Kane, Michael; May, Joseph E.; Frank, Michael M.

doi:10.1172/jci107193

Cited by 62 publications

(19 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The precise mechanisms of the endotoxin effect are probably complex and not yet fully understood. The classical complement (C) pathway is involved in endotoxin-induced thrombocytopenia in guinea-pigs [ 1 ].…”

Section: Introductionmentioning

confidence: 99%

Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs

Bult

Herman

1979

Agents and Actions

View full text Add to dashboard Cite

Endotoxin lipopolysaccharides Escherichia coli O26:B6 and E. coli O127:B8 were weak inducers of aggregation in normal guinea-pig platelet-rich plasma (PRP), even in the presence of Ca2+. Indomethacin hardly inhibited endotoxin-induced aggregation, indicating that biosynthesis of thromboxane A2 (TXA2) was of little importance. In accordance with this conclusion TXA2 was not detectable by means of bioassay during endotoxin-induced aggregation in normal guinea-pig PRP. Pretreatment of the guinea-pigs with endotoxin sensitized their PRP to endotoxin. This was due to a humoral factor with a selectively directed towards the polysaccharide moiety of endotoxin. The combination of this factor with endotoxin indued a marked biosynthesis of TXA2 and concomitant platelet aggregation.

show abstract

Section: Introductionmentioning

confidence: 99%

Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs

Bult

Herman

1979

Agents and Actions

View full text Add to dashboard Cite

show abstract

“…We therefore speculate that the differences between their study and ours resulted from different experimental conditions, de- The vindesine-induced neutropenia occurred maximally after 30 min, which is slower than the neutropenia that occurs within 15 min after intravenous injection with lipopolysaccharide and fMLR This difference may be due in part to slower induction of polarization by vindesine than induction by lipopolysaccharide or fMLR In support of this view, Keller et al [36] showed that neutrophils required at least 3 min to start to polarize after exposure to colchicine, whereas fMLP induced polarization within 1 min. The more rapid appearance of neutropenia induced by lipopolysaccharide or fMLP is probably not due to their stimulatory effect on neutrophil adhesiveness to the vascular endothelium, since lipopolysaccharide-induced adherence of neutrophils in vitro was minimal at 15 min and did not reach a maximum until 40-60 rain [40].…”

Section: Cytochalasln B Washmentioning

confidence: 95%

Transient neutropenia after intravenous injection of vindesine in patients with lung cancer

Aoshiba¹,

Nagai²,

Ueno³

et al. 1994

Eur J Clin Pharmacol

View full text Add to dashboard Cite

We have found transient circulating neutropenia and pulmonary sequestration of neutrophils after the intravenous injection of vindesine, a microtubule disruptor. Experiment 1 Ten patients with lung cancer were given a bolus intravenous injection of 3 mg.m-2 vindesine (Fildesine(r)). In all patients, total leukocyte and neutrophil counts in the venous blood fell to 65% and 47% of baseline values respectively within 30 min, and returned to baseline values within 6 h. In contrast, the lymphocyte count was stable. Experiment 2 Male Wistar rats were given saline or 0.08 mg.kg-1 vindesine intravenously and were sacrificed after 30 min. Vindesine produced a 58% reduction in the neutrophil count in the systemic circulation and a threefold increase in the neutrophil/erythrocyte ratio in the pulmonary microvasculature. Experiment 3 We studied the effects of vindesine in vitro on neutrophils and lymphocytes isolated from the venous blood of healthy volunteers. Vindesine (10(-5)-10(-8) mol.l-1) reduced neutrophil deformability (filterability) and induced neutrophil polarization, with reversibility of both effects after washout. These effects of vindesine were completely inhibited by cytochalasin B, an actin filament disrupter. Vindesine did not stimulate the neutrophil functions of adherence to polystyrene tubes, chemotaxis, or superoxide anion generation. The filterability and morphology of lymphocytes were not altered by vindesine. Thus, we conclude that a bolus injection of vindesine produces pulmonary sequestration of neutrophils, which produces circulatory neutropenia, and that it is primarily mediated by a decrease in neutrophil deformability that occurs without activation of the cells.

show abstract

“…(3) endothelial damage, with subsequent Hageman factor activation and platelet aggregation (Gaynor and Bouvier, 1970): and (4) complement mediated platelet damage (Brown, 1973;Kane, 1973).…”

Section: Disseminated Intravascular Coagulationmentioning

confidence: 99%

“…Plasmin activates the first and third components of complement in addition to initiating fibrinolysis and activation of Hageman factor (Ryan and Majno, 1977). In addition, complement fixation with subsequent platelet damage (Brown, 1973;Kane, 1973) causes the release of platelet factor 3 (FF3), which potentiates coagulation because of the factor Xl-like activity of this chemical. FF3 is considered by some to be a major initiator of the intrinsic coagulation system (Davie and Fujikawa, 1975).…”

Section: Effects Upon the Complement Systemmentioning

confidence: 99%

See 1 more Smart Citation

The biologic effects of bacterial endotoxin: A short review

Culbertson

Osburn

1980

Vet Res Commun

View full text Add to dashboard Cite

Culbertson, Jr., R. and Osburn, B.I., 1980. The biologic effects of bacterial endotoxin: a short review. Vet. Sci. Commun., 4: 3-14=This short reveiw considers some of the more widely accepted biological actions of bacterial endotoxin. Early sections concern endotoxin chemical composition, assay techniques, and species variation in toxigenicity. Individual specific actions and classical endotoxin-induced phenomena are presented under headings of pyrogenic effect, hemodynamic effects, disseminated intravascular coagulation, complement system effects, induction of the generalized Shwartzman reaction, effects upon cellular constituents of blood, metabolic and endocrinologic effects, immunologic effects, nervous system effects, hepatic effects, and abortifacient action. The relationship of these effects to clinical manifestations is discussed where warranted.

show abstract

Interactions of the Classical and Alternate Complement Pathway with Endotoxin Lipopolysaccharide EFFECT ON PLATELETS AND BLOOD COAGULATION

Cited by 62 publications

References 24 publications

Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs

Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs

Transient neutropenia after intravenous injection of vindesine in patients with lung cancer

The biologic effects of bacterial endotoxin: A short review

Contact Info

Product

Resources

About