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W W Spink

Publications and source records attributed to W W Spink.

At least 19 recordsLinked to original sources

Significane of intravascular coagulation in canine endotoxin shock.

The contribution of disseminated fibrin clot formation to the pathogenesis of canine endotoxin shock was explored in control dogs and in those defibrinated with a purified fraction of Malayan pit viper venom. The hemodynamic and humoral responses after the administration of an intravenous challenge dose of Escherichia coli endotoxin were comparable as was mortality. It is concluded that, although the role of the coagulation sequence in canine endotoxin shock is unclear, it does not appear to be determinative.

Animals↗

Complement in endotoxin shock: effect of complement depletion on the early hypotensive phase.

The complement (C) inhibition caused by bacterial endotoxin is well known, but the relationship of this reaction to endotoxin shock is unclear. Anesthetized dogs were therefore given Escherichia coli endotoxin intravenously with or without prior C depletion by a purified cobra venom factor (CVF). Mean aortic blood pressures (MAP) and C levels were measured. Intravenous CVF usually caused an early transient drop of MAP and a profound, long-lasting drop in C. Bacterial lipopolysaccharide (LPS) alone always caused a sudden (within 2 min) drop in MAP which was followed by partial recovery and then more long-lasting depression. Moderate drops in C usually occurred. In animals pretreated with CVF so that C levels were markedly depressed (<25% of control), LPS did not elicit the immediate MAP drops; however, a later (after 5 to 20 min) MAP drop always occurred. CVF pretreatment did not modify LPS-induced mortality. CVF effects were not caused by LPS contamination. These data show that the early hemodynamic responses of the dog to LPS may be mediated through the complement system.

Journal Article↗