Cardiovascular effects of Shigella sonnei endotoxin in the rat.
Shigella sonnei lipopolysaccharide (LPS), either in phase I (extracted from the smooth strains), or in phase II (extracted from the rough strains) reduced mean arterial pressure and heart rate following a 640 micrograms/Kg intravenous (iv) bolus injection in the urethane-anesthetized rat. Lower doses were without significant effects. Escherichia coli LPS (640 micrograms/Kg iv) produced a greater and more prolonged hypotension, however the negative chronotropic effect was less severe. The iv injection of the lipid A moiety of the LPS molecule of Shigella sonnei resulted in a more pronounced hypotensive effect than that obtained with the parent LPS, thus showing that lipid A is the vasodilatating fraction of the molecule. When lipid A was injected in rats pretreated with aspirin or with naloxone, the hypotensive effect was significantly reduced and the decrease in heart rate was reverted in tachycardia. In atropine-pretreated, surgically bivagotomized rats, iv injection of lipid A was followed by a long-lasting pressor effect. The date indicate that Shigella sonnei endotoxin has cardiovascular effects, mainly due to its lipid A moiety of the molecule. The hypotensive effect involves a wide range of mechanisms.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology; D001285:Atropine / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects*; D004731:Endotoxins / Q000633:toxicity*; D006339:Heart Rate / Q000187:drug effects*; D008050:Lipid A / Q000633:toxicity; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D009270:Naloxone / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D012764:Shigella sonnei / Q000472:pathogenicity*
D004731:Endotoxins; D008050:Lipid A; D008070:Lipopolysaccharides; D009270:Naloxone; D001285:Atropine; D001241:Aspirin