[Site of endotoxic pulmonary vasoconstriction and the effect of anisodamine].
Using arterial and venous occlusion techniques in an in situ, isolated left goat lung preparation, the total arteriovenous pressure drop across the lung was partitioned vertically into pressure drops across the relatively indistensable arteries (delta Pa) and veins (delta Pv) and the middle distensible vessels (delta Pm). Endotoxin primarily increased delta Pv and Pc. Anisodamine only showed a slight effect on pressure drops in different segment under normal conditions. It could attenuate the endotoxin effect however. Serotonin mainly increased delta Pa and showed no effect on delta Pv and delta Pm. Norepinephrine and histamine increased delta Pv and Pc while it showed almost no effect on delta Pa. It is possible that the norepinephrine and histamine mediate the pulmonary hypertension caused by endotoxin.
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D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D004731:Endotoxins; D004926:Escherichia coli; D006041:Goats; D011651:Pulmonary Artery / Q000187:drug effects; D011667:Pulmonary Veins / Q000187:drug effects; D012991:Solanaceous Alkaloids / Q000494:pharmacology*; D014661:Vasoconstriction / Q000187:drug effects*; D014665:Vasodilator Agents
D004731:Endotoxins; D012991:Solanaceous Alkaloids; D014665:Vasodilator Agents; C003922:anisodamine