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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.

Two new steroidal alkaloids named capsimine and isocapsicastrine were isolated from the root bark of Solanum capsicastrum. Their structures were elucidated by chemical degradation and spectral data as (22R, 25R)-22,26-epiminocholest-5-ene-3 beta, 16 alpha-diol and (22S,25S)-O(3)-beta-D-glucopyranosyl-22,26-epiminocholest-5-ene-3 beta-16 alpha-diol, respectively. Capsicastrine, capsicastrine acetate, isoteinemine acetate, and etioline exhibited strong activity against liver damage induced by CCl4.

[3H]Arachidonic acid (AA)-prelabeled mouse peritoneal macrophages were stimulated by calcium ionophore A-23187 to release [3H]AA metabolites. The major labeled products which were co-chromatographed with the authentic PG and LT standards by TLC and determined by liquid scintillation were 6-keto-PGF1 alpha, PGE2, LTC4, and LTB4. Anisodamine (Ani) significantly inhibited the A-23187-induced release of PG and LT from mouse macrophages in a dose-dependent manner. In the presence of Ani at 0.5 mmol/L, the A-23187-induced release of 6-keto-PGF1 alpha, PGE2, LTC4 and LTB4 was reduced by 57%, 20%, 53% and 49%, respectively. A-23187-induced release of 6-keto-PGF1 alpha measured by RIA from bovine aorta endothelial cells was also significantly inhibited by Ani in a dose-dependent manner. These results indicate that the calcium-antagonistic effects of Ani may not only play a significant role in its inhibiting release of PG and LT, but also contribute to its salutary effects in the treatment of septic shock.