6-ketoprostaglandin-f1-alpha and anisodamine

The short term effect of anisodamine, an alkaloid isolated from the chinese herb anisodas tonguticus, on blood flow of uterine and umbilical arteries in 16 pregnant women with pregnancy-induced hypertension (PIH) was investigated by means of pulsed doppler ultrasound technique Results have shown that anisodamine could decrease the A/B ratio, resistant index (RI), and pulsative index (PI) of blood velocity in these arteries with statistical significant difference. Its mechanism of action might be the improving of the rheology in PIH and adjusting the imbalance of TXA2/PGI2. It was suggested that the resistance in uteroplacental circulation was decreased and its perfusion improved, so that favors the fetal growth and development.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Blood Viscosity; Female; Humans; Microcirculation; Placenta; Pre-Eclampsia; Pregnancy; Regional Blood Flow; Solanaceous Alkaloids; Thromboxane B2; Umbilical Arteries; Uterus; Vascular Resistance

Anisodamine, a Chinese traditional medicine herb, has been used for treatment of adult respiratory distress syndrome effectively, but little is known about its mechanism. We attempted to investigate if anisodamine could protect bovine pulmonary endothelial cell injury induced by exogenous oxygen-free radicals that were generated by xanthine/xanthine oxidase or opsonized zymosan-stimulated polymorphonuclear leukocytes. Results showed that with the addition of xanthine/xanthine oxidase into cultured bovine pulmonary endothelial cells, production of malondialdehyde and release of lactate dehydrogenase in supernatant increased, and synthesis of prostacyclin decreased. Damaged cellular membranes were revealed by scanning electron microscopy. The same was true for the addition of opsonized zymosan-stimulated polymorphonuclear leukocytes. While treatment with anisodamine greatly attenuated all of the above-mentioned parameters, results showed that (1) cultured bovine pulmonary endothelial cells could be damaged by oxygen-free radicals, (2) anisodamine had a protective effect on this injury as effective as that of superoxide dismutase and catalase, and (3) the membrane-stable action might contribute to the mechanism of protective effect against this injury.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Catalase; Cattle; Cells, Cultured; Drugs, Chinese Herbal; Endothelium, Vascular; Free Radicals; L-Lactate Dehydrogenase; Malondialdehyde; Microscopy, Electron, Scanning; Neutrophils; Oxygen; Pulmonary Artery; Solanaceous Alkaloids; Superoxide Dismutase; Xanthine; Xanthine Oxidase; Xanthines; Zymosan

The effects of dauricine (Dau), aniso amine (Ani), platelet activating factor (PAF), leukotriene C4 (LTC4) and leukotriene D4 (LTD4) on the production of TXB2 and 6-keto-PGF1 alpha (the stable metabolites of TXA2 and PGI2, respectively) in bovine anterior cerebral arterial smooth muscle cells were studied. The normal quantities of TXB2 and 6-keto-PGF1 alpha produced by bovine anterior cerebral arterial smooth muscle cells were 16 +/- 5 and 464 +/- 24 pg/10(5) cells, respectively, when measured by radioimmunoassay (RIA). The levels of TXB2 and 6-keto-PGF1 alpha in bovine anterior cerebral arterial smooth muscle cells decreased significantly when the cells were treated with Dau or Ani over 20 min. Both drugs inhibited the production of TXB2 and 6-keto-PGF1 alpha in dose (1-100 mumol/L) dependent manner. The bovine anterior cerebral arterial smooth muscle cells were stimulated markedly by LTC4 and LTD4 to produce TXB2 and 6-keto-PGF1 alpha on the same condition even at 0.01 mumol/L. When the cells were treated with PAF over 20 min, TXB2 increased significantly, but 6-keto-PGF1 alpha remained unchanged. If the cells were preincubated with Dau or Ani 20 min before PAF, LTC4 or LTD4 stimulation, the production of TXB2 and 6-keto-PGF1 alpha especially TXB2 were inhibited significantly compared with that of PAF, LTC4 or LTD4 group, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: 6-Ketoprostaglandin F1 alpha; Alkaloids; Animals; Benzylisoquinolines; Cattle; Cells, Cultured; Cerebral Arteries; Isoquinolines; Muscle, Smooth, Vascular; Solanaceous Alkaloids; Tetrahydroisoquinolines; Thromboxane B2

The effect of anisodamine on arachidonic acid metabolism in macrophages was studied. The results indicated that the synthesis of PGI2, TXA2 and PGF2 alpha stimulated by phorbol-12-myristate-13-acetate (PMA) and calcium ionophore A23187 was dose and time-dependently inhibited by anisodamine, and preincubation of the cells with anisodamine significantly decreased subsequent PMA and A23187-stimulated synthesis of prostaglandins. An isodamine failed to inhibit exogenous arachidonic acid-stimulated synthesis of prostaglandins. It is suggested that the site of action of anisodamine could be the phospholipase A2 reaction.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Anti-Inflammatory Agents, Non-Steroidal; Calcimycin; Macrophages; Mice; Peritoneal Cavity; Solanaceous Alkaloids; Tetradecanoylphorbol Acetate; Thromboxane B2

[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.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Aorta; Calcimycin; Cattle; Cells, Cultured; Dose-Response Relationship, Drug; Endothelium, Vascular; Female; Leukotriene B4; Macrophages; Male; Mice; Peritoneal Cavity; Prostaglandins; Prostaglandins E; Solanaceous Alkaloids; SRS-A

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Adult; Blood Platelets; Cardiopulmonary Bypass; Child; Child, Preschool; Cyclic AMP; Humans; Solanaceous Alkaloids; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Cells, Cultured; Dinoprost; Female; Macrophages; Mice; Peritoneal Cavity; Shock, Septic; Solanaceous Alkaloids; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Pressure; Drugs, Chinese Herbal; Infusions, Intravenous; Male; Rats; Rats, Inbred Strains; Shock, Septic; Solanaceous Alkaloids; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Cattle; Dinoprost; Endotoxins; Epithelium; Macrophages; Mice; Solanaceous Alkaloids; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Acetylcholine; Animals; Dinoprostone; Dose-Response Relationship, Drug; Iris; Norepinephrine; Parasympatholytics; Prostaglandins E; Rabbits; Solanaceous Alkaloids

Acute disseminated intravascular coagulation (DIC) is a life-threatening condition that may be encountered in many situations, especially in cases of shock with uncontrollable hemorrhage. Anisodamine, an alkaloid extracted from a Chinese herb, is well known for its dramatic therapeutic effect on DIC. Sixty male rabbits were used to establish an acute DIC model. A total of 240 blood samples were taken for laboratory assays of changes in blood coagulation factors, platelet count, platelet adhesion, platelet aggregation, malondialdehyde (MDA), thromboxane B2 (TXB2), and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). Changes of the microcirculatory status and the rate of the blood flow in the conjunctival capillaries of 60 rabbits were observed with WXS-II microcirculation microscope. Pathological sections of the lungs and kidneys were studied. Our investigation showed the presence of microthrombi in the microvasculature. After treatment with anisodamine, the prothrombin time stayed in the normal range, fibrinogen consumption was lessened, adenosine-diphosphate-induced platelet aggregation was inhibited, thromboxane B2 and malondialdehyde concentrations were significantly lower than in the control group, and the elevated quantity of 6-keto-PGF1 alpha was spared. We concluded that the anti-platelet-aggregating, microcirculation-facilitating, thromboxane-B2-inhibiting, malondialdehyde-inhibiting, and 6-keto-PGF1 alpha-sparing effects of anisodamine are the important mechanisms of its dramatic therapeutic effect on DIC.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Coagulation; Disseminated Intravascular Coagulation; Kidney; Lung; Male; Malondialdehyde; Microcirculation; Platelet Aggregation; Platelet Count; Rabbits; Regional Blood Flow; Solanaceous Alkaloids; Thromboxane B2

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Blood Pressure; Dogs; Female; Male; Parasympatholytics; Platelet Aggregation; Shock, Septic; Solanaceous Alkaloids

Topics: 6-Ketoprostaglandin F1 alpha; Adolescent; Animals; Child; Child, Preschool; Dinoprost; Dogs; Epoprostenol; Female; Humans; Infant; Male; Prostaglandins E; Prostaglandins F; Shock, Septic; Solanaceous Alkaloids; Vasodilator Agents