プロトピン 塩酸塩

Danger

H301 (100%): Toxic if swallowed [Danger Acute toxicity, oral]

P264, P270, P301+P316, P321, P330, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 39 reports by companies from 1 notifications to the ECHA C&L Inventory.

Emergency treatment: Symptomatic drug ingestion; [HSDB] Intraperitoneal LD50 = 102 mg/kg; [RTECS] May cause irritation; Toxic if swallowed; Effects in high-dose animal studies include convulsions; Oral LD50 (mouse) = 160 mg/kg; [Aldrich MSDS]

FROM OPIUM: HESSE, BER 4, 693 (1871); ALSO FROM THE HERB FUMARIA OFFICINALIS L, CHELIDONIUM MAJUS L, & MANY OTHER PAPAVERACEAE & FUMARIACEAE: MANSKE IN THE ALKALOIDS VOL IV, RHF MANSKE, HL HOLMES, EDS (ACADEMIC PRESS, NEW YORK, 1954) PP 157-159. /PROTOPINE/

WHEN INJECTED IV @ 0.5-10 MG/KG INTO RABBITS OR RATS, PROTOPINE-HCL DECR THE ATRIOVENTRICULAR AND INTRACARDIAC CONDUCTIVITY LEADING TO A DECR IN THE FREQUENCY OF CARDIAC CONTRACTIONS. AT 1-100 MUG/ML, IT DECR THE CONTRACTIONS OF AN ISOLATED RAT INTESTINAL SEGMENT INDUCED BY BACL2 (0.8 MG/ML).

CACL2 (0.2 G/KG, IV) INDUCED FIBRILLATION OF THE RAT CARDIAC VENTRICLES FOR 2 SEC AND CAUSED DEATH OF THE ANIMALS. PROTOPINE-HCL (10 MG/KG) PROLONGED THE VENTRICULAR FIBRILLATION TO 186 SEC. IT ALSO RESTORED THE SINUS RHYTHM 3 MIN AFTER ITS ADMIN IN ALL TREATED ANIMALS.

Compounds with activity like OPIATE ALKALOIDS, acting at OPIOID RECEPTORS. Properties include induction of ANALGESIA or NARCOSIS.

Drugs that selectively bind to but do not activate histamine H1 receptors, thereby blocking the actions of endogenous histamine. Included here are the classical antihistaminics that antagonize or prevent the action of histamine mainly in immediate hypersensitivity. They act in the bronchi, capillaries, and some other smooth muscles, and are used to prevent or allay motion sickness, seasonal rhinitis, and allergic dermatitis and to induce somnolence. The effects of blocking central nervous system H1 receptors are not as well understood.

Drugs or agents which antagonize or impair any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.