Papaverine Pharmacology, Pharmacokinetics, Studies, Metabolism - Papaverine

Papaverine Pharmacology, Pharmacokinetics, Studies, Metabolism - Papaverine

CLINICAL PHARMACOLOGY

The main actions of papaverine are exerted on cardiac and smooth muscle. Like qathidine, papaverine acts directly on the heart muscle to depress conduction and prolong the refractory period. Papaverine relaxes various smooth muscles. This relaxation may be prominent if spasm exists. The muscle cell is not paralyzed by papaverine and still responds to drugs and other stimuli causing contraction. The antispasmodic effect is a direct one, and unrelated to muscle innervation. Papaverine is practically devoid of effects on the central nervous system. Papaverine relaxes the smooth musculature of the larger blood vessels, especially coronary, systemic peripheral, and pulmonary arteries. Perhaps by its direct vasodilating action on cerebral blood vessels, papaverine increases cerebral blood flow and decreases cerebral vascular resistance in normal subjects; oxygen consumption is unaltered. These effects may explain the benefit reported from the drug in cerebral vascular encephalopathy.

The direct actions of papaverine on the heart to depress conduction and irritability and to prolong the refractory period of the myocardium provide the basis for its clinical trial in abrogating atrial and ventricular premature systoles and ominous ventricular arrhythmias. The coronary vasodilator action could be an additional factor of therapeutic value when such rhythms are secondary to insufficiency or occlusion of the coronary arteries. In patients with acute coronary thrombosis, the occurrence of ventricular rhythms is serious and requires measures designed to decrease myocardial irritability. Papaverine may have advantages over quinidine, used for similar purpose, in that it may be given in an emergency by the intravenous route, does not depress myocardial contraction or cause cinchonism, and produces coronary vasodilation.