NCTI- Pharmacology- Mechanism of Action

Inhibits aggregation (clumping) of platelets by blocking the formation of the substance thromboxane (A2) ; prolonging bleeding time

Provides analgesia by inhibiting prostaglandins and other substances that sensitize pain receptors (blocking of prostaglandins also accounts for the drug’s anti-inflammatory effects).

Relieves fever by acting upon the hypothalamic heat regulating center

Alters pain perception and produces euphoria

Decreases myocardial oxygen demand by decreasing preload (venous pooling due to peripheral vasodilation) and decreasing afterload (decreased systemic vascular resistance due to peripheral vasodilation)

Depresses the CNS by interacting with opiate receptors in the brain

Binds (adsorbs) toxic substances inhibiting gastrointestinal absorption, leaving less toxic substance in body circulation; increasing fecal elimination of drug/charcoal complex

• Relaxes smooth muscles causing venous dilation
• Reduces preload and afterload to the heart
• Dilates the coronary arteries resulting in increased perfusion of the myocardium

Increases percentage of oxygen in inspired air (FiO2)

• Suppresses the spread of seizure activity and raises the seizure threshold in the motor cortex
• Sedative effects depress the CNS and reduce anxiety
• Skeletal muscle relaxant
• Induces amnesia

• Reduces anxiety
• Relaxes skeletal muscles
• Produces short term CNS depression and amnesia

Reverses the respiratory depression and CNS sedation of narcotics by competing for opiate receptor sites in the brain

• Elevates blood glucose level by converting stored liver glycogen into glucose
• Increases heart rate and myocardial contractility and improves AV conduction in a manner similar to that produced by catecholamines

Provides immediate source of glucose for cellular metabolism

Coenzyme necessary for carbohydrate metabolism of glucose