| Indication | For the rapid relief of angina pectoris. |
| Pharmacodynamics | Amyl nitrite, in common with other alkyl nitrites, is a potent vasodilator. It expands blood vessels, resulting in lowering of the blood pressure. Alkyl nitrite functions as a source of nitric oxide, which signals for relaxation of the involuntary muscles. Physical effects include decrease in blood pressure, headache, flushing of the face, increased heart rate, dizziness, and relaxation of involuntary muscles, especially the blood vessel walls and the anal sphincter. There are no withdrawal symptoms. |
| Mechanism of action | Amyl nitrite's antianginal action is thought to be the result of a reduction in systemic and pulmonary arterial pressure (afterload) and decreased cardiac output because of peripheral vasodilation, rather than coronary artery dilation. As an antidote (to cyanide poisoning), amyl nitrite promotes formation of methemoglobin, which combines with cyanide to form nontoxic cyanmethemoglobin. |
| Absorption | Amyl nitrite vapors are absorbed rapidly through the pulmonary alveoli, manifesting therapeutic effects within one minute after inhalation. |
| Volume of distribution | Not Available |
| Protein binding | Not Available |
| Metabolism | Hepatic. The drug is metabolized rapidly, probably by hydrolytic denitration; approximately one-third of the inhaled amyl nitrite is excreted in the urine. |
| Route of elimination | Not Available |
| Half life | Not Available |
| Clearance | Not Available |
| Toxicity | Overdose symptoms include nausea, emesis (vomiting), hypotension, hypoventilation, dyspnea (shortness of breath), and syncope (fainting) |
No comments:
Post a Comment