The explosive power of nitroglycerin derives from detonation: energy from the initial decomposition causes a strong pressure wave that detonates the surrounding fuel. This is a self-sustained shock wave that propagates through the explosive medium at 30 times the speed of sound as a near-instantaneous pressure-induced decomposition of the fuel into a white-hot gas. Detonation of nitroglycerin generates gases that would occupy more than 1,200 times the original volume at ordinary room temperature and pressure. The heat liberated raises the temperature to about 5,000 °C (9,000 °F). This is entirely different from deflagration, which depends solely upon available fuel regardless of pressure or shock. The decomposition results in a much higher ratio of energy to gas moles released compared to other explosives, making it one of the hottest detonating high explosives. Manufacturing
Nitroglycerin can be produced by acid-catalyzed nitration of glycerol (glycerin). The industrial manufacturing process often reacts glycerol with a nearly 1:1 mixture of concentrated sulfuric acid and concentrated nitric acid. This can be produced by mixing white fuming nitric acid—a quite expensive pure nitric acid in which the oxides of nitrogen have been removed, as opposed to red fuming nitric acid, which contains nitrogen oxides—and concentrated sulfuric acid. More often, this mixture is attained by the cheaper method of mixing fuming sulfuric acid, also known as oleum—sulfuric acid containing excess sulfur trioxide—and azeotropic nitric acid (consisting of about 70% nitric acid, with the rest being water). The sulfuric acid produces protonated nitric acid species, which are attacked by glycerols nucleophilic oxygen atoms.
These agents all exert their effect by being converted to nitric oxide in the body by mitochondrial aldehyde dehydrogenase (ALDH2), and nitric oxide is a potent natural vasodilator. In medicine, nitroglycerin is probably most commonly prescribed for angina pectoris, a painful symptom of ischemic heart disease caused by inadequate flow of blood and oxygen to the heart and as a potent antihypertensive agent. Nitroglycerin corrects the imbalance between the flow of oxygen and blood to the heart and the heart’s energy demand. There are plenty of formulations on the market at different doses. At low doses, nitroglycerin dilates veins more than arteries, thereby reducing preload (volume of blood in the heart after filling); this is thought to be its primary mechanism of action. By decreasing preload, the heart has less blood to pump, which decreases oxygen requirement since the heart does not have to work as hard. Additionally, having a smaller preload reduces the ventricular transmural pressure (pressure exerted on the walls of the heart), which decreases the compression of heart arteries to allow more blood to flow through the heart. At higher doses, it also dilates arteries, thereby reducing afterload (decreasing the pressure against which the heart must pump). An improved ratio of myocardial oxygen demand to supply leads to the following therapeutic effects during episodes of angina pectoris: subsiding of chest pain, decrease of blood pressure, increase of heart rate, and orthostatic hypotension.