Isosorbiddinitrate

Author: Prof. Dr. med. Peter Altmeyer

All authors of this article

Last updated on: 29.10.2020

Dieser Artikel auf Deutsch

Synonym(s)

3,6-Bisnitrooxyhexahydrofuro[3,2-b]-furan (IUPAC); CAS number: 87-33-2; ISDN

Definition
This section has been translated automatically.

Isosorbide dinitrate (ISDN) is a drug with the molecular formula C6H8N2O8 for the treatment of angina pectoris or coronary sclerosis. It improves the oxygen supply to the myocardium and at the same time reduces oxygen consumption in the myocardium by reducing the so-called preload. Isosorbide mononitrate has an analogous effect.

Pharmacodynamics (Effect)
This section has been translated automatically.

Isosorbide dinitrate is a very fast but short-acting nitrate, which is therefore well suited for the treatment of an acute attack. After application in the oral cavity (e.g. in tablet or spray form) it takes effect after only a few minutes. The effect lasts for about one hour. The dilatation of veins and vessels reduces the preload of the heart (lowering the end-diastolic pressure). This improves the blood flow in the coronary vessels during diastole. Only in high, non-therapeutic doses do nitrates also have a slight arterial dilating effect.

You might also be interested in

Indication
This section has been translated automatically.

Acute treatment and prevention of angina pectoris (stage of coronary heart disease CHD caused by coronary sclerosis)

Acute left heart failure .

Coronary spasms (special form of angina pectoris, they are called prinzmetal angina after their discoverer).

Acute heart attack

Undesirable effects
This section has been translated automatically.

Headaches

Blood pressure drop

Flush

Skin irritation

Tolerance development

Contraindication
This section has been translated automatically.

Acute circulatory failure

Cardiogenic shock

Heart valve stenosis

Pronounced hypotension

Pregnancy and lactation

Preparations
This section has been translated automatically.

Isoket (D, A, CH), Isomack (A)

Note(s)
This section has been translated automatically.

All therapeutically applied nitrovasodilators develop their antiischemic efficacy uniformly via the same mechanism. They release radical NO (nitric oxide), albeit via different bioactivation pathways. This corresponds to the physiologically released "Endothelium Derived Relaxing Factor", in short EDRF, in healthy tissue. NO has the greatest relaxation effect where there is the greatest lack of physiological NO. Apparently there is an inverse correlation between the amount of NO formed, which is normally necessary for dilation, and the reaction to organic nitro compounds. Improvement of myocardial function and increase of oxygen supply to poorly perfused parts of the myocardium. NO activates guanylate cyclase. This increases the intracellular content of cGMP. This in turn lowers the cytosolic calcium concentration and thus causes the smooth muscle cells to relax. It is important to note that in vessels with altered endothelium, e.g. in arteriosclerosis, the release of EDRF is disturbed.

Tolerance development: All nitrate compounds from which nitric oxide (NO) is released enzymatically with the help of aldehyde dehydrogenase-2 are subject to tolerance development(glycerol trinitrate, ISMN). This tolerance decreases very quickly after weaning, a nitrate-free interval of 6-8 h is usually sufficient. The effectiveness in acute application is therefore not impaired.

NO is not released enzymatically from molsidomine. It is suitable for bridging the nitrate pause of other preparations. Cross-tolerances to the other nitrate compounds must also be taken into account.

Authors

Last updated on: 29.10.2020