It is a stimulant and the form I of caffeine is metastable. Zabot, in Green Sustainable Process for Chemical and Environmental Engineering and Science, 2020 3 Why extracting caffeine?Ĭaffeine (C 8H 10N 4O 2, molar mass of 194.1906 g/mol, also known as 1H-Purine-2,6-dione, 3,7-dihydro-1,3,7-trimethyl- or 1,3,7-trimethyl-2,6-dioxopurine) is a methylxanthine alkaloid found in several parts of plants, like beans, nuts, seeds, and leaves.
Caffeine is an adenosine receptor antagonist.Īpproximate caffeine content of common products Donovan and DeVane (2001): Chronic use of caffeine results not only in tolerance, but also in physical dependence, as reflected by the emergence of signs and symptoms of withdrawal upon the abrupt cessation of drug intake Holtzman (1990). The average world consumption of caffeine is 70 mg/person/day in the US it is 211 mg/person/day and in the United Kingdom it is 444 mg/person/day (highest in the world) Donovan and DeVane (2001). It is a natural constituent of more that 60 plant species and has been used for thousands of years for its stimulant effects. Bylund, in xPharm: The Comprehensive Pharmacology Reference, 2007 IntroductionĬaffeine is the most widely used and abused psychoactive drug in the world Donovan and DeVane (2001), Holtzman (1990).It is inexpensive, readily available, socially acceptable, and legal. Caffeine is also a mild diuretic, and it stimulates gastric acid secretion, respiration, and lipolysis.ĭavid B. Second, caffeine augments β2-effects and causes subsequent vasodilation with resulting hypotension.Ĭaffeine in overdose also acts as a nonselective antagonist of neuronal adenosine receptors that may lead to seizures. First, caffeine-induced tachydysrhythmias lead to inadequate filling of the heart and subsequent decrease in cardiac output. The hypotension that has been noted with overdoses of caffeine is due primarily to two mechanisms. Fourth, caffeine blocks cardiac adenosine receptors, which have been shown to be antiarrhythmic. This resulting increase in cytosolic calcium may provoke dysrhythmias. Caffeine both induces release of calcium from the sarcoplasmic reticulum and blocks calcium's reuptake into the sarcoplasmic reticulum. Third, caffeine increases myocardial intracellular calcium. Subsequently, β1-receptor effects are exaggerated and tachydysrhythmias are induced. The activity of cAMP is prolonged due to its decreased metabolism as phosphodiesterase is inhibited by caffeine. Stimulation of β1-receptors increases intracellular cAMP by G protein stimulation of adenylate cyclase. Increased circulating catecholamines after caffeine overdose increase β1-receptor stimulation. Second, caffeine inhibits phosphodiesterase.
First, caffeine increases circulating catecholamines. At least four mechanisms have been proposed for the pro-arrhythmic potential of caffeine in overdose.
Holstege, in Encyclopedia of Toxicology (Third Edition), 2014 Mechanism of ToxicityĬaffeine can have profound effects on the cardiovascular system.
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