Stimulants of central nervous system

Caffeine is a powerful stimulant of central nervous system and also stimulates the cardiac muscle. However, high amounts of the alkaloid have noticeable irritation of gastrointestinal tract as well causes matw unwanted effects [1]. 

Symptoms of exposure Irritation of eyes, nose, and throat. May cause diarrhea, stimulation of central nervous system, tremor, and convulsions (Patnaik, 1992). 

Health Hazards Information - Recommended Personal Protective Equipment Protective goggles, gloves Symptoms Following Exposure Irritation of mucous membranes and stimulation followed by depression of central nervous system. Breathing of vapor may also cause dizziness, headache, and in... 

Discuss ways to promote an optimal response to drug therapy, how to manage common adverse drug reactions, and important points to keep in mind when educating patients about the use of central nervous system stimulants. 

Examples of the xanthine derivatives (drag that stimulate the central nervous system [CNS] resulting in bronchodilation, also called methylxanthines) are theophylline and aminophylline. Additional information concerning the xanthine derivatives is found in the Summary Drag Table Bronchodilators. 

Clinical signs and symptoms of toxicity are related to the overstimulation of muscarinic, nicotinic, and central nervous system receptors in the nervous system. Muscarinic receptors are those activated by the alkaloid drug muscarine. These receptors are under the control of the parasympathetic nervous system, and their hyperactivity results in respiratory and gastrointestinal dysfunction, incontinence, salivation, bradycardia, miosis, and sweating. Nicotinic receptors are those activated by nicotine. Hyperactivity of these receptors results in muscle fasciculations even greater stimulation results in blockade and muscle paralysis (Lefkowitz et al. 1996 Tafliri and Roberts 1987). Hyperactivity of central nervous system receptors results in the frank neurological signs of confusion, ataxia, dizziness, incoordination, and slurred speech, which are manifestations of acute intoxication. Muscarine and nicotine are not... 

Similar signs of central nervous system stimulation were observed following exposure to doses of endosulfan as low as 48 mg/kg/day (females) and 81 mg/kg/day (males) during a 6-hour/day, 5-day/week, 30-day exposure period (Hoechst 1985c, 1985d). Diffuse edema was also observed in the brains of males at the 81-mg/kg/day exposure level. However, daily application of up to 62.5 mg/kg/day (males) or... 

Stolerman, I.P., and D Mello, G.D. Role of training conditions in discrirnination of central nervous system stimulants by rats. Psychopharmacology (Berlin) 73 295-303, 1981. 

Angrist B (1987). Clinical effects of central nervous system stimulants A selective update. In J Engel and L Oreland (eds), Brain Reward Systems and Abuse. Raven Press, New York. 

Hayashi, H., Campenot, R. B., Vance, D. E. and Vance, J. E. Glial lipoproteins stimulate axon growth of central nervous system neurons in compartmented cultures. J. Biol. Chem. 279 14009-14015,2004. 

Derivative 47 and related compounds proved to stimulate the central nervous system <1997H(44)117>, and the unprotected derivatives of 53 showed fungicidal activity <1999MI511>. 

Although a great many deaths have occurred from accidental, intentional, or occupational exposures to HCN, in only a few cases are specific exposure concentrations known. In a review of human fatalities (ATSDR 1997), it was stated that exposure to airborne concentrations of HCN at 180 to 270 ppm were fatal, usually within several minutes, and a concentration of 135 ppm was fatal after 30 min. The average fatal concentration for humans was estimated at 546 ppm for 10 min. The latter data point is based on the work of McNamara (1976), who considered the resistance of man to HCN to be similar to that of the goat and monkey and four times that of the mouse. Fatal levels of HCN cause a brief period of central nervous system stimulation followed by depression, convulsions, coma with abolished deep reflexes and dilated pupils, and death. Several review sources, such as Dudley et al. (1942),... 

As for the indole alkaloids harmaline and harmine (Fig. 4), their biosynthesis was stimulated in emhryogenic callus of T. terrestris at concentrations of 66.4 0.5 and 82.7 0.6 /rg/g dw, respectively." Harmaline stimulates the central nervous system while harmine is cytotoxic to human leukemia cell lines HL-60 and K562. 

Dextroamphetamine is a powerful stimulant of the nervous system that manifests its effects by releasing dopamine and norepinephrine from presynaptic nerve endings, thus stimulating central dopaminergic and noradrenergic receptors. In certain doses it strengthens the excitatory process in the CNS, reduces fatigue, elevates mood and the capacity to work, reduces the need for sleep, and decreases appetite. 

The principal xanthines of medical interest include caffeine, theophylline and aminophylline. Caffeine is synthesized by several plants and was originally isolated from tea in 1838. It is a methylxanthine (Figure 1.12) which stimulates the central nervous system, increasing mental alertness. It also acts as a diuretic and stimulates gastric acid secretion. It is absorbed upon oral administration and is frequently included in drugs containing an analgesic, such as aspirin or paracetamol. 

Head trauma, meningitis, childhood fevers, brain tumors, and degenerative diseases of the cerebral circulation are conditions often associated with the appearance of recurrent seizures that may require treatment with anticonvulsant drugs. Seizures also may be a toxic manifestation of the action of central nervous system (CNS) stimulants and certain other drugs. Seizures often occur in hyperthermia (febrile seizures are very common in infants) sometimes in eclampsia, uremia, hypoglycemia, or pyridoxine deficiency and frequently as a part of the abstinence syn-... 

Mechanism of Action An isoindole that stimulates the central nervous system and primarily exerting its effect on the limbic system. Therapeutic Effect Stimulates the hypothalamus to reduce appetite. 

Mecfianism of Action A phenylalkylamine sympathomimetic with activity similar to amphetamines that stimulates the central nervous system (CNS) and elevates blood pressure (BP) most likely mediated via norepinephrine and dopamine metabolism. Causes stimulation of the hypothalamus. Therapeutic Effect Decreases appetite. Pharmacokinetics The pharmacokinetics of phendimetrazine tartrate has not been well established. Metabolized to active metabolite, phendimetrazine. Excreted in urine. Half-life 2-4 hr. 

Despite the documented efficacy and safety of the psychostimulants, their mechanism of action is not fully understood. Stimulants affect central nervous system (CNS) dopamine (DA) and norepinephrine (NE) pathways crucial in frontal lobe function. The stimulants act by causing release of catecholamines from the DA axons and blocking their reuptake. Methylphenidate releases catecholamines from long-term stores, so its effects can be blocked by pretreatment with reserpine. Amphetamines, on the other hand, release catecholamines from recently formed storage granules near the surface of the presynaptic neuron, so their action is not blocked by reserpine. In addition, the stimulants bind to the DA transporter in striatum (see Figures 2.6 and 2.7) and block the reuptake of both DA and NE. This action reduces the rate that catecholamines are removed from the synapse back into the axon and leads... 

These are the group of drugs which are used to stimulate the central nervous system. Some of them are also known as analeptics, but they are not much useful clinically due to non-selectivity of action. 

Castells X, Casas M, Vildal X, Bosch R, Roncero C, Ramos-Quiroga JA Capella D (2007) Efficacy of central nervous system stimulant treatment for cocaine dependence a systematic review and meta-analysis of randomized controlled clinical trials. Addiction, 102, 1871-87 Chaisson RE, Bacchetti P, Osmond D, Brodie B, Sande MA Moss AR (1989). Cocaine use and HIV infection in intravenous drug users in San Francisco. Journal of the American Medical Association, 261, 561-5 Chapleo CB Walter DS (1997). The bupre-norphine-naloxone combination product. Research and Clinical Forums, 19, 55-8 Cheskin LJ, Fudala PJ Johnson RE (1994). A controlled comparison of buprenorphine and clonidine for acute detoxification from opioids. Drug and Alcohol Dependence, 36, 115-21... 

A number of antidepressants do not fit neatly into the other classes. Among these are bupropion,mirtazapine, amoxapine, and maprotiline (Figure 30-5). Bupropion has a unicyclic aminoketone structure. Its unique structure results in a different side-effect profile than most antidepressants (described below). Bupropion somewhat resembles amphetamine in chemical structure and like the stimulant, has central nervous system (CNS) activating properties. 

Amphetamines stimulate the central nervous system (CNS), producing feelings of euphoria, providing relief from fatigue, and increasing alertness. CNS stimulation provoked by amphetamines can also intensify emotions, increase aggression, and alter self-esteem. 

Because it stimulates the central nervous system, dextroamphetamine fights mental fatigue. The drug can also improve mood and give users a sense of power, euphoria, and well-being. With chronic use, however, it may cause obsessive thoughts and feelings of paranoia, anxiety, hypersensitivity—and, in extreme cases, psychosis. 

In earlier decades, use of dinitrophenol dropped as dieters discovered amphetamine, a medication developed in 1887. Amphetamine stimulates the central nervous system, which can reduce a person s appetite. Caffeine, which is found in beverages like coffee, is a weak stimulant. During the twentieth century, dieters would drink coffee and take amphetamines to lose weight. 

This toxicity may be partially caused by direct effects on the gastrointestinal tract but is also the result of central nervous system actions, including chemoreceptor trigger zone stimulation. 

B. Caddy, F. Fish, and D. Scott, Chromatographic screening for drugs of abuse using capillary columns, part 1, comparison of open tubular columns and support coated open tubular columns for the analysis of central nervous system stimulant drugs, Chro-matographia, 6 251 (1973). 

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