Dopamine dosage

Taper the dopamine dosage before discontinuing the drug because abrupt cessation of dopamine therapy may result in marked hypotension... 

Levodopa is a chemical formulation found in plants and animals that is converted into dopamine by nerve cells in the brain. Levodopa does cross die blood-brain barrier, and a small amount is dien converted to dopamine. This allows the drug to have a pharmacologic effect in patients witii Parkinson s disease (Pig. 29-1). Combining levodopa witii another drug (carbidopa) causes more levodopa to reach die brain. When more levodopa is available, the dosage of levodopa may be reduced. Carbidopa has no effect when given alone. Sinemet is a combination of carbidopa and levodopa and is available in several combinations (eg, Sinemet 10/100 has 10 mg of carbidopa and 100 mg of levodopa Sinemet CR is a time-released version of die combined drugs). 

There is an increased risk of CNS depression when tiie dopamine receptor agonists are administered witii otiier CNS depressants. When administered witii levodopa, the dopamine receptor agonists increase the effects of levodopa (a lower dosage of levodopa may be required). hi addition, when the dopamine receptor agonists are administered with levodopa, there is an increased risk of hallucinations. When administered witii ciprofloxacin, there is an increased effect of the dopamine receptor agonist. 

Disulfiram produces a variety of adverse effects, which commonly include drowsiness, lethargy, and fatigue (Chick 1999). Other more serious adverse effects, such as optic neuritis, peripheral neuropathy, and hepatotoxicity, are rare. Psychiatric effects of disulfiram are also uncommon. They probably occur only at higher dosages of the drug and may result from the inhibition by disulfiram of a variety of enzymes in addition to ALDH. Included among the enzymes inhibited by disulfiram is dopamine P-hydroxylase, inhibition of which increases dopamine levels, which in turn can exacerbate psychotic symptoms in patients with schizophrenia and occasionally may result in psychotic or depressive symptoms in patients without schizophrenia. 

In an attempt to simulate in rats the dosage regimen commonly employed by abusers of amphetamines, METH was administered (10 or 15 mg/kg every 6 hours four to six doses), after which the animals were killed (Koda and Gibb 1971 Koda and Gibb 1973). TH activity and catecholamine con-eentrations were measured in various brain regions and in the adrenal. Neostriatal TH aetivity was depressed in a dose-dependent manner and reaehed its nadir at 36 hours. Dopamine (DA) and norepinephrine concentrations were initially elevated, but then deereased in parallel with TH aetivity. Adrenal TH aetivity was elevated, presumably because of stress assoeiated with the toxie doses of METH. 

Benzodiazepines and barbiturates are self-administered by animals (Koob, 1992). Unlike other rewarding drugs, these are not believed to release dopamine from the nucleus accumbens or prefrontal cortex (Nutt, 1996 Di Chiara Im-perato, 1988 Spanagel Weiss, 1999). However, it is possible that they do so when used for euphoric effects in the high dosages used by benzodiazepine abusers (Strang et al., 1993). 

Levodopa + carbidopa (Sinemet) Carbidopa inhibits peripheral metabolism of levodopa to dopamine and reduces required dosage and toxicity. Carbidopa does not enter CNS. 

Substituted benzamides include metodopramide (discussed previously) and trimethobenzamide. Their primary mechanism of antiemetic action is believed to be dopamine-receptor blockade. Trimethobenzamide also has weak antihistaminic activity. For prevention and treatment of nausea and vomiting, metodopramide may be given in the relatively high dosage of 10-20 mg orally or intravenously every 6 hours. The usual dose of trimethobenzamide is 250 mg orally, 200 mg rectally, or 200 mg by intramuscular injection. The principal adverse effects of these central dopamine antagonists are extrapyramidal restlessness, dystonias, and parkinsonian symptoms. 

The hypericin fraction was initially reported to have MAO-A and -B inhibitor properties. Later studies found that the concentration required for this inhibition was higher than that achieved with recommended dosages. In vitro studies using the commercially formulated hydroalcoholic extract have shown inhibition of nerve terminal reuptake of serotonin, norepinephrine, and dopamine. While the hypericin constituent did not show reuptake inhibition for any of these systems, the hyperforin constituent did. Chronic administration of the commercial extract has also been reported to significantly down-regulate the expression of cortical 13 adrenoceptors and up-regulate the expression of serotonin receptors (5-HT2) in a rodent model. 

As noted, vitamin C is needed for the production of collagen in the body, but it is also essential in the production of certain hormones such as dopamine and adrenaline. Ascorbic acid is also essential in the metabolism of some amino acids. It helps protect cells from free radical damage, helps iron absorption, and is essential for many metabolic processes. The dietary need of vitamin C is not clearly established, but the U.S. National Academy of Science has established a recommended dietary allowance (RDA) of 60 mg per day. Some groups and individuals, notably Linus Pauling in the 1980s, recommend dosages as high as... 

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