Stimulants acute effects

One feature of the response to oxidants (in particular, ozone) that has stimulated considerable interest is the apparent development of tolerance to the acute effects of short-term exposure to these agents in laboratory animals. Fairchild reviewed possible mechanisms of this phenomenon. Tolerance has been defined as the increased capacity of an organism that has been pre-exposed to oxidant to resist the effects of later exposures to ordinarily lethal (or otherwise injurious) doses of the same agent or of different agents (cross-tolerance) with similar toxicologic properties. 

The acute effects of psychomotor stimulant overdoses are related to their CNS stimulant properties and may include euphoria, dizziness, tremor, irritability, and insomnia. At higher doses, convulsions and coma may ensue. These drugs are cardiac stimulants and may cause headache, palpitation, cardiac arrhythmias, anginal pain, and either hypotension or hypertension. Dextroamphetamine produces somewhat less cardiac stimulation. Chronic intoxication, in addition to these symptoms, commonly results in weight loss and a psychotic reaction that is often diagnosed as schizophrenia. 

The effects of LSD may be observed for 8 hours. The specific acute effects of a drug like LSD include euphoria, depersonalization, enhanced awareness of sensory input, alterations in the perception of time or space or body image, and to some extent, minor stimulant effects. Sometimes the dreamlike quality of the experience produces relaxation, good humor, and a sense of wonder or euphoria. 

Recent investigations into intracellular events have begun to define the postsynaptic events through which TCAs appear to exert their effects (Morinobu et ah, 1995). One of the observations made was down-regulation of transcription factors for early gene products such as c-Fos. C-Fos is normally produced in response to periods of stress. In research with rats, TCAs as well as other antidepressants have been shown to decrease the expression of c-Fos in areas of frontal cortex after chronic but not acute treatment. Other psychotropic medications (e.g., cocaine and haloperidol) with similar acute effects on norepinephrine/serotonin neurotransmission have not shown this same chronic effect. It has been speculated that the decreased production of c-Fos is the end product of a cascade of events stimulated by increased norepinephrine levels (Morinobu et ah, 1995). 

Newhouse PA, Potter A, Corwin J, et al Acute nicotinic blockade produces cognitive impairment in normal humans. Psychopharmacology 108 480-484, 1992a Newhouse PA, Penetar D, Fertig J Stimulant drug effects after prolonged total sleep deprivation a comparison of amphetamine, nicotine, and deprenyl. Mil Psychol 4 207-234, 1992b... 

The use of rumble strips on highways to prevent sleepiness-related accidents represents the clearest example of society adapting a countermeasure. Rumble strips combine multiple stimuli (i.e., noise, cutaneous stimulation) in an attempt to arouse the driver and prevent accidents. Like the other countermeasures discussed, there is no question about its acute effectiveness. There is a decrease in accidents proximal to the rumble strip. However, a question remains about its overall efficacy. Some research has described a phenomenon called migration, the movement of accidents from the location of the rumble strips to other locations on the highway. The question yet to be resolved is whether rumble strips prevent accidents or merely postpone them. 

Acute exposure to high doses of lindane is known to cause CNS stimulation (usually developing within 1 hour), mental/motor impairment, excitation, clonic (intermittent) and tonic (continuous) convulsions, increased respiratory rate and/or failure, pulmonary edema, and dermatitis. Toxic symptoms in humans are more behavioral in nature (e.g., loss of balance, teeth grinding, and hyperirritability. Most acute effects in humans have been the result of accidental or intentional ingestion, although inhalation toxicity occurred (especially among children) when lindane was used in vaporizers. 

Hundreds of patients have received huge doses of atropine and scopolamine (up to 250 mg), sometimes given three times a week for up to 4 mo, and this form of therapy continues in Eastern Europe today. A chronic behavioral syndrome of toxicity appears unlikely, and single or even multiple exposures to the anticholinergic drugs used In the volunteers, frequently at low doses, are deemed Insufficient to stimulate a persistent toxic syndrome. Of course. Individual susceptibility to acute effects, which may trigger a long-term effect, cannot be excluded. 

In addition to its acute effects on contractile function of vascular and cardiac muscle, ET-1 influences cell growth, proliferation and migration. ET-1 stimulates DNA synthesis, as indicated by increased H-thymidine uptake [31-33], stimulates cellular Na /H exchange [33] and increases the expression of the proto-oncogenes, c-fos and c-myc [31] in vascular smooth muscle cells. ET-1 also induces cardiac gene expression [34]. 

The Coca Leaf Early Use of Cocaine The Amphetamines Cocaine Epidemic II The Return of Meth Pharmacokinetics of Stimulants Mechanism of Stimulant Action Acute Effects at Low and Moderate Doses... 

Nicotine is classified as a stimulant drug, but people who use it often report decreased arousal. That is, the perception is that nicotine has a calming effect, and nicotine users find this effeet reinforcing (Todd, 2004). The reasons for this perception of lowered arousal are complex. One factor may be nicotine s acute effect of relaxing the skeletal muscles (see Table 7.5 also see Jones, 1987b). Another pharmacological reason is nicotine s biphasic action at higher doses its effects are more depressant. 

Nicotine s acute effects involve the CNS and ANS. It tends to have stimulant effects at lower doses but more depressant effects at higher doses. 

The acute effects of caffeine include diuresis, stimulation of the heart and CNS, relaxation of smooth muscles, and stimulation of gastric acid. 

Recently Opmeer and Van Ree (33) have shown that the inhibition of the contractile response in the ileum which follows high-frequency stimulation and is presumably partially due to release of endogenous opiates (38) is also antagonized by increased Ca + concentrations. However, Opmeer and Van Ree also found that in vitro tolerance development was not affected when strips were incubated in Ca + free buffer containing EGTA. Thus it was proposed that although Ca + appears to be involved in the acute effects of opiates on the guinea pig ileum, it was much less important for In vitro tolerance development. 

Release of Aldosterone from the Adrenal Cortex Angll stimulates the zona glomerulosa of the adrenal cortex to increase the synthesis and secretion of aldosterone and also exerts permissive effects that augment responses to ACTH and K+. Increased output of aldosterone is elicited by concentrations of Angll that have little or no acute effect on blood pressure. Aldosterone acts on the distal and collecting tubules to cause retention of Na+ and excretion of K+ and H+. Angll-induced stimulation of aldosterone synthesis is enhanced by hyponatremia or hyperkalemia. 

However, ethanol ingestion also has acute effects on liver metabolism, including inhibition of fatty acid oxidation and stimulation of triacylglycerol synthesis, leading to a fatty liver. It also can result in ketoacidosis or lactic acidosis and cause hypoglycemia or hyperglycemia, depending on the dietary state. These effects are considered reversible. 

A. PCP. In tablet form the usual street dose is 1-6 mg, which results in hallucinations, euphoria, and disinhibition. Ingestion of 6-10 mg causes toxic psychosis and signs of sympathomimetic stimulation. Acute ingestion of 150-200 mg has resulted in death. Smoking PCP produces rapid onset of effects and thus may be an easier route for users to titrate to the desired level of intoxication. 

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