Depressant effect

TrialkylPhosphates. Triethyl phosphate [78-40-0] C H O P, is a colorless Hquid boiling at 209—218°C containing 17 wt % phosphoms. It may be manufactured from diethyl ether and phosphoms pentoxide via a metaphosphate intermediate (63,64). Triethyl phosphate has been used commercially as an additive for polyester laminates and in ceHulosics. In polyester resins, it functions as a viscosity depressant as weH as a flame retardant. The viscosity depressant effect of triethyl phosphate in polyester resins permits high loadings of alumina trihydrate, a fire-retardant smoke-suppressant filler (65,66). 

Geriatric factors a variety of factors, both pharmacokinetic and pharmacodynamic, that contribute to variable dmg responses in the elderly. These responses are not seen for every class of dmg. Thus, the depressant effects of the glycosides also appear to increase with aging (116,117). 

Nitrous oxide produces respiratory depression (38,39). It has been shown to produce a direct myocardial depressant effect in dogs (40) and in humans breathing a 40% N2O/60% oxygen mixture (41) however, this may be offset by the activation of the sympathetic nervous system (42). The combination of nitrous oxide and opioids can produce decreases in myocardial contractiHty, heart rate, and blood pressure (43). 

Overexposure to tetrachloroethylene by inhalation affects the central nervous system and the Hver. Dizziness, headache, confusion, nausea, and eye and mucous tissue irritation occur during prolonged exposure to vapor concentrations of 200 ppm (15). These effects are intensified and include incoordination and dmnkenness at concentrations in excess of 600 ppm. At concentrations in excess of 1000 ppm the anesthetic and respiratory depression effects can cause unconsciousness and death. A single, brief exposure to concentrations above 6000 ppm can be immediately dangerous to life. Reversible changes to the Hver have been reported foUowing prolonged exposures to concentrations in excess of 200 ppm (16—22). Alcohol consumed before or after exposure may increase adverse effects. 

Fused isoxazoles (631) were prepared as GABA analogs (75MI41604) and some exhibited CNS depression effects (74JAP(K)7480062) or were effective as minor tranquilizers, muscle relaxants and/or sleep inducers (76USP3966748, 79USP4163057). 

Both Cushny and Dale found the amorphous gelsemium alkaloids represented by such fractions as gelseminine much more active than gelsemine. Cushny stated that gelseminine resembled coniine in action and showed a greater depressant effect on the central nervous system, but unlike coniine it exerted no pressor effect. It was also a powerful mydriatic. Dale found that 0-001 gm. of the hydrochlorides of the amorphous alkaloids injected into rabbits caused death from respiratory failure in 25 minutes, preceded by convulsions. These results are explained by the subsequent isolation from such amorphous fractions, of the potent alkaloids sempervirine and gelsemicine. 

VMATs are irreversibly inhibited by the potent antihypertensive drug reserpine. The depressive effects of reserpine helped to formulate the original monoamine hypothesis of affective disorders. Reseipine also appears to interact with the transporters near the site of substrate recognition. Tetrabenazine, which is used in treatment of movement disorders, inhibits VMAT2 much more potently than VMAT1, consistent with the less hypotensive action of this agent. 

Drug that counteract the effects of the narcotic analgesics are the narcotic antagonists. These drugp compete with the narcotics at the receptor sites and are used to reverse the depressant effects of the narcotic analgesics. Both types of drug are discussed in this chapter. 

Respiratory-depressant effects on respiratory rate (caused by a reduced sensitivity of the respiratory center to carbon dioxide)... 

The risk of respiratory depression is a concern for many nurses administering a narcotic and may cause some nurses to hesitate to administer the drug. However, respiratory depression rarely occurs in patients using a narcotic for pain. In fact, these patients usually develop tolerance to the respiratory depressant effects of the drug very quickly. Naloxone (see Chap. 20) can be administered to reverse the narcotic effects if absolutely necessary. 

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. 

There is an increased risk of toxicity of MTX when administered with the NSAIDs, salicylates, oral antidiabetic drugs, phenytoin, tetracycline, and probenecid. There is an additive bone marrow depressant effect when administered with other drug known to depress the bone marrow or with radiation therapy. There is an increased risk for nephrotoxicity when MTX is administered with other drug that cause nephrotoxicity. When penicillamine is administered with digoxin, decreased blood levels of digoxin may occur. There is a decreased absorption of penicillamine when the dmg is administered with food, iron preparations, and antacids. 

The barbiturates are contraindicated in patients with known hypersensitivity to the drugs. The barbiturates are used cautiously in patients with liver or kidney disease and those with neurological disorders. The barbiturates (eg, phenobarbital) are used with caution in patients with pulmonary disease and in hyperactive children. When barbiturates are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. See Chapter 26 for additional information on the barbiturates. 

Pregnancy Category C drug and is used with caution during pregnancy. As with all anticonvulsants, when the succinimides are used with other CNS depressants (eg, alcohol, narcotic analgesics, and antidepressants), an additive CNS depressant effect may occur. 

Other central nervous system (CNS) depressants and alcohol may cause additive depressant effects when administered with antitussives containing codeine. 

Some adverse reactions are desirable, for example, the depressing effect of certain antineoplastic drugs on the bone marrow because this adverse drag reaction is essential in the treatment of the leukemias. Other adverse reactions are not desirable, for example, severe vomiting or diarrhea. 

Plasma digoxin levels may decrease when the drug is administered with bleomycin. When bleomycin is used witii cisplatin, there is an increased risk of bleomycin toxicity Pulmonary toxicity may occur when bleomycin is administered with other antineoplastic drugs. Plicamycin, mitomycin, mitoxantrone, and dactino-mycin have an additive bone marrow depressant effect when administered with other antineoplastic drugs. In addition, mitomycin, mitoxantrone, and dactinomycin decrease antibody response to live virus vaccines. Dactinomycin potentiates or reactivates skin or gastrointestinal reactions of radiation therapy There is an increased risk of bleeding when plicamycin is administered witii aspirin, warfarin, heparin, and the NSAIDs. 

Additive bone marrow depressive effects occur when the miotic inhibitor drugs are administered with other anti-neoplastic dragp or radiation therapy. Administration of vincristine with digoxin results in a decreased therapeutic effect of tlie digoxin and decreased plasma digoxin levels. There is a decrease in serum concentrations of phenytoin when administered widi vinblastine... 

When an antineoplastic drug has a depressing effect on the bone marrow, laboratory tests, such as a complete blood count, are ordered to determine the effect of... 

The nurse reviews the results of all laboratory tests at the time they are reported. The primary health care provider is notified of the results before the administration of successive doses of an antineoplastic drug. If these tests indicate a severe depressant effect on the bone marrow or other test abnormalities, the primary health care provider may reduce the next drug dose or temporarily stop chemotherapy to allow the affected body systems to recover. 

Dohrn CS, Lichtor JL, Finn RS, et al Subjective and psychomotor effects of nitrous oxide in healthy volunteers. Behav Pharmacol 3 19-30, 1992 Dohrn CS, Lichtor JL, Coalson DW, et al Reinforcing effects of extended inhalation of nitrous oxide in humans. Drug Alcohol Depend 31 263-280, 1993 Evans AC, Raistrick D Phenomenology of intoxication with toluene-based adhesives and butane gas. Br J Psychiatry 130 769-773, 1987 Evans EB, Balster RL CNS depressant effects of volatile organic solvents. Neurosci Biobehav Rev 13 233—241, 1991... 

Alcohol can affect the metabolism of trichloroethylene. This is noted in both toxicity and pharmacokinetic studies. In toxicity studies, simultaneous exposure to ethanol and trichloroethylene increased the concentration of trichloroethylene in the blood and breath of male volunteers (Stewart et al. 1974c). These people also showed "degreaser s flush"—a transient vasodilation of superficial skin vessels. In rats, depressant effects in the central nervous system are exacerbated by coadministration of ethanol and trichloroethylene (Utesch et al. 1981). 

Rubinstein HS, Painter E, Hame OG. 1939. Neural depressing effect of trichloroethylene. J Lab Clin Med 1238-1241. 

These opposing effects of tryptamine and 5-HT are also seen when they are applied directly to cortical neurons by iontophoresis. Tryptamine is predominantly depressant while 5-HT is mainly excitatory. Surprisingly, the 5-HT antagonist metergoline is more effective against tryptamine and the depressant effects. When the medial Raphe nucleus... 

Figure 15.2(b) A schematic presentation of possible basal ganglia circuitry in Parkinson s disease. In PD there is little or no inhibitory nigrostriatal input to the striatum so the Ind Path is active and GPext is inhibited. This will then have less depressant effect on the SThN which will be free to drive the GPint (and SNr) and so reduce cortico-thalamic traffic and produce akinesia. See text for detail. Pathway activity — low — normal — high... 

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