Central depressants

Benzodiazepines, especially lorazepam, are used to prevent and treat CINV.5,10 Lorazepam is thought to prevent input from the cerebral cortex and limbic system from reaching the central vomiting center in the brain stem.10 Sedation and amnesia are common side effects. Respiratory depression can occur with high doses or when other central depressants such as alcohol are combined with benzodiazepines. 

An elevated growth with a central depression that bleeds occasionally. This growth type increases in size rapidly. 

Morphine may be administered orally, intravenously, or epidurally. An advantage of epidural administration is that it provides effective analgesia while minimizing the central depressant effects associated with systemic administration. The mechanism of action with the epidural route of administration involves opioid receptors on the cell bodies of first-order sensory neurons in the dorsal root ganglia as well as their axon terminals in the dorsal hom. Stimulation of these receptors inhibits release of substance P and interrupts transmission of the pain signal to the second-order sensory neuron. 

The temperature patterns follow a transition from the more oceanic western area (milder temperatures) to the central depression (high temperatures in summer and intense cold and fog in winter). The northwest-southeast cold and dry wind ( cierzo ) is characteristic of the central depression of the Ebro basin, especially in spring. The cierzo at the middle Ebro valley (around Zaragoza) can lead to soil erosion and salt transport [17]. The wind intensity at this area is highly correlated with evapotranspiration [18]. A mild warm wind is sometimes occurring (especially in summer) following the opposite direction (southeast-northwest). 

A number of 1-benzazepine derivatives show a variety of biological activities. Among them, of particular interest are central depressant (12) [ 21 ], cardiotonic (16) [27], antiarrhythmic (17,18) [30, 36] and ACE-inhibitory (23,26) [52, 55] benzazepines. However none of them has yet reached the goal. The most promising agents are (28) [54, 57] and (30) [64], both ACE inhibitors are now undergoing clinical evaluation. 

Therapeutic doses of scopolamine produce CNS depression, characterized by drowsiness, amnesia, and dreamless sleep (Brown and Taylor 1996). It reduces arousal and increases the effort required to awaken (Parrott 1987). Higher therapeutic doses of atropine cause central excitation, characterized by restlessness, irritability, confusion, disorientation, hallucinations, and delirium. Larger doses produce central depression, paralysis, coma, and death by respiratory failure and cardiovascular collapse. 

Manolov P, Petkov VD, Ivancheva S. (1977). Studies on the central depressive action of methanol extract from Geranium macrorrhizum L. DokI Bolg Akad Nauk. 30(11) 1657-59. 

Central depressants and stimulants (e.g., analgesics, antipyretics, barbiturates)... 

There are some clinically important pharmacodynamic drug-drug interactions to be mentioned. Antipsychotics will potentiate the central depressant effects of sedatives and of alcohol. They will also increase the risk of respiratory-depressant effects of opiates. Inducers of drug metabolic enzymes like for example rifampicin and several antiepileptics, may increase the elimination rate of antipsychotic agents and thus decrease their efficacy. 

Mechanism of Action A central depressant whose exact mechanism is unknown. Many effects due to its central depressant actions. TherapeuticEffect Relieves pain or muscle spasms. 

Pre-anaesthetic medication These agents reduce the salivary and respiratory secretion and are administered half an hour before general anaesthesia. They also prevent laryngospasm. Atropine is given in combination with morphine as a preanaesthetic medication to antagonize the central depressant action of morphine on respiration. 

An excellent brief article on buprenorphine treatment has been provided by Taikato et al. (2005), which notes the common possible side-effects (headaches, nausea and vomiting, sweating, constipation, etc.) and drug interactions. The limited central depressant effect of buprenorphine may be compounded by alcohol and antidepressants, while the metabolism of buprenorphine can be enhanced by anticonvulsants, with therefore possibly reduced efficacy. There have been some case reports of liver toxicity from buprenorphine that is reversible if the medication is stopped (Herve et al. 2004), and often clinical guidelines will recommend that liver function tests are included in buprenorphine treatment, as they definitely should be with naltrexone. 

Adonis vernalis L. China Cymarol, corchoroside A, convallatoxin, adonilide, isoramanone, pergularin.33 This herb is toxic. Treat heart disease and central depression, diuretic. 

Toxic substances can interfere with normal neurotransmission in a variety of ways, either directly or indirectly, and cause various central effects. For example, cholinesterase inhibitors such as the organo phosphate insecticides cause accumulation of excess acetylcholine. The accumulation of this neurotransmitter in the CNS in humans after exposure to toxic insecticides leads to anxiety, restlessness, insomnia, convulsions, slurred speech, and central depression of the respiratory and circulatory centers. 

The cause of death is usually respiratory failure due partly to neuromuscular paralysis, central depression, and bronchoconstriction. 

The result of formate accumulation is metabolic acidosis. However, at later stages, the acidosis may also involve the accumulation of other anions such as lactate. This may be a result of inhibition of cytochrome oxidase and hence of mitochondrial respiration, tissue hypoxia due to reduced circulation of blood, or an increase in the NADH/NAD ratio. The acidosis that results from methanol poisoning will result in more formic acid being in the nonionized state and hence more readily able to enter the CNS. This will cause central depression and hypotension and increased lactate production. This situation is known as the "circulus hypoxicus."... 

Analgesic efficacy and clinical use Levallorphan (Leimgruber et al., 1973) is an opioid antagonist with a minor agonistic component and practically no analgesic action. It has been used as one of the first relative pure antagonists for the treatment of opioid overdose, to reverse opioid central depression and to antagonize opioid-induced respiratory impairment (Foldes et al., 1969). 

The metabolic effects of morphine are not marked and are clinically unimportant. The metaholic rale may be decreased slightly due to the lowered activity and tone of the skeletal muscles resulting front the central depression. A rise in blood sugar may be observed after the injection of... 

Benzodiazepines exert central depressant effects on spinal reflexes, in part mediated by the brainstem reticular system.3 For example, chlordiazepoxide depresses the duration of electrical after-discharge in the limbic system. Most benzodiazepines elevate the seizure threshold and therefore may be used as anticonvulsant medications. Diazepam, clonazepam, and clorazepate may be prescribed for this therapeutic purpose. 

Jacobson KA, Nikodijevic D, Shi D, Gallo-Rodriguez C, Olah ME, Stiles G, Daly JW (1993) A role for central Aj-adenosine receptors mediation of central depressant effects. FEBS Lett 336 57-60... 

Colchicine also exhibits a variety of other pharmacological effects. It lowers body temperature, increases the sensitivity to central depressants, depresses the respiratory center, enhances the response to sympathomimetic agents, constricts blood vessels, and induces hypertension by central vasomotor stimulation. It enhances gastrointestinal activity by neurogenic stimulation but depresses it by a direct effect, and alters neuromuscular function. 

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