Anesthetics behavior

Fire Hazards - Flash Point (deg. F) -213 (approx.) CC Flammable Limits in Air (%) 2.75 - 28.6 Fire Extinguishing Agents Stop flow of gas if possible. Use carbon dioxide, dry chemical, water fog Fire Extinguishing Agents Not To Be Used Not pertinent Special Hazards of Combustion Products Vapors are anesthetic Behavior in Fire Container may explode Ignition Temperature (deg. F) 842 Electrical Hazard Class I, Group D Burning Rate 7.4 mm/min. 

AHopregnanolone and similar A-ring-reduced pregnanes potentiate GABA effects at these receptors. These steroids mimic the effects of the benzodiazepines, changing chloride ion conductance and producing sedative and hypnotic behavioral effects (276,277). Neuroactive steroids can be therapeutically useful as anticonvulsants, anxiolytics, or anesthetics (qv) (see also Hypnotics, sedatives, anticonvulsants, and anxiolytics). 

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

But there are those in my lab who believe that the excitation is being seen by a bias toward large cells and that they represent a large cell population in the neostriatum. I don t necessarily believe that. I don t know why, in the anesthetized animal, you can flip a nerve cell that is inhibited by amphetamine by increasing the dose. It has been postulated that the excitation is related to the occurrence of both the stereotyped behaviors, and that this may be provoked at doses that produce neurotoxicity. We have also done a number of studies looking at the neurotoxicity of amphetamine administration in animals, most of which replicate Lou Seiden s work. 

Phencyclidine (PCP), a dissociative anesthetic agent, which is subject to abuse, produces behavioral effects in man that frequently resemble schizophrenia (Luisada 1978). Manifestations of persistent psychopathology frequently remain after the acute effects of PCP have diminished. With PCP, subjects may display autistic and delusional thinking typical of schizophrenics (Luby et al. 1959). A more striking link between schizophrenia and PCP comes from observations of cases in which PCP was given to hospitalized schizophrenics (Luisada 1978). After receiving PCP, these patients showed extreme exacerbation of their psychoses the reaction persisted for up to 6 weeks. By contrast, LSD produced no more severe effects in schizophrenics than in normal subjects. 

Although PCP was developed as an anesthetic, its profile as an anesthetic is very different from typical general anesthetics of the CNS-depressant class (Domino 1964). Nonetheless, PCP has a number of behavioral and pharmacological effects similar to those of depressants such as the barbiturates (Balster and Wessinger 1983). PCP has profound motor effects, as evidenced by effects on rotorod performance and similar measures (Kalir et al. 1969 ... 

The hypothesis that HNO is not involved during NO-release from sydnonimines was confirmed by the study of NO-release from C78-0652 109, the dimethyl derivative of SIN-1A (Scheme 6.19). This product closely resembles SIN-1A in its biological and pharmacological behavior, showing a clear NO-dependent vasodilating effect on guinea pig pulmonary arteries and hypotensive action in anesthetized and conscious dog models [105]. 

Excess consumption of alcohol is not healthful, as many people will testify. Ethanol is a depressant and can be a mild tranquilizer or a general anesthetic, depending on how much is consumed over what period of time. At low doses, ethanol depresses some of the brain s inhibitory systems and acts as a social lubricant. It can also exacerbate seizure disorders such as epilepsy by depressing the inhibitory systems in the brain that suppress seizures and convulsions. At higher doses, alcohol leads to the classical symptoms of intoxication unsteady walk, slurred speech, altered sensory perception, slow reaction times, bizarre behavior, and finally, loss of consciousness. Consnmption of a fiffh of a gallon of hard liqnor over a short time period can be fatal. 

At the endocrinological level, the VNO mediates the surge of luteinizing hormone and testosterone in males after exposure to females. This surge does not occur if a male with deafiferentiated VNO is exposed to an anesthetized female or her urine (Wysocki etal., 1983). But VNO-deafferentiated males will show a surge in luteinizing hormone in response to awake females (Coquelin etal., 1984). In female mice, stimulation of the VNO by male urinary cues activates the limbic system (discussed in Ch. 8). The roles of the VNO in the behavior of some rodents are listed in Table 5.3. 

PCP receptor (NMDA charmel) GRINl Agonism Anesthetic properties, may induce psychosis (schizophrenia like). hallucination, delirium and disoriented behavior, may cause seizures, neurotoxicity. 

It is true that a more hydrophobic anesthetic is more potent, but not all hydrophobic substances are anesthetics. There exist substances such as 1,2-dichlorohexafluorocyclobutane and 2, 3-dichlorooctafluorobutane that would be predicted to be anesthetic based on their hydrophobicity, but that do not have anesthetic properties. These substances are called either non-anesthetics or non-immobilizers depending on the behaviors that have been tested and found lacking (Koblin et ak, 1994). 

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