Brain inhalant effects

Amyl nitrite is rapidly absorbed into the blood stream and quickly reaches the brain, with effects usually beginning five to 10 seconds after inhaling. The initial effects are often referred to as a rush or head rush and last from two to five minutes. It causes the walls of blood vessels to relax, resulting in lowered blood pressure. This increases pulse rate because the heart is beating faster than usual to restore normal blood pressure. It also causes facial flushing and dizziness. The dilation of blood vessels in the brain appears to trigger an increase in pressure in the brain, which may give rise to the euphoria reportedly experienced by users. Amyl nitrite also causes muscles to involuntarily relax. Adverse reactions include skin and throat irritation, nausea, and headache. 

HUMAN TOXICITY DATA oral-human LDLo 50mg/kg inhalation-human TCLo 200 ppm toxic effect central nervous system, blood effects, brain inhalation-man TCLo 100 ppm toxic effect central nervous system eye-human 300 ppm. 

In other applications of CT, orally administered barium sulfate or a water-soluble iodinated CM is used to opacify the GI tract. Xenon, atomic number 54, exhibits similar x-ray absorption properties to those of iodine. It rapidly diffuses across the blood brain barrier after inhalation to saturate different tissues of brain as a function of its lipid solubility. In preliminary investigations (99), xenon gas inhalation prior to brain CT has provided useful information for evaluations of local cerebral blood flow and cerebral tissue abnormalities. Xenon exhibits an anesthetic effect at high concentrations but otherwise is free of physiological effects because of its nonreactive nature. 

Toluene, volatile nitrites, and anesthetics, like other substances of abuse such as cocaine, nicotine, and heroin, are characterized by rapid absorption, rapid entry into the brain, high bioavailability, a short half-life, and a rapid rate of metabolism and clearance (Gerasimov et al. 2002 Pontieri et al. 1996, 1998). Because these pharmacokinetic parameters are associated with the ability of addictive substances to induce positive reinforcing effects, it appears that the pharmacokinetic features of inhalants contribute to their high abuse liability among susceptible individuals. 

Rea TM, Nash JF, Zabik JE, et al Effects of toluene inhalation on brain biogenic amines in the rat. Toxicology 31 143-1450, 1984 Rebert CS, Matteucci MJ, Pryor GT Acute electrophysiologic effects of inhaled toluene on adult male Long-Evans rats. Pharmacol Biochem Behav 33 157—165, 1989 Reynolds JEF Martindale The Extra Pharmacopoeia, 28th Edition. London, Pharmaceutical Press, 1982, pp 745-746... 

Yanagita T, Takahashi S, Ishida K, et al Voluntary inhalation of volatile anesthetics and organic solvents by monkeys. Jpn J Clin Pharmacol 1 13—16, 1970 Yavich L, Zvartau E A comparison of the effects of individual organic solvents and their mixture on brain stimulation reward. Pharmacol Biochem Behav 48 661— 664, 1994... 

Savolainen H, Pfaffli P, Tengen M, et al. 1977. Trichloroethylene and 1,1,1- trichloroethane Effects on brain and liver after five days intermittent inhalation. Arch Toxicol 38 229-237. 

Respiratory Effects. In most case reports of acute accidental exposure to hydrogen sulfide and occupational studies, exposure concentrations and duration were not reported. However, acute inhalation exposure to >500 ppm hydrogen sulfide is considered to result in respiratory failure. Death is often the result of respiratory depression as a result of the action of hydrogen sulfide on the respiratory center in the brain. Respiratory distress was reported in 2 workers exposed to >40 ppm hydrogen sulfide for... 

Pharmacologically, carbofuran inhibits cholinesterase, resulting in stimulation of the central, parasympathetic, and somatic motor systems. Sensitive biochemical tests have been developed to measure cholinesterase inhibition in avian and mammalian brain and plasma samples and are useful in the forensic assessment of carbamate exposure in human and wildlife pesticide incidents (Bal-lantyne and Marrs Hunt and Hooper 1993). Acute toxic clinical effects resulting from carbofuran exposure in animals and humans appear to be completely reversible and have been successfully treated with atropine sulfate. However, treatment should occur as soon as possible after exposure because acute carbofuran toxicosis can be fatal younger age groups of various species are more susceptible than adults (Finlayson et al. 1979). Carbofuran labels indicate that application is forbidden to streams, lakes, or ponds. In addition, manufacturers have stated that carbofuran is poisonous if swallowed, inhaled, or absorbed through the skin. Users are cautioned not to breathe carbofuran dust, fumes, or spray mist and treated areas should be avoided for at least 2 days (Anonymous 1971). Three points are emphasized at this juncture. First, some carbofuran degradation... 

Both oral and inhalation exposures to high concentrations of hexachloroethane were associated with hyperactivity, ataxia, convulsions, and/or prostration in rats, sheep, and dogs. The mechanism for these neurological effects is not clear since there were no apparent histopathological lesions in the brains of the affected animals. Neurological effects were only noted with the high-dose exposures. 

To confirm their results and check for methodological problems, some studies have been carried out. As there was a probability that hypothermic conditions during temporary removal from dam may have affected the results, Pauluhn and Schmuck administered S-bioallethrin and deltamethrin to neonatal mice from postnatal day 10 to 16 under a hypo-, normo-, or hyperthermic environment, and measured the MAChR density at the age of 17 days [51]. Increase in MAChR in Cortex at PND 17 in animals treated with S-bioallethrin was observed. Meanwhile, no changes were observed in animals treated with deltamethrin. In addition, an enormous influence of environmental temperature on the density of MAChR receptors in the crude synaptosomal fraction of the cerebral cortex was ascertained. Tsuji et al. exposed mouse dams with their litters to D-allethrin by inhalation for 6 h from postnatal day 10 to 16. The inhalation administration method is the most relevant route of exposure for humans, including babies and infants, after indoor use of D-allethrin. The neonatal exposure to D-allethrin by inhalation did not induce effects either on the brain MAChR density or motor activity at 17 days and 4 months of age, or on performance in the leaming/memory test at 11 months of age [52]. Other unpublished studies with D-allethrin, S -bioallethrin, or deltamethrin were examined to confirm the results of Eriksson et al. and showed inconsistent results [53]. The reasons for discrepancy among these findings are unknown. 

An effect on blood pressure was shown in the study by Clark and Litchfield (1969) in which subcutaneous injections of PGDN to anesthetized rats at 5, 10, 20, 40, 80, or 160 mg/kg resulted in a dose-related fall in mean arterial blood pressure (measured in the cannulized femoral artery) within 30 min with recovery over the next 12 h. The maximum drop in blood pressure correlated with the maximum concentration of PGDN in the blood. However, a drop in blood pressure did not occur in human volunteers who inhaled 0.5 ppm PGDN for 7.3 h. Rather, a mean elevation of diastolic blood pressure of 12 mm Hg was associated with severe and throbbing headaches (Stewart et al. 1974). A drop in blood pressure and decreasing stroke volume can result in brain ischemia, causing the dizziness and weakness reported by one subject after exposure at 0.5 ppm for 6 h in the Stewart et al. (1974) study as well as in occupationally exposed workers (Horvath et al. 1981). 

---