Nitrous oxide nervous system

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). 

Toxicology. Nitrous oxide is an asphyxiant at high concentrations prolonged exposure has been associated with damage to the hematopoietic system, the central nervous system, and the reproductive system. 

Central nervous system toxicity from either social abuse of nitrous oxide or extremely heavy occupational exposure has been characterized by symptoms of numbness, paresthesias, impairment of equilibrium, and difficulty in concentration. In severe cases, the patient becomes incontinent, impotent, and unable to walk. Neurological signs include ataxic gait, muscle weakness, impaired sensation, and diminished reflexes. 

Inhaled (volatile) anesthetics potentiate the neuromuscular blockade produced by nondepolarizing muscle relaxants in a dose-dependent fashion. Of the general anesthetics that have been studied, inhaled anesthetics augment the effects of muscle relaxants in the following order isoflurane (most) sevoflurane, desflurane, enflurane, and halothane and nitrous oxide (least) (Figure 27-9). The most important factors involved in this interaction are the following (1) nervous system depression at sites proximal to the neuromuscular junction (ie, central nervous system) (2) increased muscle blood flow (ie, due to peripheral vasodilation produced by volatile anesthetics), which allows a larger fraction of the injected muscle relaxant to reach the neuromuscular junction and (3) decreased sensitivity of the postjunctional membrane to depolarization. 

The exact mechanism of action of most volatile substances remains unknown. Altered function of ionotropic receptors and ion channels throughout the central nervous system has been demonstrated for a few. Nitrous oxide, for example, binds to NMDA receptors and fuel additives enhance GABAa receptor function. Most inhalants produce euphoria increased excitability of the VTA has been documented for toluene and may underlie its addiction risk. Other substances, such as amyl nitrite ("poppers"), primarily produce smooth muscle relaxation and enhance erection, but are not addictive. With chronic exposure to the aromatic hydrocarbons (eg, benzene, toluene), toxic effects can be observed in many organs, including white matter lesions in the central nervous system. Management of overdose remains supportive. 

In cases of severe abuse, published studies have described chronic symptoms such as impairment of the nervous system, tingling and/or numbness of the hands and feet, and uncontrolled muscle twitching and movement. These side effects may be related to the depletion of vitamin B12 and folate caused by nitrous oxide abuse. They are usually reversible if nitrous use is stopped. 

Nitrous oxide, once commonly known as laughing gas, is used as an oxidant gas and in dental surgery as a general anesthetic. It is a central nervous system depressant and can act as an asphyxiant. 

People who breathe nitrous oxide for more than a few minutes at a time may experience nausea especially if they have just eaten. They may also feel hung over for some time after. Addiction to nitrous oxide is a real possibility. Addicts may suffer serious mood and personality changes in addition to the bone marrow and nervous system damage already mentioned. 

Nitrous oxide use has been associated with damage to the nervous system and in particular the spinal cord. Nitrous oxide deactivates vitamin Bj2, which is vital for making the sheath... 

Since nitrous oxide has some effects on the nervous system, it is not entirely surprising to note a further report that under experimental conditions it can affect memory. That memory changes can occur has been known for a long time, but the pattern of the effects now appears to be distinctly odd. 

Nervous System When administered alone, NjO can significantly increase cerebral blood flow and ICP. When nitrous oxide is coadministered with intravenous anesthetic agents, increases in cerebral blood flow are attenuated or abolished. When N O is added to a halogenated inhalational anesthetic, its vasodUatory effect on the cerebral vasculature is slightly reduced. 

Toxicity and irritant effects of nitrous oxide in humans are very low. It is an anesthetic. Inhalation of this gas at high concentrations can produce depression of the central nervous system, decrease in body temperature, and fall in blood pressure. The LC50 value of a 4-hour exposure in mice is in the range of 600 ppm. 

B. Chronic toxicity to the hematologic and nervous systems results from inactivation of vitamin following irreversible oxidation of its cobalt atom. Vitamin Bi2 is required for the synthesis of methionine, which is essential for DNA synthesis and maintenance of myelin. Use of nitrous oxide can precipitate neurological symptoms in patients with subclinical B,2 or folic acid deficiency. 

Nervous system A peripheral neuropathy associated with chronic nitrous oxide abuse has been reported [19 ]. 

Nitrous oxide s primary physiological effect is central nervous system (CNS) depression. At... 

Nitrous oxide s primary physiological effect is central nervous system (CNS) depression. At high concentrations, anesthetic levels can be obtained, but the low potency of nitrous oxide necessitates concomitant administration of other depressant drugs. Ni-... 

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