Galaxy Gas Is Destroying Young Black Men

I was scraping to score N2O, and could only get the gas from the upright containers of Instant Whipped Cream...
Bit of a piss off actually.

Long time ago.

Medically - I have been quite ignorant on this subject.


https://en.wikipedia.org/wiki/Nitrous_oxide

When used chronically, nitrous oxide has the potential to cause neurological damage through inactivation of vitamin B12.

Inhalation of nitrous oxide is used frequently to relieve pain associated with childbirth, trauma, oral surgery and acute coronary syndrome (including heart attacks). Its use during labour has been shown to be a safe and effective aid for birthing women.[33] Its use for acute coronary syndrome is of unknown benefit.[34]

In Canada and the UK, Entonox and Nitronox are used commonly by ambulance crews (including unregistered practitioners) as rapid and highly effective analgesic gas.

Fifty per cent nitrous oxide can be considered for use by trained non-professional first aid responders in prehospital settings, given the relative ease and safety of administering 50% nitrous oxide as an analgesic. The rapid reversibility of its effect would also prevent it from precluding diagnosis.[35]

While casual use of nitrous oxide is understood by most recreational users to be a route to a "safe high", many are unaware that excessive consumption has the potential to cause neurological harm which, if left untreated, can result in permanent neurological damage.[41] In Australia, recreation use became a public health concern following a rise in reported cases of neurotoxicity and a rise in emergency room admissions, and in (the state of) South Australia legislation was passed in 2020 to restrict canister sales.[42]

Nitrous oxide is a significant occupational hazard for surgeons, dentists and nurses. Because nitrous oxide is minimally metabolised in humans (with a rate of 0.004%), it retains its potency when exhaled into the room by the patient, and can pose an intoxicating and prolonged exposure hazard to the clinic staff if the room is poorly ventilated. Where nitrous oxide is administered, a continuous-flow fresh-air ventilation system or N
2O scavenger system is used to prevent a waste-gas buildup.[citation needed]

The National Institute for Occupational Safety and Health recommends that workers' exposure to nitrous oxide should be controlled during the administration of anaesthetic gas in medical, dental and veterinary operators.[43] It set a recommended exposure limit (REL) of 25 ppm (46 mg/m3) to escaped anaesthetic.[44]
Mental and manual impairment

Exposure to nitrous oxide causes short-term decreases in mental performance, audiovisual ability and manual dexterity.[45] These effects coupled with the induced spatial and temporal disorientation could result in physical harm to the user from environmental hazards.[46]

Neurotoxicity and neuroprotection

Nitrous oxide is neurotoxic and there is evidence that medium or long-term habitual consumption of significant quantities can cause neurological harm with the potential for permanent damage if left untreated.[42][41]

Like other NMDA receptor antagonists, it has been suggested that N
2O produces neurotoxicity in the form of Olney's lesions in rodents upon prolonged (several hour) exposure.[47][48][49][50] It has been argued that, because N
2O is rapidly expelled from the body under normal circumstances, it is less likely to be neurotoxic than other NMDAR antagonists.[51] Indeed, in rodents, short-term exposure results in only mild injury that is rapidly reversible, and neuronal death occurs only after constant and sustained exposure.[47] Nitrous oxide also may cause neurotoxicity after extended exposure because of hypoxia. This is especially true of non-medical formulations such as whipped-cream chargers (also known as "whippets" or "nangs"),[52] which never contain oxygen, since oxygen makes cream rancid.[53]

In heavy (≥400 g or ≥200 L of N2O gas in one session) or frequent (regular, i.e., daily or weekly) users reported to poison control centers, signs of peripheral neuropathy have been noted: the presence of ataxia (gait abnormalities) or paresthesia (perception of abnormal sensations, e.g. tingling, numbness, prickling, mostly in the extremities). These are considered an early sign of neurological damage and indicates chronic toxicity.[54]

Nitrous oxide at 75% by volume reduces ischemia-induced neuronal death induced by occlusion of the middle cerebral artery in rodents, and decreases NMDA-induced Ca2+ influx in neuronal cell cultures, a critical event involved in excitotoxicity.[51]
DNA damage

Occupational exposure to ambient nitrous oxide has been associated with DNA damage, due to interruptions in DNA synthesis.[55] This correlation is dose-dependent[56][57] and does not appear to extend to casual recreational use; however, further research is needed to confirm the duration and quantity of exposure needed to cause damage.
Oxygen deprivation

If pure nitrous oxide is inhaled without oxygen, oxygen deprivation can occur, resulting in low blood pressure, fainting, and even heart attacks. This can occur if the user inhales large quantities continuously, as with a strap-on mask connected to a gas canister. It can also happen if the user engages in excessive breath-holding or uses any other inhalation system that cuts off a supply of fresh air.[citation needed]
Vitamin B12 deficiency

Long-term exposure to nitrous oxide may cause vitamin B12 deficiency. This can cause serious neurotoxicity if the user has preexisting vitamin B12 deficiency.[58] It inactivates the cobalamin form of vitamin B12 by oxidation. Symptoms of vitamin B12 deficiency, including sensory neuropathy, myelopathy and encephalopathy, may occur within days or weeks of exposure to nitrous oxide anaesthesia in people with subclinical vitamin B12 deficiency.

Symptoms are treated with high doses of vitamin B12, but recovery can be slow and incomplete.[59]

People with normal vitamin B12 levels have stores to make the effects of nitrous oxide insignificant, unless exposure is repeated and prolonged (nitrous oxide abuse). Vitamin B12 levels should be checked in people with risk factors for vitamin B12 deficiency prior to using nitrous oxide anaesthesia.[60]
Prenatal development

Several experimental studies in rats indicate that chronic exposure of pregnant females to nitrous oxide may have adverse effects on the developing fetus.[61][62][63]
Chemical/physical risks

At room temperature (20 °C [68 °F]) the saturated vapour pressure is 50.525 bar, rising up to 72.45 bar at 36.4 °C (97.5 °F)—the critical temperature. The pressure curve is thus unusually sensitive to temperature.[64]

As with many strong oxidisers, contamination of parts with fuels have been implicated in rocketry accidents, where small quantities of nitrous/fuel mixtures explode due to "water hammer"-like effects (sometimes called "dieseling"—heating due to adiabatic compression of gases can reach decomposition temperatures).[65] Some common building materials such as stainless steel and aluminium can act as fuels with strong oxidisers such as nitrous oxide, as can contaminants that may ignite due to adiabatic compression.[66]

There also have been incidents where nitrous oxide decomposition in plumbing has led to the explosion of large tanks.[20]
Mechanism of action

The pharmacological mechanism of action of N
2O in medicine is not fully known. However, it has been shown to directly modulate a broad range of ligand-gated ion channels, and this likely plays a major role in many of its effects. It moderately blocks NMDAR and β2-subunit-containing nACh channels, weakly inhibits AMPA, kainate, GABAC and 5-HT3 receptors, and slightly potentiates GABAA and glycine receptors.[67][68] It also has been shown to activate two-pore-domain K+
channels.[69] While N
2O affects quite a few ion channels, its anaesthetic, hallucinogenic and euphoriant effects are likely caused predominantly, or fully, via inhibition of NMDA receptor-mediated currents.[67][70] In addition to its effects on ion channels, N
2O may act to imitate nitric oxide (NO) in the central nervous system, and this may be related to its analgesic and anxiolytic properties.[70] Nitrous oxide is 30 to 40 times more soluble than nitrogen.

The effects of inhaling sub-anaesthetic doses of nitrous oxide have been known to vary, based on several factors, including settings and individual differences;[71][72] however, from his discussion, Jay (2008)[46] suggests that it has been reliably known to induce the following states and sensations:

Intoxication
Euphoria/dysphoria
Spatial disorientation
Temporal disorientation
Reduced pain sensitivity

A minority of users also will present with uncontrolled vocalisations and muscular spasms. These effects generally disappear minutes after removal of the nitrous oxide source.[46]
Anxiolytic effect

In behavioural tests of anxiety, a low dose of N
2O is an effective anxiolytic, and this anti-anxiety effect is associated with enhanced activity of GABAA receptors, as it is partially reversed by benzodiazepine receptor antagonists. Mirroring this, animals that have developed tolerance to the anxiolytic effects of benzodiazepines are partially tolerant to N
2O.[73] Indeed, in humans given 30% N
2O, benzodiazepine receptor antagonists reduced the subjective reports of feeling "high", but did not alter psychomotor performance, in human clinical studies.[74][75]
Analgesic effect

The analgesic effects of N
2O are linked to the interaction between the endogenous opioid system and the descending noradrenergic system. When animals are given morphine chronically, they develop tolerance to its pain-killing effects, and this also renders the animals tolerant to the analgesic effects of N
2O.[76] Administration of antibodies that bind and block the activity of some endogenous opioids (not β-endorphin) also block the antinociceptive effects of N
2O.[77] Drugs that inhibit the breakdown of endogenous opioids also potentiate the antinociceptive effects of N
2O.[77] Several experiments have shown that opioid receptor antagonists applied directly to the brain block the antinociceptive effects of N
2O, but these drugs have no effect when injected into the spinal cord.

Apart from an indirect action, nitrous oxide, like morphine [78] also interacts directly with the endogenous opioid system by binding at opioid receptor binding sites.[79][80]

Conversely, α2-adrenoceptor antagonists block the pain-reducing effects of N
2O when given directly to the spinal cord, but not when applied directly to the brain.[81] Indeed, α2B-adrenoceptor knockout mice or animals depleted in norepinephrine are nearly completely resistant to the antinociceptive effects of N
2O.[82] Apparently N
2O-induced release of endogenous opioids causes disinhibition of brainstem noradrenergic neurons, which release norepinephrine into the spinal cord and inhibit pain signalling.[83] Exactly how N
2O causes the release of endogenous opioid peptides remains uncertain.
Properties and reactions

Nitrous oxide is a colourless gas with a faint, sweet odour.

Nitrous oxide supports combustion by releasing the dipolar bonded oxygen radical, and can thus relight a glowing splint.

N2O is inert at room temperature and has few reactions. At elevated temperatures, its reactivity increases. For example, nitrous oxide reacts with NaNH2 at 187 °C (369 °F) to give NaN3:

2 NaNH2 + N2O → NaN3 + NaOH + NH3

The above reaction is the route adopted by the commercial chemical industry to produce azide salts, which are used as detonators.[84]

Kool aid, Aids, Abortion and Fentanyl can't kill them fast enough they need that fast gas to ruin their brains and send em to the reaper quicker than the ZIONIST JEWS COULD EVER DREAM.