"Long-term side effects
Main article: Olney's lesions
In 1989, psychiatry professor John Olney reported that ketamine caused reversible changes in two small areas of the rat brain. 40mg/kg resulted in fluid-filled bags ("vacuoles") appearing inside cells. The bags disappeared after several days, unless high doses of the far more toxic PCP or close relative MK801 were repeatedly given, in which case some cell death was seen. Roland Auer injected monkeys with MK801 and was unable to produce any vacuoles. I asked Auer in 1998 whether persons undergoing anesthesia with Ketalar were at risk of these changes. His reply was that he doubted that it was even a remote possibility because of fundamental differences in metabolism between the rat and human brain. Ketamine can block excito-toxicity (brain damage due to low oxygen, low sugar, epilepsy, trauma etc.) but it can also excite the brain at low doses by switching off the inhibitory system. Why isn't this damaging in monkeys and humans? The answer probably lies in the fact that ketamine binds to an increasingly wide range of different receptors as the dose level rises, and some of these receptors act to shut down the excitement. In humans, by the time a potentially toxic dose is reached, the "excitement window" has been passed and the drug is starting to activate other systems that switch cells off again, a result of ketamine's promiscuity that improves its safety relative to MK801. MK801 binds very specifically to N-P receptors. The other part of the explanation is that rats have rates of brain metabolism that are almost twice as high as those in humans to start with. It is because of this higher base rate of metabolism that ketamine causes over-excitement in rats at doses below those at which it activates shutdown systems.”[50][51][52]
Vutskits et al from Geneva showed that short-term exposure of cultures to ketamine at concentrations of > or =20 microg/ml leads to a significant cell loss of differentiated cells and that non-cell death-inducing concentrations of ketamine (10 microg/ml) can still initiate long-term alterations of dendritic arbor in differentiated neurons, including dendritic retraction and branching point elimination. They also demonstrated that chronic (>24 h) administration of ketamine at concentrations as low as 0.01 microg/ml can interfere with the maintenance of dendritic arbor architecture. These results raise the possibility that chronic exposure to low, subanesthetic concentrations of ketamine, while not affecting cell survival, could still impair neuronal morphology and thus might lead to dysfunctions of neural networks.[53]
Ketamine effects on horses, which where applied by the US army in Arizona during the 1980's proved ketamine provided horses with the faculty to jump notably higher than when they were not under the influence of ketamine.
There is a long list of medicines that could counteract these potential toxic effects, including clonidine, anticholinergics, benzodiazepines and barbiturates.[51][52]
On 21 June 2007 Hong Kong Medical Journal has put up a report regarding the misuse of 'street K'. The report suggests that long term use may result in damage to the liver or urinary bladder, or even acute renal failure. However, the researchers suspect that the damage "may be due to other toxins that the 'street ketamine' has been contaminated with".[54]
In a study of 9 daily ketamine users, Shahani et al found "marked thickening of the bladder wall, a small capacity, and perivesicular stranding, consistent with severe inflammation. At cystoscopy, all patients had severe ulcerative cystitis. Biopsies in 4 patients revealed epithelial denudation and inflammation with a mild eosinophilic infiltrate. Cessation of ketamine use, with the addition of pentosan polysulfate, appeared to provide some symptomatic relief."[55]
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In: Schadelijkheid ketamine
1-1-2024