Ketamine Injectable opiates Red Discussion: Ketamine and Injectable opiates

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Ketamine and Injectable opiates​

Ketamine is a dissociative anesthetic that has gained attention for its use in both clinical settings and as a recreational drug. Ketamine primarily works by blocking the N-methyl-D-aspartate (NMDA) receptor, a subtype of glutamate receptor. Glutamate is the most abundant excitatory neurotransmitter in the brain and plays a key role in synaptic plasticity, learning, and memory.

By inhibiting NMDA receptors, ketamine reduces the activity of glutamate, leading to a state of dissociation. This dissociative state is characterized by a feeling of detachment from reality, the environment, and even one’s own body, which is why ketamine is referred to as a dissociative anesthetic.

Ketamine indirectly increases dopamine levels in the brain, contributing to its mood-enhancing effects. This dopaminergic activity is part of why ketamine can have antidepressant properties. Besides, ketamine has some action on the opioid system, which may contribute to its analgesic (pain-relieving) properties.


Injectable opiates, also known as opioids, are a class of drugs that include natural, semi-synthetic, and synthetic substances derived from the opium poppy or created to mimic its effects. These drugs are primarily used for their powerful pain-relieving properties but are also known for their potential for abuse.

Injectable opiates work by binding to specific receptors in the brain, spinal cord, and other parts of the body known as opioid receptors. The three main types of opioid receptors are:

1. Mu (μ) Receptors: The primary site for pain relief, euphoria, and respiratory depression.
2. Delta (δ) Receptors: Involved in modulating mood and analgesia.
3. Kappa (κ) Receptors: Associated with pain relief, dysphoria, and hallucinations.

When opiates bind to these receptors, they inhibit the release of neurotransmitters like substance P and glutamate that are involved in transmitting pain signals. This action decreases the perception of pain and increases tolerance to pain. Opiates also depress the central nervous system, leading to sedation, drowsiness, and, at high doses, respiratory depression, which is a major risk factor in overdose situations.

Opiates trigger the release of dopamine in the brain’s reward pathway, particularly in areas like the nucleus accumbens. This surge in dopamine creates feelings of intense pleasure and euphoria, which contribute to the addictive potential of these drugs.

Examples of Injectable Opiates:

• Morphine: Often used in medical settings for severe pain management, such as post-surgical pain, cancer pain, and in palliative care. Morphine is a potent mu receptor agonist, providing strong analgesic effects along with sedation and euphoria.
• Heroin (Diacetylmorphine): Although originally developed for medical use, heroin is now an illegal drug with no accepted medical use in many countries. It is highly addictive and is commonly abused for its intense euphoric effects. Once injected, heroin rapidly crosses the blood-brain barrier and is converted to morphine, which then binds to opioid receptors, leading to powerful euphoria and pain relief.
• Fentanyl: Fentanyl is a synthetic opioid used in medical settings for severe pain, such as during surgery or for cancer pain. It is also commonly used in anesthesia. Fentanyl is extremely potent, about 50-100 times stronger than morphine, and acts quickly by binding strongly to mu receptors. Its potency makes it highly effective in pain relief but also increases the risk of overdose, especially when used improperly.
• Hydromorphone (Dilaudid): Another potent opioid used for severe pain, often in cases where other opioids are ineffective. Similar to morphine, hydromorphone acts primarily on mu receptors to produce analgesia, sedation, and euphoria.

Combining ketamine with injectable opiates can produce complex and potentially dangerous effects due to the way these substances interact within the brain and body.

1. Increased Risk of Respiratory Depression: Both ketamine and opiates can depress the respiratory system, but they do so through different mechanisms. Opiates primarily act on the brainstem to reduce the drive to breathe, while ketamine, though generally less likely to cause respiratory depression on its own, can exacerbate this effect when combined with opiates. This combination significantly increases the risk of fatal respiratory depression, especially in cases of overdose.
2. Enhanced Sedation and Cognitive Impairment: Both drugs cause sedation, but when used together, this effect is amplified. Users may experience profound sedation, which can impair cognitive function and motor skills, increasing the risk of accidents, especially if the individual attempts to perform tasks like driving.
3. Cardiovascular Complications: Ketamine can elevate blood pressure and heart rate, while opiates tend to have the opposite effect, lowering both. The combination can create unpredictable cardiovascular responses, potentially leading to arrhythmias, hypertension, or hypotension, depending on the dose and individual susceptibility.
4. Unpredictable Psychological Effects: Ketamine’s dissociative effects, combined with the euphoric and potentially dysphoric effects of opiates, can lead to unpredictable psychological experiences. Users might experience intense hallucinations, delusions, or severe anxiety, especially at higher doses or in those with pre-existing mental health conditions.
5. Overdose Risk: The risk of overdose is significantly higher when these substances are combined. In many reported cases, the lethal outcome was due to the compounded effects of respiratory depression, extreme sedation, and cardiovascular collapse, particularly in non-therapeutic settings where dosages are not carefully controlled.

All things considered, we recommend avoiding this combination under any conditions.