The researchers found that "noxious" anesthesia drugs - which most of the general anesthetics are - activate and then sensitize specific receptors on neurons in the peripheral nervous system. These are the sensory nerves in the inflammation and pain pathway that are not affected by general anesthesia drugs that target the central nervous system – the brain and the spinal cord.
Investigators know that while they suppress the central nervous system, they can activate so called "pain-sensing" or nociceptive nerve cells on the peripheral nervous system – anesthesiologists sometimes use a drug to suppress pain before delivering the anesthesia. But what has not been understood is the mechanism by which anesthetics affect sensory neurons, or that they can continue to cause pain and inflammation even as they are being used during surgery, so the scientists.
The researchers tested the hypothesis that two specific receptor on the nerves cells (TRPV1 and TRPA1) which are often expressed together and which also react to other irritants, such as garlic and wasabi, were the ones activated by the noxious drugs. TRPA1 is more commonly known as the mustard-oil receptor, and is a principal receptor in the pain pathway.
Experiments showed that general anesthetics appear to regulate TRPA1 in a direct fashion, and are thus responsible for the acute noxious effects of the drugs. Mice bred without TRPA1 genes demonstrate no pain when the drugs are administered and used.
The scientists argue: Most general anesthetics activate the mustard oil receptor, and animals that don't have the receptor don't have irritation. The research team also found that nerve-mediated inflammation was greater when pungent (chemical irritants) versus non-pungent inhaled general anesthetics were used. What both findings suggest is that sensory nerve stimulation throughout the body just before and during surgery adds to the pain that is felt after the patient is awake.
MEDICA.de; Source: Georgetown University Medical Center