Should Soda Lime be Abolished

Anesthesia & Analgesia, 2005

Certain dietary proteins and oils are capable of decreasing chronic neuropathic pain levels in rats after partial sciatic nerve ligation injury. We tested, for the first time, the role of dietary polyunsaturated fatty acids in suppressing pain in partial sciatic nerve ligation-injured rats. Six groups of male Wistar rats were fed an identical casein-based, fatfree diet for 1 wk preceding partial sciatic nerve ligation injury and for 1 wk thereafter. In addition, rats received, via gavage, 1 mL/day of pure canola, corn, hemp, soy, or sunflower oil, differing significantly in their -3 and -6 polyunsaturated fatty acid content, or 1 mL of plain water. Responses to tactile and noxious heat stimuli were recorded before and after surgery and a difference score was calculated for each group by subtracting the preoperative from the post-partial sciatic nerve ligation values. Heat hyperalgesia, but not tactile allodynia, was significantly different among the dietary groups (P ϭ 0.005). Heat hyperalgesia of rats fed hemp oil, developing the most robust response, was significantly larger compared with rats fed corn oil, developing the least pain model (difference score: 24.3 Ϯ 4.1 s versus 6.1 Ϯ 3.1 s, respectively; P Ͻ 0.001). These oils contain similar levels of -6 polyunsaturated fatty acids (hemp, 60%; corn, 58%) but their -3 levels are 28-fold different (20% versus 0.7%, respectively). A significant correlation was found among dietary levels of -3, but not -6 or the -3/-6 ratio, of the six dietary groups and heat hyperalgesia (P ϭ 0.006). We conclude that dietary oil might predict levels of neuropathic pain in rats and that this effect may be associated with dietary -3 levels.

Pharmacological Research, 2011

Fish oil has been used to alleviate pain associated with inflammatory conditions such as rheumatoid arthritis. The anti-inflammatory property of fish oil is attributed to the n-3 fatty acids docosahexaenoic acid and eicosapentaenoic acid. Contrarily, vegetable oils such as safflower oil are rich in n-6 fatty acids which are considered to be mediators of inflammation. This study investigates the effect of n-3 and n-6 fatty acids rich oils as dietary supplements on the thermally induced pain sensitivity in healthy mice. C57Bl/6J mice were fed diet containing regular fish oil, concentrated fish oil formulation (CFO) and safflower oil (SO) for 6 months. Pain sensitivity was measured by plantar test and was correlated to the expression of acid sensing ion channels (ASICs), transient receptor potential vanilloid 1 (TRPV1) and c-fos in dorsal root ganglion cells. Significant delay in sensitivity to thermal nociception was observed in mice fed CFO compared to mice fed SO (p<0.05). A significant diminution in expression of ion channels such as ASIC1a (64%), ASIC13 (37%) and TRPV1 (56%) coupled with reduced expression of c-fos, a marker of neuronal activation, was observed in the dorsal root ganglion cells of mice fed CFO compared to that fed SO. In conclusion, we describe here the potential of fish oil supplement in reducing sensitivity to thermal nociception in normal mice.

Neuroscience Letters, 2010

TRPA1 agonists cinnamaldehyde (CA) and mustard oil (allyl isothiocyanate= AITC) induce heat hyperalgesia and mechanical allodynia in human skin, and sensitize responses of spinal and trigeminal dorsal horn neurons to noxious skin heating in rats. TRPA1 is also implicated in cold nociception. We presently used behavioral methods to investigate if CA affects sensitivity to thermal and mechanical stimuli in rats. Unilateral intraplantar injection of CA (5-20%) induced a significant, concentration-dependent reduction in latency for ipsilateral paw withdrawal from a noxious heat stimulus, peaking (61.7% of pre-injection baseline) by 30 min with partial recovery at 120 min. The highest dose of CA also significantly reduced the contralateral paw withdrawal latency. CA significantly reduced mechanical withdrawal thresholds of the injected paw that peaked sooner (3 min) and was more profound (44.4% of baseline), with no effect contralaterally. Bilateral intraplantar injections of CA resulted in a significant cold hyperalgesia (cold-plate test) and a weak enhancement of innocuous cold avoidance (thermal preference test). The data are consistent with roles for TRPA1 in thermal (hot and cold) hyperalgesia and mechanical allodynia.

European Journal of Pain, 2008

Diabetic neuropathic pain, an important microvascular complication of diabetes mellitus is recognized as one of the most difficult types of pain to treat. The development of tolerance, inadequate relief and potential toxicity of classical antinociceptives warrant the investigation of the newer agents to relieve this pain. The aim of the present study was to explore the antinociceptive effect of lycopene and its effect on tumour necrosis factor-a (TNF-a) and nitric oxide (NO) release in streptozotocin induced diabetic mice. Four weeks after a single intraperitoneal injection of streptozotocin (200 mg/kg), mice were tested in the tail immersion and hot-plate assays. Diabetic mice exhibited significant hyperalgesia alongwith increased plasma glucose and decreased body weights as compared with control mice. Lycopene (1, 2 and 4 mg/kg body weight; per oral) treatment, from the 4th to 8th week after streptozotocin injection, significantly attenuated thermal hyperalgesia and the hot-plate latencies. Lycopene also inhibited the TNF-a and NO release in a dose dependent manner. These results indicate an antinociceptive activity of lycopene possibly through its inhibitory action on NO and TNF-a release and point towards its potential to attenuate diabetic neuropathic pain.

Applied Sciences

Neuropathic pain, a prevalent concern associated with various pathological conditions, poses a significant public health risk due to its poorly understood pathophysiology and treatment complexities. Multimodal therapy is often the most efficacious approach to managing neuropathic pain, yet it is also highly labour intensive. The exact underlying causes of neuropathic pain are unclear; evidence suggests that cytokines, neuropeptides, and neurotrophic factors may play a role in its pathogenesis. The current study aimed to investigate the anti-neuropathic pain activity of caraway oil and the molecular mechanisms underlying its actions in rats with CCI, a model of neuropathic pain. Behavioural evaluations of cold allodynia, heat hyperalgesia, mechanical allodynia, and mechanical hyperalgesia were conducted using the acetone spray test, hot plate test, Von Frey hair test, and pinprick test, respectively. Additionally, the level of TNF-α in the sciatic nerve was examined as an indicator o...

Pain, 2008

Palmitoylethanolamide (PEA) is an endogenous lipid that is thought to be involved in endogenous protective mechanisms activated as a result of stimulation of inflammatory response. In spite of the well demonstrated anti-inflammatory properties of PEA, its involvement in controlling pain pathways still remains poorly characterized. On this basis, we tested the efficacy of PEA in vivo against a peculiar persistent pain, such as neuropathic one. PEA was administered i.p. to mice with chronic constriction injury of sciatic nerve (CCI) once a day for one week starting the day after the lesion. This therapeutic regimen evoked a relief of both thermal hyperalgesia and mechanical allodynia in neuropathic mice. Various selective receptor antagonists were used in order to clarify the relative contribution of cannabinoid, vanilloid and peroxisome proliferator-activated receptor to PEA-induced effects. The results indicated that CB 1 , PPARc and TRPV1 receptors mediated the antinociception induced by PEA, suggesting that the most likely mechanism might be the so-called ''entourage effect" due to the PEA-induced inhibition of the enzyme catalyzing the endocannabinoid anandamide (AEA) degradation that leads to an enhancement of its tissue levels thus increasing its analgesic action. In addition, the hypothesis that PEA might act through the modulation of local mast cells degranulation is sustained by our findings showing that PEA significantly reduced the production of many mediators such as TNFa and neurotrophic factors, like NGF. The findings presented here, in addition to prove the beneficial effects of PEA in chronic pain, identify new potential targets for analgesic medicine.

2008

The intake of n-3 polyunsaturated fatty acids (PUFAs) in many industrialized countries is relatively low and its increased consumption has protective and modifying effects on such diverse conditions as atherosclerosis, ventricular arrhythmias, multiple sclerosis, major depression and inflammatory and autoimmune diseases. In addition, n-3 PUFAs have been shown to alleviate pain in patients with rheumatoid arthritis, inflammatory bowel disease and in a number of other painful conditions. This has been attributed to the inhibition of pro-inflammatory eicosanoid and cytokine production by peripheral tissues. n-3 PUFAs have also been shown to inhibit eicosanoid production in glial cells, block voltage-gated sodium channels (VGSCs), inhibit neuronal protein kinases and modulate gene expression. They also appear to have mood-stabilizing and sympatholytic effects. The present article explores the possibility that, based on what is known about their neural and non-neural effects, n-3 PUFAs directly attenuate the neuronal and glial processes that underlie neuropathic and inflammatory pain. r

2010

The transient receptor potential vanilloid 1 (TRPV1) channel is the principal detector of noxious heat in the peripheral nervous system. TRPV1 is expressed in many nociceptors and is involved in heat-induced hyperalgesia and thermoregulation. The precise mechanism or mechanisms mediating the thermal sensitivity of TRPV1 are unknown. Here, we have shown that the oxidized linoleic acid metabolites 9-and 13-hydroxyoctadecadienoic acid (9-and 13-HODE) are formed in mouse and rat skin biopsies by exposure to noxious heat. 9-and 13-HODE and their metabolites, 9-and 13-oxoODE, activated TRPV1 and therefore constitute a family of endogenous TRPV1 agonists. Moreover, blocking these substances substantially decreased the heat sensitivity of TRPV1 in rats and mice and reduced nociception. Collectively, our results indicate that HODEs contribute to the heat sensitivity of TRPV1 in rodents. Because oxidized linoleic acid metabolites are released during cell injury, these findings suggest a mechanism for integrating the hyperalgesic and proinflammatory roles of TRPV1 and linoleic acid metabolites and may provide the foundation for investigating new classes of analgesic drugs. Conflict of interest: The University of Texas has claimed intellectual property on this discovery. The authors have declared that no other conflict of interest exists.

2012

Transient receptor potential (TRP) channels are being ardently pursued as targets for pain therapies. They play an important role in transducing thermal, mechanical and chemical stimuli for somatic sensation. Several TRP channels exhibit sensitivity to increases or decreases in temperature as well as chemical ligands that elicit similar thermal or painful sensations; these include mustard oil, cinnamaldehyde from cinnamon, menthol from mint, gingerol, camphor, capsaicin from chili peppers, eugenol from cloves, and others. Mustard oil (allyl isothiocyanate (AITC)) and cinnamaldehyde (CA), agonists of the ion channel TRPA1 expressed in sensory neurons, elicit a burning sensation and heat hyperalgesia. In this work, we tested whether these phenomena are reflected in the responses of lumbar spinal wide-dynamic range (WDR) neurons recorded in anesthetized male rats. Responses to electrical and graded mechanical and noxious thermal stimulation were tested before and after cutaneous applic...