Effect of systemic lidocaine on visceral and somatic nociception in conscious horses

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Abstract

Commonly used analgesics (nonsteroidal anti-inflammatory agents, opioids and alpha2-agonists) have unwanted side effects. An effective alternative with minimal adverse effects would benefit clinical equine pain management. To compare the effect of lidocaine or saline on duodenal and rectal distension threshold pressure and somatic thermal threshold in conscious mature horses. Systemically administered lidocaine would increase somatic and visceral nociceptive thresholds. Lidocaine (2 mg/kg bwt bolus followed by 50 microg/kg bwt/min for 2 h) or saline was administered to 6 horses each carrying a permanently implanted gastric cannula, in a randomised, blinded cross-over design. Thermal threshold was measured using a probe containing a heater element placed over the withers which supplied heat until the horse responded. A barostatically controlled intraduodenal balloon was distended until a discomfort response was obtained. A rectal balloon was inflated until extruded or signs of discomfort noted. Thermal threshold was increased significantly 30 and 90 mins after the start of lidocaine infusion. There was no change in duodenal distension pressure and a small but clinically insignificant change in colorectal distension pressure in the lidocaine group. At the dose used, systemically administered lidocaine produced thermal antinociception but minimal changes in visceral nociception. At these doses, lidocaine may play a role in somatic analgesia in horses.

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Systemic lidocaine for neuropathic pain relief.

L. Chen, Jun Mao (2000)

The effectiveness of systemic lidocaine in relieving acute and chronic pain has been recognized for over 35 years. In particular, systemic lidocaine has been utilized both as a diagnostic and therapeutic tool for intractable neuropathic pain during the last decade. The introduction of oral lidocaine congeners such as mexiletine has significantly extended the usage of lidocaine therapy in chronic pain settings. However, a number of clinical issues remain to be addressed including (1) an effective, meaningful dose range for the clinical lidocaine test, (2) the predictive value of the lidocaine test for an oral trial of lidocaine congeners, (3) identification of pain symptoms and signs relieved by systemic lidocaine, (4) comparisons of therapeutic effects between systemic lidocaine and its oral congeners, and (5) long-term outcomes of systemic lidocaine and its oral congeners. Mechanisms of neuropathic pain relief from lidocaine therapy are yet to be understood. Both central and peripheral mechanisms have been postulated. Systemic lidocaine is thought to have its suppressive effects on spontaneous ectopic discharges of the injured nerve without blocking normal nerve conduction. However, there remain inconsistencies in the scientific basis underlying the clinical application of lidocaine therapy. Recent demonstration of changes in tetrodotoxin (TTX)-sensitive and TTX-resistant sodium channels following nerve injury and their link to certain neuropathic pain symptoms may lead to the development of subtype-specific sodium channel blockers. The thoughtful use of lidocaine therapy and the potential application of subtype-specific sodium channel blockers could provide better management of distinctive neuropathic pain symptoms.

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Low-dose lidocaine reduces secondary hyperalgesia by a central mode of action.

R Sittl, W. Koppert, N Ostermeier … (2000)

Sodium channel blockers are approved for intravenous administration in the treatment of neuropathic pain states. Preclinical studies have suggested antihyperalgesic effects on the peripheral as well as the central nervous system. The objective of this study was to determine mechanisms of action of low-dose lidocaine in experimental induced, secondary hyperalgesia. In a first experimental trial, participants (n=12) received lidocaine systemically (a bolus injection of 2 mg/kg in 10 min followed by an intravenous infusion of 2 mg kg(-1)h(-1) for another 50 min). In a second trial, a modified intravenous regional anesthesia (IVRA) was administered to exclude possible central analgesic effects. In one arm, patients received an infusion of 40 ml lidocaine, 0.05%; in the other arm 40 ml NaCl, 0.9%, served as a control. In both trials capsaicin, 20 microgram, was injected intradermally and time course of capsaicin-induced pain, allodynia and hyperalgesia as well as axon reflex flare was determined. The capsaicin-induced pain was slightly reduced after systemic and regional application of the anesthetic. The area of pin-prick hyperalgesia was significantly reduced by systemic lidocaine, whereas the inhibition of hyperalgesia was absent during regional administration of lidocaine. In contrast, capsaicin-induced flare was significantly decreased after both treatments. We conclude that systemic lidocaine reduces pin-prick hyperalgesia by a central mode of action, which could involve blockade of terminal branches of nociceptors. A possible role for tetrodotoxin resistant sodium channels in the antihyperalgesic effect of low-dose lidocaine is discussed.

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Intravenous lidocaine inhibits visceral nociceptive reflexes and spinal neurons in the rat.

Jennifer Ness (2000)

Systemically administered local anesthetics and other sodium channel blockers produce analgesia in patients with hypersensitivity disorders. To assess whether these agents have a role in the treatment of visceral pain, the present study examined the effects of intravenous lidocaine on neuronal and reflex responses to colorectal distension. In decerebrate, cervical spinal cord-transected male rats, the lumbosacral spinal cord was exposed by a laminectomy. Dorsal horn neurons demonstrating excitatory responses to colorectal distension were identified using microelectrodes. Sequential doses of lidocaine were administered intravenously. In chronically instrumented, unanesthetized rats, visceromotor responses, pressor responses, and increases in heart rate were elicited by colorectal distension and sequential doses of lidocaine. Intravenous lidocaine dose-dependently inhibited visceromotor and cardiovascular reflexes and the evoked and spontaneous activity of neurons excited by colorectal distension. There were statistically greater effects on one of the neuronal subgroups (sustained neurons) than on another subgroup (abrupt neurons.) Intravenous lidocaine had dose-dependent, inhibitory effects on two spinal neuronal populations excited by colorectal distension and dose-dependently inhibited reflex responses to the same stimulus. This suggests there may be utility of sodium channel blockers in the treatment of pain of visceral origin.