Tissue acidosis in nociception and pain

This chapter focuses on the tissue acidosis in nociception and pain. Local imbalance of perfusion and metabolism may be suggested to be the common mechanism generating tissue acidosis. Even in inflammation, the metabolic turn-over may be more enhanced, for example, by accumulation of inflammatory cells, than the local blood flow that should lead to lactic acid accumulation. Leukocytes, as well as myocytes, can actively transport lactic acid into the interstitial space. The delayed hyperalgesia observed with experimental tissue acidosis in humans seems to be reflected in a concomitantly delayed decrease of mechanical thresholds of cutaneous nociceptors, in vitro, which occurs upon repeated or prolonged exposure to low pH. A striking feature of pH-induced pain and nociceptor excitation is the synergism with mediators of inflammation encountered with tissue acidosis in inflamed areas. Preventing tissue acidosis may neither be possible nor even desirable; however, blocking pH-induced nociceptor excitation may be of great help to controlling pain of various origins. © 1996 Elsevier Science B.V.