“…Investigation of the endocrine responses to acid stress have largely concentrated on the HPI axis and there are several reports of increased plasma cortisol which may be at least partially responsible for the widely reported parallel increases in plasma glucose (Edwards et al, 1987;Brown et al, 1989). There is, however, strong evidence that catecholamines have a hyperglycaemic action (Sheridan & Muir, 1988;Epple et al, 1989). Catecholamines are released into circulation during disturbed acid/base balance or low arterial oxygen tension (Tang & Boutilier, 1988;Ristori & Laurent, 1989;Perry & Reid, 1992;, events which can occur in acid/aluminium stress .…”