Abstract
Sodium lactate injection into rat brain produces coagulation necrosis consistent with infarction when pH0 is held at less than or equal to 5.30 for 20 min. Such injury may result from excessive astroglial acidification. If true, then brain damage from acidosis in elasmobranchs might evolve differently since glial reaction there to another necrotizing injury, exposure to extreme cold, is dissimilar from that seen in mammals. Accordingly, pH0 was monitored and sodium lactate (pH 4.00-7.00) injected into skate (Raja erinacea) cerebella. Necrosis was seen only when pH0 was less than or equal to 4.86 for 20 min; and pH0 rise after injections was unaffected by those which destroyed brain, and not slowed as in rat. Thus elasmobranchs are less susceptible to irreversible brain injury from acidosis, a capacity which may result from their lower body temperature compared to mammals.