Abstract

We have recently shown that brain temperature can drop even though rectal and skull readings are maintained near 37°C during global forebrain ischemia in the gerbil. In this study gerbils were subjected to 5 min of ischemia followed by 85 min of extended halothane anesthesia, while rectal and skull temperatures were kept at normal values. This extended anesthesia procedure prevented the development of spontaneous postischemic hyperthermia. However, it occasionally produced mild brain hypothermia both during ischemia and throughout anesthesia. In addition, the degree of brain hypothermia positively correlated with CA1 preservation; with some gerbils showing complete protection. In contrast, animals with normal brain temperature displayed extensive CA1 cell loss. These data suggest that postischemic hyperthermia is not a prerequisite for extensive CA1 loss in gerbils exposed to 5 min of ischemia. Second, rectal and skull recordings are not always reliable indicators of brain temperature, especially during anesthesia.

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