Abstract

AbstractPaired, serial blood samples were collected for a minimum of 6 hr to a maximum of 15 days from cannulae chronically placed in the internal carotid artery (A) to the brain and the anterior cardinal sinus (V) from the brain of the spiny dogfish shark (Squalus acanthias). Previously fed animals were fasted for either 3 to 8 days (short‐fasted) or 20 to 29 days (long‐fasted) before the surgery to implant the cannulae and during the subsequent sampling periods. Plasma β‐hydroxybutyrate, acetoacetate, glucose, lactate, and alanine levels were measured by standard enzymatic procedures. The internal carotid artery plasma β‐hydroxybutyrate and acetoacetate levels were in the approximate ratio of 4 to 6:1, were greater in the long‐fasted than in the short‐fasted animals, and both ketones increased throughout the observation periods. In contrast, plasma lactate and alanine levels declined by postoperative day 2 to levels that, like glucose, remained relatively stable and were characteristic of the individual animal. The A‐V metabolite differences between the short‐ and long‐fasted animals were not significantly different and the data from the two groups of animals were combined for purpose of analysis. β‐Hydroxybutyrate was extracted from the plasma by the brain during both the surgery and recovery period (⩽ 2 days) and the “normal” under the observational conditions period (> 2 days). The small negative A‐V differences in acetoacetate during both periods, and in glucose during the > 2 day period, were not statistically significant. There were no evident A‐V differences in plasma alanine. Lactate was released by the brain during both the ⩽ 2 days and > 2 day periods. The uptake of β‐hydroxybutyrate and the release of lactate indicate that the spiny dogfish brain used both β‐hydroxybutyrate and glucose during the observation periods. The data suggest that the plasma was the immediate source of β‐hydroxybutyrate, but, as proposed by previous authors, the proximate glucose source may have been provided by the mobilization of endogenous brain glycogen stores. © 1994 Wiley‐Liss, Inc.

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