This study investigated the relationship between energy failure and neurotransmitter release in the frog (Rana pipiens) brain during 1-3 h of anoxia. Unlike truly anoxia-tolerant species, the frog does not defend its brain energy charge. When exposed to anoxia at 25 degrees C, there is an immediate fall in brain ATP levels, which reach approximately 20% of normoxic levels in approximately 60 min. The frog, nevertheless, survives another 1-2 h of anoxia. At 100 min of anoxia, there is an increase in extracellular adenosine concentration, probably originating from the increased intracellular adenosine concentration caused by the breakdown of intracellular ATP. Increases in the levels of extracellular glutamate and GABA do not occur until 1-2 h after ATP depletion. This response is quite unlike that recorded for other vertebrates, anoxia-tolerant or anoxia-intolerant, where energy failure quickly results in an uncontrolled and neurotoxic release of excitatory neurotransmitters. In the frog, the delay in excitotoxic neurotransmitter release may be one of the factors that allow a period of survival after energy failure. Clearly, energy failure by itself is not a fatal event in the frog brain.

The remarkable ability of the turtle brain to survive anoxia is based on its ability to match energy demand flexibly to energy production. Earlier studies indicate that reduced ion leakage is an important mechanism for energy conservation during anoxia. We tested the hypothesis that extracellular adenosine plays a role in the reduction of K+ flux (channel arrest) that occurs in the anoxic turtle brain. Changes in extracellular K+ concentration ([K+]o in the in situ brain of the turtle Trachemys scripta were monitored following inhibition of Na+/K(+)-ATPase with ouabain. The time to reach full depolarization ([K+]o plateau) was three times longer in the anoxic brain than in normoxic controls and the initial rate of K+ leakage was reduced by approximately 70%. Superfusing the brain before the during anoxia with the general adenosine receptor blocker theophylline, or the specific adenosine A1 receptor blocker 8-cyclopentyltheophylline, significantly shortened the time to full depolarization in the ouabain-challenged anoxic brain and increased the rate of K+ efflux. The results suggest that adenosine A1 receptors are involved in the expression of anoxia-induced ion channel arrest in the turtle brain.

In the mammalian brain, nitric oxide (NO) is responsible for a vasodilatory tonus as well as the elevation of cerebral blood flow (CBF) induced by hypercapnia. There have been few comparative studies of cerebral vasoregulation in lower vertebrates. Using epi-illumination microscopy in vivo to observe CBF velocity on the brain surface (cerebral cortex), we show that turtles (Trachemys scripta) exposed to hypercapnia (inspired PCO2 = 4.9 kPa) displayed a 62% increase in CBF velocity, while systemic blood pressure remains constant. Exposing turtles to a PCO2 of 14.9 kPa caused an additional increase in CBF velocity, to 104% above control values, as well as a 30% increase in systemic blood pressure. The elevated CBF velocity during hypercapnia could not be blocked by a systemic injection of the NO synthase (NOS) inhibitor NG-nitro-L-arginine (L-NA). However, L-NA injection caused a temporary stop in CBF as well as a persistent increase in systemic blood pressure, suggesting that there is a NO tonus that is attenuated by the NOS inhibitor and that CBF is strongly dependent on this tonus, although compensatory mechanisms exist. Thus, although the cerebrovascular reaction to hypercapnia appeared to be NO-independent, the results suggest that there is a NO-dependent vasodilatory tonus affecting both cerebral and systemic blood circulation in this species.

Anoxia-tolerant turtles and carp (Carassius) exhibit contrasting strategies for anoxic brain survival. In the turtle brain, the energy consumption is deeply depressed to the extent of producing a comatose-like state. Brain metabolic depression is brought about by activating channel arrest to reduce ion flux and through the release of inhibitory gamma-aminobutyric acid (GABA) and the upregulation of GABAA receptors. Key glycolytic enzymes are down-regulated during prolonged anoxia. The result is a suppression of neurotransmission and a substantial depression in brain electrical activity. By contrast, Carassius remain active during anoxia, though at a reduced level. As in the turtle, there is an adenosine-mediated increase in brain blood flow but, in contrast to the turtle, this increase is sustained throughout the anoxic period. Key glycolytic enzymes are up-regulated and anaerobic glycolysis is enhanced. There is no evidence of channel arrest in Carassius brain. The probable result is that electrical activity in the brain is not suppressed but instead maintained at a level sufficient to regulate and control the locomotory and sensory activities of the anoxic carp. The key adaptations permitting the continued high level of glycolysis in Carassius are the production and excretion of ethanol as the glycolytic end-product, which avoids self-pollution by lactate produced during glycolysis that occurs in other vertebrates.

Pulmonary CO diffusion capacity (DL CO ), lung volume (VL), oxygen uptake (V o 2 ) and pulmonary blood flow (QL) were measured simultaneously in the loggerhead sea turtle Caretta caretta (Linnaeus) (8–11 kg) using a gas rebreathing technique (syringe pump ventilation). Calculated DL CO and V o 2 values in the loggerhead turtle are approximately twice those of non-varanid reptiles and about 25 % of values for resting mammals. Evidence based on an estimated lung-capillary O 2 gradient, δP o 2 , shows that only a small driving gradient is required for O 2 conductance across the loggerhead turtle lung. Pulmonary blood flow values are high compared to those for other reptiles; on the basis of the Fick principle, this implies a substantial blood convection requirement. Differences in oxygen transport mechanisms between the loggerhead sea turtle and other highly aerobic but terrestrial reptiles may result from divergent lung structures and breathing patterns. In sea turtles, the coupling of respiration with locomotory behaviour is one factor that may limit aerobic performance. Since sea turtles have only intermittent access to air, they are required to load both arterial and venous blood with O 2 before submerging

1. An electrolytic method was used to plot the oxygen dissociation curves of whole blood from both the larva and adult of the lamprey Lampetra fluviatilis at a temperature of 10 degrees C and over a pH range of 6-5-8-1. 2. Larval blood has a far higher affinity for oxygen than that of adults, the respective calculated P50's at a pH of 7–75 being 1-9 and 10-7 mmHg. 3. The high affinity of larval blood is of use to a relatively sedentary animal living in burrows, and the increased oxygen delivery pressure brought about by the shift of the curve to the right in the adult is of advantage to an animal exhibiting greater activity. 4. The n value obtained from the Hill plots increased with increasing saturation and were lower in larvae than adults at the same level of blood saturation. 5. The Bohr effect in larvae at 10 degrees C over the pH range 6-5-8-1 was --0-25, a value which did not differ significantly from the −0-22 found in adults.