The present study was designed to investigate the role of adenosine in the hypoxic depression of synaptic transmission in rat hippocampus. An in vivo model of hypoxic synaptic depression was developed in which the common carotid artery was occluded on one side in the urethane-anesthetized rat. Inspired oxygen levels were controlled through a tracheal cannula. Rats were placed in a stereotaxic apparatus for stimulation and recording of bilateral hippocampal field excitatory postsynaptic potentials. The percent inspired oxygen could be reduced to levels that produced a reversible and repeatable depression of evoked synaptic transmission restricted to the hippocampus ipsilateral to the occlusion. Further reduction in the level of inspired oxygen depressed synaptic transmission recorded from both hippocampi. The adenosine nonselective antagonist caffeine and the A(1) selective antagonist 8-cyclopentyltheophylline prevented the initial depression in synaptic transmission. We conclude that the initial depression of synaptic transmission observed in the rat hippocampus in vivo is due to endogenous adenosine acting at neuronal adenosine A(1) receptors.

Nine alligators, Alligator mississippiensis, were injected with 133Xe and the clearance half times measured in response to heating and cooling. Mean half times for thermostable, heating, and cooling conditions were 12.2, 8.6, and 28.3 min, respectively, indicating cutaneous vasodilation in response to local heating and reduced blood flow during cooling. Alterations of cutaneous blood flow occurred before changes in body temperature or heart rate. Warming portions of the animal while shading the injection site resulted in reduced blood flow when heat loss occurred. Skin thickness (S in cm) was related to body mass (M in kg) as S = 0.08 M0.38. Cutaneous blood flow per unit area was found to increase with increasing body mass from approximately 0.0025 to 0.025 ml blood-cm-2 of skin-min-1 during warming and from 0.0018 to 0.0045 during cooling for the 0.18--8.6 kg animals, respectively.

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This study was performed to test the effect of the chemical composition of the blood on cerebral blood flow (CBF) regulation in turtles. The CBF response to increases in arterial PCO2 (PaCO2) (hypercapnia) was measured during normoxia and anoxia in anesthetized freshwater turtles Pseudemys scripta. The radioactive-microsphere technique was used to measure CBF. CBF increased with increases in PaCO2. The sensitivity of the CBF response to hypercapnia (delta CBF/delta PaCO2) was 0.68 ml.min-1.100 g-1. Torr-1 during normoxia. delta CBF/delta PaCO2 increased to 3.44 ml.min-1.100 g-1. Torr-1 during anoxia. The increases in CBF occurred at constant mean arterial blood pressure, which indicates that cerebral vascular resistance decreased. The increased CBF response during asphyxia (hypercapnia-anoxia) could be beneficial for survival during prolonged dives by increasing glucose delivery for brain anaerobic metabolism. In addition, increased CBF could aid in regulating brain acid-base composition by controlling extracellular fluid PCO2.

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Gas exchange and arterial blood acid-base status were measured in 13 conscious alligators, Alligator mississipiensis, at 15, 25, and 35 degrees C. Arterial pH decreased by 0.250 units (from 7.635 to 7.385) and arterial carbon dioxide partial pressure increased by 11.4 Torr (from 11.8 to 23.2) as body temperature increased from 15 to 35 degrees C. No statistically significant changes occurred in arterial bicarbonate concentration. When OH-/H+ and alpha-imidazole were compared at each temperature, more variability was observed in OH-/H+, which increased from 8.7 to 12.0 as temperature increased from 15 to 35 degrees C. alpha-Imidazole remained essentially constant (0.76 at 15 degrees C and 0.80 at 35 degrees C). Body temperature increase caused marked increases in minute ventilation (VE), oxygen consumption (VO2), and carbon dioxide production (VCO2). The relative changes in these parameters resulted in a decrease in both VE/VO2 and VE/VCO2. The data of the present study are consistent with the concept that poikilotherms regulate their alveolar ventilation with changes in body temperature in order to keep OH-/H+ or alpha-imidazole constant.