The thermoregulatory responses to 10 degrees C (for 3 h) were investigated in 1) 12 natives from sea level (lowlanders) at 150 m, and on arrival at 3,350 and 4,340 m; 2) 6 of these during a 6-wk sojourn at 4,360 m, and on return to sea level; and 3) 5 natives from each of the two altitudes (highlanders) in their respective habitat, and after descent to 150 m. The cold-induced increase in the rate of O2 consumption (Vo2) of the lowlanders was significantly smaller at both altitudes than at sea level. It did not recover substantially during the 6 wk at altitude, but was restored to its initial rate on return to sea level. By contrast, visible shivering activity was augmented on arrival at altitude. It persisted throughout the 6 wk there, but was greatly depressed on return to sea level, despite the increased Vo2. Mean skin temperatures (Tsk) stabilized in the cold at significantly higher values at altitude. Rectal temperature (Tre) decreased similarly at all altitudes. Vo2 of the highlanders in the cold was significantly greater at sea level than at their resident altitudes, although shivering activity was less intense; Tsk stabilized at significantly lower levels at 150 m than at either altitude. These results indicate that altitude exposure reduces the calorigenic response of man to cold, and that this effect is not moderated by acclimatization to altitude, yet is reversible immediately on descent to sea level. The component of cold thermogenesis which appeared to be reduced by altitude exposure was nonshivering thermogenesis rather than visible shivering.
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.
Electrical stimulation of the ventromedial region of the rostral fastigial nucleus (FN) in the cat produced marked quantifiable changes in respiration that were highly correlated with the concurrently elicited cardiovascular responses. The threshold- and stimulus-response curves were very similar for the two responses. Stimulation at relatively low frequencies produced increases in respiratory rate at all active sites. At approximately half the sites biphasic responses were observed with increases in stimulus frequency. These were characterized by a transient period of apnea beginning with onset of the stimulus, followed by an increased respiratory rate. At the remaining sites respiratory rate increased at all stimulation frequencies tested. Inspiratory duration decreased, and mean inspiratory flow increased. Tidal volume was not significantly altered. Similar changes were also observed when the pressor response was blocked by phenoxybenzamine. These observations, together with the frequent demonstration of expiratory-to-inspiratory and inspiratory-to-expiratory phase switching with short-burst stimulation, suggest that the FN can influence a respiratory central pattern generator. Based on these findings, a possible role for the FN in integrating cardiovascular and respiratory responses is suggested.
In previous studies, bilateral lesions of the rostral fastigial nucleus (rFN) of the cerebellum impaired recovery of mean arterial pressure (MAP) after many forms of hypotension. This study examined effects of cerebellar lesions on baroreflex responses during transient, isovolaemic, non-orthostatic changes in MAP in anaesthetized cats. Bilateral rFN lesions did not alter the rate or extent of fall in MAP induced by nitroprusside, but reduced by 39% the reflex increase in heart rate per unit decrease in pressure (delta HR/delta MAP). Femoral artery resistance remained below control levels. Lesions prolonged the time for 50% MAP recovery after nitroprusside by 93%. During phenylephrine-induced MAP increases, bilateral rFN lesions augmented reflex delta HR/delta MAP by 68%. In intact cats, the reflex decrease in HR after phenylephrine was blocked by electrical stimulation of the rFN, but appeared immediately after stimulation was stopped. Stimulation alone increased both MAP and HR. Propranolol failed to block either the increased HR or the suppression of reflex cardiodeceleration induced by rFN stimulation. Decreases in resting HR after rFN lesions may reflect removal of tonic cerebellar inhibition of cardiac parasympathetic tone. Thus, the cerebellum can influence autonomic output and modify baroreflex sensitivity by augmenting cardiovascular responses mediated by the sympathetic nervous system and inhibiting those mediated by the parasympathetic nervous system.
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