In the ears of anaesthetized rabbits cutaneous efferent sympathetic nerve activity (SkNA) and blood flow (Q) to capillaries have been measured during various thermal treatments. Warming the spinal cord or skin of the body midside caused a marked decrease in SkNA but capillary Q increased only slightly. Exposure to a warm environment or localized warming of the ear alone induced either a decrease, an increase, or no change in SkNA, but capillary Q always increased markedly. The usual slight increase in capillary Q during spinal warming, was abolished by preventing the usual marked increase in skin temperature. When the spinal cord of the conscious rat was warmed, a marked increase in temperature of the tail (which contains arteriovenous anastomoses, AVA's) indicated dilatation, whereas there was no change in ear temperature (where there are no AVA's). When these results are considered together with recently defined differential influences of reflex and direct effects of temperature on blood flow through cutaneous AVA's and capillaries, it is concluded: (1) That thermally-induced reflex changes in skin blood flow are mediated via sympathetic nervous action on AVA's; (2) Changes in blood flow evoked by direct heating take place through the capillaries, not the AVA's, quite independently of SkNA.
The patterns of regional changes of sympathetic efferent activity evoked by thermal stimulation of the spinal cord and by arterial and primary tissue hypoxia were investigated in decerebrated, anesthetized and immobilized rabbits. Decerebration was performed either at the mid- or infracollicular level. The responses of the decerebrated rabbits evoked by spinal thermal stimulation were the same as those of intact rabbits, i.e., splanchnic and cardiac sympathetic activity increased and cutaneous sympathetic activity decreased during warming, while the reverse response was elicited by cooling. It is concluded that the typical thermoregulatory response pattern of the sympathetic nervous system can be produced also after the loss of hypothalamic integration, i.e., by integrative mechanisms in the lower brain stem and the spinal cord. In contrast, the responses of decerebrated rabbits to arterial and primary tissue hypoxia differed from those of intact rabbits in that they consisted in an overall activation in all investigated sympathetic branches. It is confirmed by this result that suprabulbar integration is essential for the generation of the inhibitory components in the differential sympathetic responses to hypoxia, which typically consist in cutaneous and cardiac sympathetic inhibition with splanchnic activation during arterial hypoxia and in cutaneous sympathetic inhibition with cardiac and splanchnic sympathetic activation during primary tissue hypoxia.
The responses of renal sympathetic nerve activity (RSNA) to changes in mean arterial pressure (MAP) during normoxia and hypoxia was studied in conscious rabbits and during anesthesia with pentobarbitone (PB) by determining the RSNA baroreflex curves. In conscious rabbits, the gain in RSNA response was greater and the range of MAP between minimum and maximum levels of RSNA was narrower than in anesthetized rabbits. The renal sympathetic baroreflex was augmented by hypoxia, indicating a central excitatory interaction between the effects of baro- and chemoreceptor stimulation. However, hypoxia produced no significant change in median blood pressure. During anesthesia with PB, resting MAP was decreased, median blood pressure was lowered, and renal sympathetic baroreflexes were less pronounced. Renal sympathetic baroreflex was augmented by hypoxia, and there was a significant increase in median blood pressure. These results provide direct evidence of an inhibitory effect of PB on the response of RSNA to baro- and chemoreceptor stimulation.
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