English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

Experiments were performed to determine the influence of cardiac sympathetic efferent nerve stimulation on the discharge rate of atrial type B stretch receptors in the anesthetized, open-chest dog. In all experiments, the left stellate ganglion was stimulated following volume expansion. To determine the effects of stellate stimulation, the responses of atrial receptors were observed during the withdrawal of blood in steps following intravascular volume expansion. Stimulation of the stellate ganglion decreased receptor discharge and left atrial pressure in all experiments. A change from a control left atrial pressure of 2.5 cm H2O (in peak left atrial u-wave pressure) resulted in a mean increase in receptor discharge of 6.6 ±1. 4 spikes/cardiac cycle during stellate stimula- tion; however, a change from a control pressure of 0.0 cm H2O resulted in a mean decrease in receptor discharge of 1.5 ± 1.5 spikes/cardiac cycle. The curves relating the change in atrial receptor discharge to the change in left atrial pressure during hemor- rhage and the curve for these parameters during stellate stimulation were not signifi- cantly different from each other. Apparently, the decreased discharge during sym- pathetic stimulation was the result of a decline in left atrial pressure rather than a result of any direct effect on the receptor per se.

Evidence for an Indirect Sympathetic Control of Atrial Stretch Receptor Discharge in the Dog