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  • Journal
    Digital Access PubMed Central v. 1-4, 1992-95.
  • Article
    Koizumi K, Nishino H, Brooks CM.
    Proc Natl Acad Sci U S A. 1977 May;74(5):2177-81.
    Stretching the atria in anesthetized dogs produces reflex changes in heart rate, and in cardiac and renal sympathetic nerve activity. Anemic decerebration, cord transection at C4-C5, and severance of vagal or sympathetic cardiac nerves was done to identify the pathways and centers essential for these reflexes. Stretching the right atrium produced an aceleration of the heart and a definite increase in sympathetic nerve activity. Left atrial-stretch caused biphasic responses: an initial sympathetic nerve inhibition and slower heartbeat folowed by sympathetic excitation and heart acceleration. The afferents responsible were carried mainly by the vagi; efferent neural control of the heart was mostly sympathetic. The reflex inhibition observed was integrated chiefly at the medullary level, but supramedullary structures contributed to the augmentation in sympathetic activity and heart rate. When central connections between vagal afferent and sympathetic efferent pathways were separated by cord transection, atrial stretch caused a decrease in heart rate due to reflex action through the vagal loop. After the cord was sectioned, we found that some afferent impulses from the atria traveling in sympathetic nerves produced a slight reflex augmentation of sympathetic efferent activity, though insufficient to affect the heart rate. Somatosympathetic reflexes evoked in cardiac and renal sympathetic nerves by stimulation of various somatic afferent pathways were also affected by atrial stretch indicating central nervous system interactions. Reflex responses to right atrial stretch were superimposed on accelerations of myogenic origin.
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