Distribution of left ventricular sympathetic afferents demonstrated by reflex responses to transmural myocardial ischemia and to intracoronary and epicardial bradykinin.
BACKGROUND. Stimulation of left ventricular (LV) receptors with sympathetic afferents generally results in reflex sympathoexcitatory responses. Stimulation of LV receptors with vagal afferents results in reflex sympathoinhibitory responses. Vagal afferents are known to be preferentially distributed to the inferoposterior (IP) wall of the LV. We tested the hypothesis that there is also a preferential distribution of LV sympathetic afferents. METHODS AND RESULTS. We measured reflex responses to stimulation of sympathetic afferents located in the anterior and IP LV. We used myocardial ischemia and chemical stimuli to increase the activity of the sensory endings in 15 chloralose-anesthetized, mechanically ventilated dogs with sinoaortic denervation and vagotomy. Reflex responses were assessed by direct recordings of efferent renal sympathetic nerve activity (RSNA). In nine dogs, maximal RSNA changes elicited by transmural anterior myocardial ischemia (22.6 +/- 3.9% increase from baseline nerve traffic) were not significantly different from maximal RSNA changes observed during transmural IP ischemia (27.1 +/- 4.4%). Similar changes in mean arterial and left atrial pressures were noted during transmural anterior and IP ischemia. In eight dogs, maximal changes of RSNA elicited by epicardial or intracoronary bradykinin to the anterior LV were not significantly different from those observed during bradykinin to the IP LV (anterior epicardial bradykinin, 76.7 +/- 11.7%; IP epicardial bradykinin, 72.2 +/- 10.0%; anterior intracoronary bradykinin, 84.6 +/- 21.0%; IP intracoronary bradykinin, 88.8 +/- 17.3%). CONCLUSIONS. We conclude that cardiac receptors with sympathetic afferents are distributed equally to the IP and anterior regions of the LV.[1]References
- Distribution of left ventricular sympathetic afferents demonstrated by reflex responses to transmural myocardial ischemia and to intracoronary and epicardial bradykinin. Minisi, A.J., Thames, M.D. Circulation (1993) [Pubmed]
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