Reflex control of sympathetic outflow and depressed baroreflex sensitivity following myocardial infarction.
Reflex control of heart rate is frequently impaired following myocardial infarction. This is referred to as depressed baroreflex sensitivity. The aim of these experiments was to assess the function of other autonomic reflexes in dogs with depressed baroreflex sensitivity. Comparisons were made to dogs in whom baroreflex sensitivity was preserved or unchanged after myocardial infarction. Under chloralose-barbiturate anesthesia, reflex control of sympathetic outflow by the sinoaortic baroreceptors was determined by measurement of changes in systolic arterial pressure and efferent renal sympathetic nerve activity during infusion of phenylephrine. Following sinoaortic denervation, reflex control of sympathetic outflow by cardiac receptors with vagal afferent fibers was determined by measurement of changes in pulmonary capillary wedge pressure and renal nerve activity during blood volume expansion. Reflex decreases in renal nerve activity in response to increases in arterial pressure were similar in the two groups of dogs. In contrast, elevation of pulmonary capillary wedge pressure elicited significantly greater reflex decreases in renal nerve activity in dogs with depressed baroreflex sensitivity following myocardial infarction compared to dogs with preserved baroreflex sensitivity. Hemodynamic parameters and infarct sizes were similar in each group. In conclusion, activation of cardiac receptors with vagal afferent fibers elicited greater reflex inhibition of sympathetic outflow in dogs with depressed baroreflex sensitivity following myocardial infarction. These data suggest that these receptors are "sensitized". These results provide additional support for the hypothesis that depressed reflex control of heart rate following myocardial infarction is related to augmented afferent input from the left ventricle.
Department of Internal Medicine (Cardiology), Medical College of Virginia Campus of Virginia Commonwealth University, United States; Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond, Virginia 23249, United States.
Christine M
CM
Jones
Department of Internal Medicine (Cardiology), Medical College of Virginia Campus of Virginia Commonwealth University, United States; Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond, Virginia 23249, United States.
M Susan
MS
Quinn
Department of Internal Medicine (Cardiology), Medical College of Virginia Campus of Virginia Commonwealth University, United States; Hunter Holmes McGuire Department of Veterans Affairs Medical Center, Richmond, Virginia 23249, United States. Electronic address: anthony.minisi@va.gov.
Anthony J
AJ
Minisi
D000344:Afferent Pathways / Q000502:physiology / Q000503:physiopathology; D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D017704:Baroreflex / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002346:Carotid Sinus / Q000294:innervation / Q000503:physiopathology* / Q000601:surgery; D003714:Denervation / Q000009:adverse effects / Q000379:methods; D004285:Dogs; D006321:Heart / Q000294:innervation / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology; D006339:Heart Rate / Q000502:physiology; D007261:Infusions, Intra-Arterial; D007668:Kidney / Q000294:innervation / Q000503:physiopathology; D009203:Myocardial Infarction / Q000473:pathology / Q000503:physiopathology*; D009433:Neural Inhibition / Q000502:physiology; D010656:Phenylephrine / Q000008:administration & dosage; D011311:Pressoreceptors / Q000503:physiopathology*; D011669:Pulmonary Wedge Pressure / Q000502:physiology; D013564:Sympathetic Nervous System / Q000503:physiopathology*; D014630:Vagus Nerve / Q000503:physiopathology; D014662:Vasoconstrictor Agents / Q000008:administration & dosage
D014662:Vasoconstrictor Agents; D010656:Phenylephrine