Cardiorespiratory reflex control in rats with left ventricular dysfunction

Am J Physiol. 1995 Jan;268(1 Pt 2):H218-25. doi: 10.1152/ajpheart.1995.268.1.H218.

Abstract

Patients with heart failure exhibit a neurohumoral excitatory state and abnormal baroreflex control of the cardiovascular system. We determined whether arterial baroreflexes are impaired during left ventricular dysfunction (LVD) caused by chronic myocardial infarction in the absence of congestive heart failure and whether abnormal central mechanisms contribute to this impairment. Baroreceptors were stimulated in anesthetized rats with and without LVD by increasing arterial pressure with phenylephrine. Lumbar sympathetic nerve and phrenic nerve activity as well as heart rate were recorded. Rats were divided into different groups based on infarct size. Rats with moderate LVD showed impaired baroreflex control of sympathetic, ventilatory, and heart rate responses. Baroreflex gains were inversely related to the size of the infarct. The central gain for sympathetic nerve activity, obtained by using electrical stimulation of the aortic depressor nerve, also was impaired. Baroreflex control of the cardiorespiratory system is thus impaired in rats with moderate LVD in the absence of congestive heart failure. The attenuated baroreflexes are likely due to abnormal afferent mechanisms, although central mechanisms contribute to the impaired barosympathetic reflex.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Afferent Pathways / physiology
  • Animals
  • Aorta / innervation
  • Baroreflex*
  • Blood Pressure
  • Coronary Vessels / physiology
  • Disease Models, Animal
  • Heart Failure / physiopathology
  • Heart Rate
  • Humans
  • Nerve Fibers / physiology
  • Rats
  • Rats, Sprague-Dawley
  • Respiration
  • Sensitivity and Specificity
  • Sympathetic Nervous System / physiology
  • Sympathetic Nervous System / physiopathology
  • Ventricular Dysfunction, Left / physiopathology*