Assessment of gain of tachycardia and bradycardia responses of cardiac baroreflex.
The cardiac baroreflex was studied in humans by means of vasoactive drugs and in conscious rabbits by the drug and perivascular cuff methods, which provide somewhat different afferent drive. Mean arterial pressure (MAP)-heart rate (HR) curves were derived using 1) a single symmetric logistic function and 2) a compound function, where the two halves of separate logistic functions were centered on the resting value, one for the tachycardia response and the other for the bradycardia response. There were some differences in overall reflex parameters (plateaus, HR range, gain) between the two methods because of minor degrees of asymmetry. But the differences were small, and the single symmetric logistic adequately describes the overall properties. With the compound function, we assessed average gain, Gt and Gb, for the tachycardia and bradycardia responses and the corresponding normalized (range-independent) gains, Ct and Cb. The resting HR has a large effect on Gt/Gb, since it determines the HR range of each logistic. Moreover, Gt/Gb depends on both resting autonomic tone and reflex changes. However, Ct and Cb provide information about "intrinsic" differences in sensitivity; they are independent of resting HR but entirely dependent on reflex autonomic changes. In rabbits Ct and Cb tended to be larger with the cuff than with the drug method; in addition, with the former Ct less than Cb, whereas with the drug method Ct greater than or equal to Cb, which was consistent with differences in afferent drive. There were also differences between humans and rabbits in Ct/Cb of the vagal component of the reflex. The assessment of the normalized gains of the compound logistic function has substantial advantages over previous methods for assessing gain of the tachycardia and bradycardia responses.
Kingwell
B A
BA
Baker Medical Research Institute, Melbourne, Victoria, Australia.
McPherson
G A
GA
Korner
P I
PI
D000328:Adult; D000818:Animals; D001013:Aorta, Thoracic / Q000502:physiology; D001262:Atenolol / Q000494:pharmacology; D001794:Blood Pressure; D003250:Constriction; D006321:Heart / Q000294:innervation / Q000502:physiology*; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D008954:Models, Biological; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D011433:Propranolol / Q000494:pharmacology; D011817:Rabbits; D013564:Sympathetic Nervous System / Q000502:physiology; D014630:Vagus Nerve / Q000502:physiology; D014682:Vena Cava, Inferior / Q000502:physiology
D009599:Nitroprusside; D010656:Phenylephrine; D001262:Atenolol; D011433:Propranolol