Pressure-heart rate relationship in intact and after stepwise elimination of three major baroreflex loops in dogs.
Systemic arterial blood pressure (BP)-heart rate (HR) relationship (the pressor test) is often used as an index of baroreflex. We evaluated this index by simultaneously comparing BP-HR, right carotid sinus pressure (CSP)-nerve action potentials (NAP), and NAP-HR relationship in dogs anesthetized with pentobarbital. BP was increased or decreased stepwise by intravenous (IV) infusions of phenylephrine or sodium nitroprusside, respectively. In nine dogs BP-HR and CSP-NAP relationships were measured and NAP-HR relationship was constructed before and after sequential and stepwise sectioning of the left aortic depressor nerve (LADN), the right aortic depressor nerve (RADN), and blockade of the left carotid sinus nerve (BLK) with 1% lidocaine. We found that HR was a negative sigmoidal function of BP in intact dogs. Linear slope of this relationship was significantly reduced after sectioning of LADN and RADN, but returned toward baseline after BLK. NAP was a positive sigmoidal function of CSP in intact dogs. Linear slope of this relationship was significantly depressed after sectioning of LADN and RADN. However, after BLK, the slope surpassed control, suggesting the existence of a central communication between the two carotid sinuses. HR was a negative function of NAP in intact dogs. However, as the other baroreflex feedback loops were eliminated, the slope of the NAP-HR relationship approached zero indicating that a closed integrated parallel feedback system is required for reflex regulation of HR. Our findings suggest that under normal conditions the pressor test is a valid index for baroreceptor function, but its use may not be warranted in chronic pathological states, such as atherosclerosis and hypertension. However, in contrast to the present acute experimental model, chronic pathological processes may not develop in sequence, and baroreceptor function on the affected site may not be completely eliminated from the baroreceptor loop such as performed in this study.
Department of Anesthesiology, Northwestern University Medical School, Chicago, Illinois 60611, USA.
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D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000759:Adjuvants, Anesthesia / Q000008:administration & dosage; D000779:Anesthetics, Local / Q000008:administration & dosage; D000818:Animals; D001011:Aorta / Q000294:innervation; D001161:Arteriosclerosis / Q000503:physiopathology; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology*; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D002346:Carotid Sinus / Q000187:drug effects / Q000294:innervation / Q000502:physiology; D004195:Disease Models, Animal; D004285:Dogs; D005246:Feedback / Q000187:drug effects; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology; D008012:Lidocaine / Q000008:administration & dosage; D016014:Linear Models; D009407:Nerve Block; D009599:Nitroprusside / Q000494:pharmacology; D010424:Pentobarbital / Q000008:administration & dosage; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology*; D015203:Reproducibility of Results; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology
D000759:Adjuvants, Anesthesia; D000779:Anesthetics, Local; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D008012:Lidocaine; D010424:Pentobarbital