Baroreflex sensitivity and carotid sinus dimensions in dogs with coarctation

Baroreflex sensitivity (BRS) has not been assessed in coarctation, though it is diminished in renal and essential hypertension. Previous experimental studies of coarctation have dealt primarily with renal mechanisms of hypertension, and have relied on constricting the aorta in adult animals. We banded the thoracic aorta in newborn puppies, and performed studies 2 yr later. Blood pressure (BP) elevations, abundant chest wall collaterals, the absence of heart failure, and subsequent necropsy confirmed the full syndrome of natural coarctation in all dogs. Transient BP elevations were induced in conscious, unrestrained dogs with intravenous phenylephrine injections. Reflex bradycardia was quantitated by plotting each pulse interval in microseconds against BP of the preceding beat, and expressing BRS as the linear regression coefficient (slope) in ms/mmHg. Mean BRS in 10 dogs with coarctation did not differ significantly (P greater than 0.1) from 8 normal controls. Carotid sinus diameter (CSD) was also assessed. Carotid arteries were fixed in vivo by prolonged exposure to glutaraldehyde to prevent contraction, then were excised and measured in a calibrated microscope. Mean CSD in 10 dogs with coarctation was significantly greater (P less than 0.01) than in 10 control dogs. The unexpectedly normal BRS in experimental coarctation may be due to changes in CSD induced by hypertension; such changes may only develop in growing animals. Experimental studies of coarctation should use a preparation that mimics the natural lesion.