Experimental Heart Failure

(pacing-induced) dogs. The sensitivity of these units was compared between the two groups of dogs. After development of clinical heart failure, the animals were anesthetized, and the left carotid sinus was vascularly isolated and perfused with oxygenated Krebs-Henseleit solution. Single-unit baroreceptor discharge was recorded from the carotid sinus nerve in response to stepwise increases in carotid sinus pressure (CSP). In addition, the carotid sinus diameter was measured with sonomicrometer crystals. In this way, both CSP-discharge and CSP-diameter curves were constructed for both normal and heart-failure dogs. Analysis of these curves demonstrated that the heart-failure group exhibited a significant decrease in peak discharge (48.1±3.0 vs. 22.2±+ 2.2 spikes/sec; p<0.001) and a significant elevation in threshold pressure compared with the normal animals (91.0 +5.0 vs. 119.1±+4.4 mm Hg; p<0.001). The peak slope of the CSP-discharge curve was also significantly lower in the heart-failure group (0.63 ±0.06 vs. 0.40 ±0.09 spikes/sec/mm Hg;p <0.05). In the heart-failure group, perfusion of the carotid sinus with ouabain (0.01 ,ug/ml) caused a significant decrease in threshold pressure and a significant increase in peak discharge frequency, as well as an increase in slope of the CSP-discharge curve. There were no changes in CSP-diameter relations in response to ouabain. This dose of ouabain had no effect on pressure-discharge relations or carotid sinus diameters in normal dogs. Perfusion of the isolated carotid sinus with a Krebs-Henseleit solution with 50% of the normal potassium ion concentration had no effect on peak discharge or slope, but this perfusion protocol significantly reduced threshold pressure in heart-failure dogs. Low potassium ion concentration had no effect in the normal dogs. From these data, we conclude that there is attenuation of the carotid sinus baroreceptor discharge sensitivity in this model of low-output heart failure. The data are consistent with the view that there is an augmentation of Na+,K+-ATPase activity in the carotid sinus baroreceptor. (Circulation 1990;81:1959-1966)