Vascular sympathetic nerve function in congestive heart failure

To determine if intrinsic abnormalities of sympathetic nerve function might contribute to enhanced vascular tone in congestive heart failure, chronic myocardial infarction (infarct) was produced in rats by coronary artery ligation 9 to 10 months previously for comparison with animals subjected to sham operation (sham). The excised pulmonary artery, preincubated with ³H-norepinephrine (NE) was superfused, and stimulated electrically at 2, 4, 8 and 16 Hz. The nonnormalized data at each frequency for electrically evoked ³H overflow in excess of basal outflow was similar in sham and infarct vessels (difference not significant); however, the shape of the frequency-response curves was different. The ³H overflow/pulse from sham vessels was constant between 2 and 16 Hz; however, for the infarct vessels there was a significant reduction (p <0.05) at the highest frequency (16 Hz). Because of an 18.4% lower peak ³H overflow at 16 Hz (difference not significant), the infarct frequency-response curve shifted significantly (4 and 8 Hz, p <0.025 and p <0.01) to the left when data were expressed as a percent of peak percent ³H overflow, suggesting an increased sensitivity of the system. These data suggest that an intrinsic vascular sympathetic nerve abnormality is not a major cause of the increased plasma NE in congestive heart failure; increased nerve activity or decreased clearance of NE may be more important.