Vascular sympathetic nerve function in congestive heart failure.

Abstract

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 less than 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 less than 0.025 and p less than 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.