Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB003

Poster Communications

Long-term recording of renal and lumbar sympathetic nerve activity in response to myocardial infarction in conscious rats

M. Yoshimoto1, S. Ikegame1, Y. Shiwa1, K. Miki1

1. Department of Environmental Health, Nara Women's University, Nara, Japan.

Sympathetic nerve activity (SNA) has been implicated in the morbidity and mortality associated with acute myocardial infarction (MI). However, little is known regarding the time course and degree of changes in SNA caused by MI. This study was designed to continuously measure renal sympathetic nerve activity (RSNA) and lumbar sympathetic nerve activity (LSNA) in a longitudinal manner for 28 days in response to MI by ligation of the left anterior descending artery (LAD). Male Wistar rats were randomly allocated to LAD ligation (MI group) or sham surgery. The rats were anaesthetized with isoflurane and pentobarbital sodium and chronically implanted with a Data Sciences International telemetry device and a bipolar renal and lumbar nerve electrode for continuous measurement of the mean arterial pressure (MAP), heart rate (HR), RSNA, and LSNA. After 7 days of surgical recovery, the MAP, HR, RSNA, and LSNA were monitored continuously for 4 days (control period; Days −4 to −1). Four days later, the animals were anaesthetized by inhalation of isoflurane (4%) and intubated, and the heart was exposed via a left thoracotomy. The LAD was ligated with a 6-0 suture near its origin. Another group of rats underwent sham ligation. Transthoracic echocardiography was performed before (Day −4) and after (Day 24) the experiment. After the experiment, the heart was excised and stained with Masson trichrome to confirm the infarct size. The rats in the MI group were divided into two subgroups: those that died within 3 days after LAD ligation (MI-3Days group) and those that survived for 24 days (MI-Survivor group). On Day 1 in the MI-3Days group, LSNA increased by 200% ± 40% and MAP decreased by 25 ± 5 mmHg while RSNA and HR did not change significantly relative to the pre-MI values. On Day 1 in the MI-Survivor group, LSNA tended to increase while RSNA and HR did not change significantly relative to the pre-MI values. In the MI-Survivor group, RSNA increased gradually from Day 9 and reached a statistically significant level by 20% ± 3% on Day 24, while LSNA and MAP remained unchanged compared with the sham group. The major differences in the response of SNA between the MI-3Days and MI-Survivor groups were the massive increase in LSNA and sustained reduction of MAP observed on Day 1. Why LSNA increased in a regionally specific manner in the MI-3Days group remains unknown; however, LSNA could serve as a marker for predicting a poor prognosis after MI. On Day 24 in the MI-Survivor group, RSNA was significantly higher than that in the sham group; however, there were no differences in MAP, HR, or LSNA. These findings suggest that RSNA is likely to play a significant role in compensating for the malfunction of cardiac performance caused by MI. This study shows that LSNA and RSNA respond to MI differently over time and in a region-specific manner after MI.

Where applicable, experiments conform with Society ethical requirements