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1 Penn State Heart and Vascular Institute, Pennsylvania State University College of Medicine, Milton S. Hershey Medical Center, Hershey, Pennsylvania, United States
* To whom correspondence should be addressed. E-mail: jianhuali{at}psu.edu.
In congestive heart failure (CHF), exaggerated sympathetic activation is observed during exercise, which elicits excess peripheral vasoconstriction. The mechanisms causing this abnormality are not fully understood. Central command is a central neural process which induces parallel activation of motor and cardiovascular systems. This study was undertaken in order to determine if central command serves as a mechanism that contributes to the exaggerated sympathetic response to exercise in CHF. In decerebrate rats, renal and lumbar sympathetic nerve responses (RSNA and LSNA) to 30 s of fictive locomotion were examined. The fictive locomotion was induced by electrical stimulation of the mesencephalic locomotor region (MLR). The study was performed in control animals [fractional shortening (FS) > 40%] and animals with myocardial infarctions (MI, FS < 30%). With low stimulation of the MLR (current intensity = 20 microA), the sympathetic responses were not significantly different in the controls (RSNA: +18±4%; LSNA: +3±2%) and MI rats (RSNA: +16±5%; LSNA: +8±3%). With intense stimulation of the MLR (50 microA), the responses were significantly greater in MIs (RSNA: +127±15%; LSNA: +57±10%) than in the controls (RSNA: +62±5%; LSNA: +21±6%). The data of this study demonstrate that RSNA and LSNA responses to intense stimulation of the MLR are exaggerated in MI rats. We suggest that intense activation of central command may play a role in evoking exaggerated sympathetic activation and inducing excessive peripheral vasoconstriction during exercise in CHF.
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