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Ischemic heart failure induces chronic sympathoexcitation in conscious Sprague Dawley rats.
Author(s) -
Burris Sarah Kimberly,
Knuepfer Mark M
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.610.13
Subject(s) - medicine , heart failure , cardiology , myocardial infarction , heart rate , cold pressor test , reflex , blood pressure , anesthesia
Indirect estimates of sympathetic nerve activity (SNA) in rats suggest increased sympathetic drive contributes to the compensatory remodeling and progression of heart failure following myocardial infarction. We examined the role of SNA during the development of ischemic heart failure by recording SNA for weeks in conscious rats. Male Sprague‐Dawley rats were instrumented to record arterial pressure, heart rate, cardiac output, electrocardiographic activity, and adrenal and renal SNA. Cardiac function and size of the infarct were assessed pre‐ and post‐infarct using 2‐D and M‐mode echocardiography and/or histology. Ganglionic blockade (trimethaphan, 10 mg/kg, i.v.) was administered daily to ensure quality of SNA recordings. Responses to acute stress (cold pressor test) were recorded prior to and for 2‐3 weeks following coronary ligation. Greater increases in resting renal and adrenal SNA were seen following myocardial infarction. Acute stress with cold water resulted in consistent increases in SNA and pressor responses in which SNA responses were attenuated following myocardial infarction. Our findings directly demonstrate that resting SNA increases during the development of ischemic heart failure yet reflex responses are blunted. We suggest that chronic sympathoexcitation contributes to the progression of heart failure. Supported by USPHS DA0017371, HL091440 & USPHS T32 GM008306.