Key result
In rats with chronic myocardial infarction, sympathetic renal nerve denervation restored volume expansion-induced natriuresis, increasing urinary sodium excretion by 1211% vs 684% in controls (P<0.01).
Why the study?
Does sympathetic renal nerve denervation improve volume expansion-induced natriuresis in a rat model of chronic myocardial infarction?
Population
Male Wistar rats with experimental chronic myocardial infarction induced by coronary ligation
Comparison
Sympathetic renal nerve denervation vs Sham-operated renal denervation
Design
Preclinical
Follow-up
3 to 16 weeks
Authors
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May enhance natriuresis in experimental post-MI HF; hypothesis-generating and should not yet change practice.
Does sympathetic renal nerve denervation improve volume expansion-induced natriuresis in a rat model of chronic myocardial infarction?
Absolute Event Rate: 1211% vs 684%
p-value: p=<0.01
Renal sympathetic nerve activity plays a key role in mediating sodium retention in congestive heart failure following myocardial infarction in a rat model.
Souza et al. (2004) studied Congestive heart failure-induced sodium retention following experimental chronic myocardial infarction (n=50). Sympathetic renal nerve denervation vs. Sham-operated renal denervation was evaluated on Increase in urinary sodium excretion (USE) after volume overload (p=<0.01). In rats with chronic myocardial infarction, sympathetic renal nerve denervation restored volume expansion-induced natriuresis, increasing urinary sodium excretion by 1211% vs 684% in controls (P<0.01).
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