April 1, 2002Clinical Science
Nitric oxide and cardiac parasympathetic control in human heart failure
Why the study?
Does inhibition of endogenous NO production with l-NMMA alter heart rate variability and baroreflex sensitivity compared to phenylephrine in heart failure patients?
Population
24 subjects: 12 heart failure patients and 12 age/sex-matched healthy control subjects.
Comparison
Inhibition of endogenous NO production with… vs Equipressor dose of the control vasoconstrictor…
Design
Other
Authors
Discussion
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Member takes
Implication
Baroreflex parasympathetic activation in heart failure depends on endogenous NO; leaves open whether NO modulation improves outcomes.
Structured PICO
Does inhibition of endogenous NO production with l-NMMA alter heart rate variability and baroreflex sensitivity compared to phenylephrine in heart failure patients?
P
Population
24 subjects: 12 heart failure patients (NYHA class II-III; mean age 52 years, range 38-67 years) and 12 age/sex-matched healthy control subjects (mean age 50 years, range 36-62 years).
I
Intervention
Inhibition of endogenous NO production with NG-monomethyl-l-arginine (l-NMMA; 3 mg/h/kg)
C
Comparator
Equipressor dose of the control vasoconstrictor phenylephrine (12-36 μg/h/kg)
O
Outcome
Heart rate variability (RMSSD and high-frequency power) and baroreflex sensitivitysurrogate
Baroreflex-mediated cardiac parasympathetic activation in human heart failure is dependent upon endogenous nitric oxide synthesis, similar to healthy subjects.
Cite This Study
Chowdhary et al. (2002) studied this question.