August 1, 1997AJP Regulatory Integrative and Comparative Physiology
Enhanced responsiveness of cardiac vagal chemosensitive endings to bradykinin in heart failure
Key result
Pacing-induced heart failure enhances cardiac vagal chemosensitive afferent sensitivity selectively to bradykinin.
Why the study?
The sensitivity of cardiac vagal chemosensitive endings to bradykinin in chronic heart failure was unclear despite evidence of enhanced cardiac chemoreflex during heart failure.
Population
Pacing-induced heart failure dogs and sham-operated dogs
Comparison
Left atrial injections of bradykinin and capsaicin with and without captopril or indomethacin in HF versus sham dogs
Design
Preclinical experimental study measuring cardiac vagal single fiber activity
Authors
Discussion
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Implication
May indicate altered vagal reflexes in experimental HF; leaves open clinical relevance and need for human studies.
Structured PICO
P
Population
Dogs with pacing-induced heart failure compared to sham-operated controls.
E
Exposure
Left atrial injections of bradykinin (0.001-1 microgram/kg) and capsaicin (1-10 micrograms/kg), with subsequent administration of captopril (2 mg/kg i.v.) or indomethacin (5 mg/kg i.v.)
C
Comparator
Sham-operated dogs
O
Outcome
Activity of cardiac vagal single fibers (afferent responses and resting discharge)surrogate
Main Result
Absolute Event Rate: 1.5% vs 1.3%
In a canine model of heart failure, cardiac vagal chemosensitive endings exhibit enhanced sensitivity to bradykinin, which is modulated by the cyclooxygenase system.
Cite This Study
Schultz et al. (1997) studied Heart failure. Pacing-induced heart failure vs. Sham-operated dogs was evaluated on Resting discharge of cardiac vagal fibers (impulses/s). In a canine model, pacing-induced heart failure enhanced the sensitivity of cardiac vagal chemosensitive endings to bradykinin but not capsaicin, without altering resting discharge rates.