May 1, 1976Cardiovascular Research
An excitatory nociceptive cardiac reflex elicited by bradykinin and potentiated by prostaglandins and myocardial ischaemia
Population
Dog heart model (exposed ventricular surface)
Design
Preclinical
Authors
Discussion
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Implication
Hypothesis-generating for ischemic reflex mechanisms in animals; leaves open translation to human anginal pain.
Key Points
- To investigate whether bradykinin evokes a cardiovascular nociceptive reflex from the ventricular surface and how prostaglandins and myocardial ischaemia modulate this response.
- Applied bradykinin topically to the exposed ventricular surface of canine hearts at varying doses.
- Co-administered prostaglandin E1 or E2, administered indomethacin, and performed temporary coronary artery occlusion to assess reflex sensitivity.
- Topical bradykinin elicited a dose-dependent reflex response characterized by increased blood pressure, tachycardia, renal vasoconstriction, and muscular vasodilation.
- Reflex responses were augmented by concomitant prostaglandin E1 or E2 and reduced by indomethacin.
- Temporary coronary occlusion sensitized the ventricular surface to topical bradykinin, indicating synergistic sensory receptor excitation during ischaemia.
Structured PICO
P
Population
Dog heart model (exposed ventricular surface)
I
Intervention
Topical application of bradykinin, with or without prostaglandin E1 or E2, indomethacin, or temporary coronary artery occlusion
O
Outcome
Reflex cardiovascular response (rise in blood pressure, tachycardia, renal vasoconstriction, and muscular vasodilation)surrogate
Bradykinin and prostaglandins released during myocardial ischemia may act in concert to excite sensory receptors, mediating both anginal pain and its accompanying cardiovascular reflexes.
Cite This Study
Staszewska-Barczak et al. (1976) studied this question.