What question did this study set out to answer?

To examine the roles and interactions of alpha- and beta-adrenergic receptors in mediating paradoxic bradycardia during inferior vena cava occlusion.

November 1, 1994Canadian Journal of Physiology and Pharmacology

Paradoxic bradycardia (vasodepressor reaction) induced by inferior vena cava occlusion: the role of α- and β-adrenergic receptors and their interaction

Q: What is the clinical evidence from this study?

Population: Paradoxic bradycardia (vasodepressor reaction) (n=44). Intervention: Inferior vena cava occlusion with adrenergic agonists/antagonists vs. Control conditions. Primary outcome: Maximum changes in R-R interval.

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Key result

Paradoxic bradycardia dependent on vagal afferents can be induced by reduced venous return during excess beta-1 stimulation or alpha-adrenergic antagonism, and is blocked by alpha-1 stimulation.

Key Points

To examine the roles and interactions of alpha- and beta-adrenergic receptors in mediating paradoxic bradycardia during inferior vena cava occlusion.
Measured maximum changes in R-R interval during 60-second inferior vena cava occlusions in 44 rats under baseline and drug-treated conditions.
Administered adrenergic agonists (isoproterenol, phenylephrine, epinephrine, norepinephrine) and antagonists (phentolamine, prazosin, propranolol).
Assessed neural pathways by evaluating responses following atropine treatment, right vagotomy, and left vagotomy.
Inferior vena cava occlusion under control, phenylephrine, and phenylephrine plus isoproterenol shortened R-R intervals (-16.8 ± 1.4 ms, -24.1 ± 2.2 ms, and -4.9 ± 1.2 ms), whereas isoproterenol, phentolamine, and prazosin prolonged R-R intervals (+89.2 ± 9.5 ms, +58.9 ± 4.1 ms, and +64.4 ± 10.2 ms).
Phentolamine-induced R-R prolongation was blocked by left vagotomy (-9.6 ± 1.1 ms) but not by atropine (+66.0 ± 2.4 ms) or right vagotomy (+73.8 ± 13.7 ms), while propranolol reversed prazosin-induced prolongation (-14.3 ± 2.8 ms).
Epinephrine shortened the R-R interval (-9.5 ± 2.2 ms) but caused prolongation following prazosin pretreatment (+13.7 ± 6.0 ms), whereas norepinephrine alone induced prolongation (+21.0 ± 6.7 ms).

PICO

Population

44 rats undergoing inferior vena cava occlusion to study paradoxic bradycardia and adrenergic receptor interactions.

Intervention / Comparator

Inferior vena cava occlusion with adrenergic agonists/antagonists vs Control conditions

Primary Outcome

Maximum changes in R-R interval

Discussion

No takes yet. Share an insight, caveat, or question.

Implication

May explain bradycardia during venodilation with beta-1 excess or alpha blockade; leaves open clinical relevance.

Cite This Study

Waxman et al. (1994) studied Paradoxic bradycardia (vasodepressor reaction) (n=44). Inferior vena cava occlusion with adrenergic agonists/antagonists vs. Control conditions was evaluated on Maximum changes in R-R interval. Paradoxic bradycardia dependent on vagal afferents can be induced by reduced venous return during excess beta-1 stimulation or alpha-adrenergic antagonism, and is blocked by alpha-1 stimulation.

synapsesocial.com/papers/6a964ecea45595e5080e19bc https://doi.org/10.1139/y94-183

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Paradoxic bradycardia (vasodepressor reaction) induced by inferior vena cava occlusion: the role of α- and β-adrenergic receptors and their interaction

Key Points

PICO

Discussion

Implication

Cite This Study

Paradoxic bradycardia (vasodepressor reaction) induced by inferior vena cava occlusion: the role of α- and β-adrenergic receptors and their interaction

Key Points

PICO

Discussion

Implication

Cite This Study

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