What question did this study set out to answer?

To determine how endogenous myocardial catecholamines and adrenergic receptor stimulation influence cellular electrophysiology and the incidence of arrhythmias during ischaemia and reperfusion.

December 1, 1984European Heart Journal

The deleterious effects of myocardial catecholamines on cellular electrophsiology and arrhythmias during ischaemia and reperfusion

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Why the study?

Does myocardial catecholamine depletion reduce arrhythmias and electrophysiological changes during ischemia and reperfusion in guinea pig hearts?

Population

Langendorff perfused guinea pig hearts

Comparison

Catecholamine depletion by pre-treatment with… vs Control hearts without catecholamine depletion…

Design

Preclinical

Follow-up

30 minutes of ischemia followed by reperfusion

Authors

WPW J PennyYale University

Discussion

Member takes

Implication

Should not yet change clinical practice; hypothesis-generating for catecholamine modulation in ischemia-reperfusion arrhythmias.

Key Points

To determine how endogenous myocardial catecholamines and adrenergic receptor stimulation influence cellular electrophysiology and the incidence of arrhythmias during ischaemia and reperfusion.
Monitored action potentials and ECG recordings from isolated Langendorff-perfused guinea pig hearts during zero flow or low flow (10% of control) ischaemia and subsequent reperfusion.
Depleted endogenous myocardial catecholamines through animal pre-treatment with 6-hydroxydopamine.
Administered methoxamine, phentolamine, and propranolol to evaluate the respective roles of alpha- and beta-adrenoceptor pathways in electrophysiological instability.
Arrhythmias occurred significantly more often during low flow ischaemia than zero flow ischaemia, with peak frequency during reperfusion following 30 minutes of ischaemia.
Catecholamine depletion significantly reduced arrhythmia incidence during both ischaemia and reperfusion, prevented spontaneous recovery of action potential amplitude and Vmax, and eliminated reperfusion-induced action potential shortening.
Methoxamine reversed the anti-arrhythmic and electrophysiological protections of catecholamine depletion, while phentolamine and propranolol modified the electrophysiological effects of ischaemia and reperfusion.

Structured PICO

Does myocardial catecholamine depletion reduce arrhythmias and electrophysiological changes during ischemia and reperfusion in guinea pig hearts?

Population

Langendorff perfused guinea pig hearts

Intervention

Catecholamine depletion by pre-treatment with 6-hydroxydopamine, with or without methoxamine, phentolamine, or propranolol

Comparator

Control hearts without catecholamine depletion undergoing ischemia and reperfusion

Outcome

Incidence of arrhythmias and cellular electrophysiological changes (action potential amplitude, Vmax, refractory period) during ischemia and reperfusionsurrogate

Endogenous myocardial catecholamines contribute to arrhythmogenesis and electrophysiological changes during ischemia and reperfusion through alpha and beta-adrenoceptor stimulation.

Cite This Study

W J Penny (1984) studied this question.

synapsesocial.com/papers/6a8aeb99b676b7d1a2fb4639 https://doi.org/10.1093/oxfordjournals.eurheartj.a061616

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The deleterious effects of myocardial catecholamines on cellular electrophsiology and arrhythmias during ischaemia and reperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The deleterious effects of myocardial catecholamines on cellular electrophsiology and arrhythmias during ischaemia and reperfusion

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Also Consider

Also Consider