January 1, 1985Journal of Cardiovascular Pharmacology
Paradoxical Role of Neuronal Uptake for the Locally Mediated Release of Endogenous Noradrenaline in the Ischemic Myocardium
Key result
Ischemia longer than 10 minutes increased noradrenaline overflow during reperfusion (1,270 pmol/g after 60 min vs 3.7 pmol/g control), which was reduced by neuronal uptake blockade.
Population
Isolated perfused (Langendorff) rat hearts
Comparison
Various periods of ischemia with or without… vs Control perfusion or ischemia without blockade
Design
Preclinical
Authors
Discussion
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Implication
Indicates carrier-mediated efflux in ischemic rat hearts; hypothesis-generating with no clinical implications yet.
Structured PICO
P
Population
Isolated perfused rat hearts subjected to various periods of ischemia to study endogenous noradrenaline overflow.
I
Intervention
Various periods of ischemia (up to 60 min) with or without blockade of neuronal uptake or lack of extracellular calcium
C
Comparator
Control perfusion or ischemia without blockade
O
Outcome
Noradrenaline overflow during reperfusionsurrogate
Main Result
Absolute Event Rate: 1270% vs 3.7%
In isolated rat hearts, noradrenaline release during 10-40 minutes of ischemia occurs via carrier-mediated efflux rather than exocytosis.
Cite This Study
Schömig et al. (1985) studied Ischemic myocardium. Ischemia and blockade of neuronal uptake vs. Control perfusion was evaluated on Noradrenaline overflow during reperfusion. Ischemia longer than 10 minutes increased noradrenaline overflow during reperfusion (1,270 pmol/g after 60 min vs 3.7 pmol/g control), which was reduced by neuronal uptake blockade.