Key result
Hypoxia produced a marked leftward shift in the dose-response curve for inositol trisphosphate production in response to norepinephrine, reducing the EC50 from 7.9 x 10^-8 M to 1.2 x 10^-8 M.
Why the study?
Does hypoxia enhance inositol trisphosphate production in response to alpha 1-adrenergic stimulation in isolated adult canine cardiac myocytes?
Population
Isolated adult canine cardiac myocytes (900,000 to 1,500,000 cells per preparation)
Comparison
Hypoxia followed by norepinephrine stimulation vs Normoxic myocytes stimulated with norepinephrine
Design
Preclinical
Authors
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May suggest mechanism for ischemia-related calcium overload and arrhythmias; leaves open relevance to human myocardium.
Does hypoxia enhance inositol trisphosphate production in response to alpha 1-adrenergic stimulation in isolated adult canine cardiac myocytes?
Absolute Event Rate: 1.2% vs 7.9%
p-value: p=<0.001
Hypoxia enhances alpha 1-adrenergic receptor-mediated production of inositol trisphosphate in cardiac myocytes, providing a potential intracellular mechanism for calcium overload and arrhythmogenesis during myocardial ischemia.
Heathers et al. (1989) studied Myocardial Ischemia (In Vitro Model). Hypoxia and norepinephrine stimulation vs. Normoxic myocytes was evaluated on EC50 for inositol trisphosphate (IP3) production in response to norepinephrine (p=<0.001). Hypoxia produced a marked leftward shift in the dose-response curve for inositol trisphosphate production in response to norepinephrine, reducing the EC50 from 7.9 x 10^-8 M to 1.2 x 10^-8 M.
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