Key result
Postischemic reperfusion in isolated rat hearts caused a greater total release of inositol phosphates compared to normoxic tissue (466 vs 345 cpm/mg protein, P<.05).
Population
Isolated perfused rat hearts
Comparison
Global myocardial ischemia followed by reperfusion vs Normoxic myocardium (nonischemic tissue)
Design
Preclinical
Authors
Loading...
Does not support clinical interventions; hypothesis-generating for alpha1-adrenergic roles in reperfusion injury.
Absolute Event Rate: 466% vs 345%
p-value: p=<.05
Postischemic reperfusion triggers a rapid, transient, and calcium-dependent release of inositol 1,4,5-trisphosphate mediated by alpha 1-adrenergic receptors, potentially initiating reperfusion injury.
Anderson et al. (1995) studied Myocardial ischemia and reperfusion. Global myocardial ischemia and reperfusion vs. Normoxic tissue was evaluated on Total release of inositol phosphates (cpm/mg protein) (p=<.05). Postischemic reperfusion in isolated rat hearts caused a greater total release of inositol phosphates compared to normoxic tissue (466 vs 345 cpm/mg protein, P<.05).
Synapse has enriched 4 closely related papers on similar clinical questions. Consider them for comparative context: