Lipid peroxidation of the sarcolemma, rather than alpha-adrenergic stimulation or lysophosphoglycerides, is a possible mechanism for calcium uptake upon reoxygenation in hypoxic myocardium.
Lipid peroxidation may mediate reoxygenation calcium uptake in hypoxic myocardium; leaves open whether targeting this pathway alters outcomes in human ischemia-reperfusion injury.
Calcium uptake on reoxygenation of hypoxic cardiac muscle is well documented. Alpha-adrenoceptor stimulation by released catecholamines, lysophosphoglycerides and lipid peroxidation have all been suggested as mediators of this effect. We have measured the uptake of Ca2+ on reoxygenation in the isolated arterially perfused interventricular septum of the rabbit heart. The alpha agonist phenylephrine (1 mumol X litre-1) did not alter calcium uptake, and the presence of either prazosin (1 mumol X litre-1) or phentolamine (10 mumol X litre-1) did not alter the reoxygenation induced Ca2+ uptake. Lysophosphatidylcholine caused an increase in Ca2+ uptake above 8 mumol X litre-1 but also produced a simultaneous increase in the distribution volume of 51Cr-EDTA, an extracellular space marker, indicating loss of membrane integrity. Hydrogen peroxide and cumene hydroperoxide both caused an increased Ca2+ uptake, but no disruption of the cell membrane; the effect on Ca2+ uptake could be inhibited by Ni2+ ions. Alpha adrenergic stimulation and lysophosphoglycerides do not appear to be key to Ca2+ uptake on reoxygenation, but lipid peroxidation of the sarcolemma is a possible mechanism.
No takes yet. Share an insight, caveat, or question.
Tones et al. (1985) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: