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Hawthorn extract is not cardioprotective in an anoxic cardiomyocyte preparation

Changes in cell function and morphology when cardiac tissue or myocytes are made anoxic and/or reoxygenated are well documented. Hawthorn extract (from the hawthorn tree, Crataegus oxycantha) has been shown to protect the heart against ischemic damage. Hawthorn extract contains a number of compounds which are potentially cardioprotective. These compounds have been proposed to protect cardiac tissue from ischemia by scavenging oxyradicals or by inhibiting cyclic AMP phosphodiesterase. We hypothesized that hawthorn extract would reduce damage to cardiac cells under anoxic conditions and decrease injury due to reoxygenation. Cardiac myocytes were subjected to aerobic or anoxic conditions for 0, 45, or 60 minutes with or without hawthorn extract; each anoxic preparation was then reoxygenated for 5 minutes. Cell viability and morphology was determined by light microscopy using trypan blue. On average, aerobic preparations began with 70% rod‐shaped cells and 80% viable. Anoxia for 60 min caused a decrease in rod count (33 ± 4%) but not much change in viability (68 ± 4%), as expected. Hawthorn extract did not protect the cells from this damage at either 80 μg/mL (25 ± 4% rods, 60 ± 4% viable) or 160 μg/mL (19 ± 4% rods, 66 ± 4% viable). We conclude from these studies that hawthorn extract is not cardioprotective as an oxyradical scavenger, but may in fact be a phosphodiesterase inhibitor.