<i>N</i>-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms

<table class="table-group" id="tab4"><tr><td><table class="table"><tr><td class="thead-hr" colspan="2"><hr/></td></tr><tr class="thead"><td align="left">Group </td><td align="center">LDH (U/mL)</td></tr><tr><td class="thead-hr" colspan="2"><hr/></td></tr><tr><td align="left">0CaCon</td><td align="center">952.70 ± 32.02</td></tr><tr><td align="left">0CaH/R</td><td align="center">1378.33 ± 72.26*</td></tr><tr><td align="left">0CaH/R + H89</td><td align="center">1389.14 ± 71.65*</td></tr><tr><td align="left">0CaH/R + Forskolin</td><td align="center">1338.78 ± 51.68*</td></tr><tr class="table-tr"><td colspan="2"><hr class="tbody-hr"/></td></tr></table></td></tr><tr class="table-fn"><td>LDH: lactate dehydrogenase; PKA: protein kinase A; H/R: hypoxia/reoxygenation.*<svg height="11.375" id="M53" style="vertical-align:-0.1638pt" version="1.1" viewbox="0 0 58.712502 11.375" width="58.712502" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink">
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</svg> versus 0CaCon group.<br/></td></tr></table>

Effects of PKA inhibitor and activator on LDH leakage of cardiomyocyte in extracellular-calcium-free H/R (<svg height="11.175" id="M52" style="vertical-align:-0.20474pt" version="1.1" viewbox="0 0 36.237499 11.175" width="36.237499" xmlns="http://www.w3.org/2000/svg" xmlns:xlink="http://www.w3.org/1999/xlink">
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</svg>).

Oxidative Medicine and Cellular Longevity

tab4

Table 4

Table 4: <i>N</i>-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms 

Table 4 | N-n-Butyl Haloperidol Iodide Ameliorates Cardiomyocytes Hypoxia/Reoxygenation Injury by Extracellular Calcium-Dependent and -Independent Mechanisms 