Background: The metabolic and hemodynamic effects of nisoldipine supplementation in cardioplegia after ischemic injury were investigated in 13 isolated rabbit hearts. Group 1 con sisted of 6 hearts, which received St. Thomas II cardioplegic solution. In group 2, nisoldipine was added to the cardioplegic solution at a concentration of 0.1 mg/kg in 7 hearts.
Methods: The explanted hearts were suspended from Langendorff apparatus and were per fused with Krebs-Henseleit solution. Left ventricular pressure, heart rate, malondialdehyde, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidized glutathione, cre atine kinase MB, (CK-MB), aspartate transaminase, and lactate dehydrogenase (LDH) were measured before and after 60 minutes of ischemia. Peak generated pressure after ischemia was significantly higher in group 2 versus group I while end-diastolic pressure was signifi cantly lower in group 2 after ischemic arrest (P < .05).
Results: Malondialdehyde levels were lower in group 2 (P < .05). Glutathione peroxidase and glutathione reductase levels were significantly higher in group 2 ( P < .05). The only enzymatic significant difference was observed between the preischemic and postischemic levels of aspartate transaminase in group 2 (P < .05).
Conclusions: These findings show beneficial effects of nisoldipine cardioplegia, although its use as a cardioplegic additive is not yet possible. We believe, however, the effects of oral nisoldipine before cardiac surgery can be studied in a clinical setting.
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