TY - JOUR
T1 - Nisoldipine cardioplegia in the isolated rabbit heart
AU - Acikel, U.
AU - Hazan, E.
AU - Sariosmanoglu, N.
AU - Catalyurek, H.
AU - Silistreli, E.
AU - Guner, G.
AU - Saydam, N.
AU - Tuncok, Y.
AU - Guven, H.
AU - Karabay, O.
AU - Oto, O.
PY - 1997
Y1 - 1997
N2 - Background: The metabolic and hemodynamic effects of nisoldipine supplementation in cardioplegia after ischemic injury were investigated in 13 isolated rabbit hearts. Group 1 consisted 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 perfused with Krebs-Henseleit solution. Left ventricular pressure, heart rate, malondialdehyde, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidized glutathione, creatine 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 1 while end-diastolic pressure was significantly 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.
AB - Background: The metabolic and hemodynamic effects of nisoldipine supplementation in cardioplegia after ischemic injury were investigated in 13 isolated rabbit hearts. Group 1 consisted 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 perfused with Krebs-Henseleit solution. Left ventricular pressure, heart rate, malondialdehyde, glutathione peroxidase, glutathione reductase, reduced glutathione, oxidized glutathione, creatine 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 1 while end-diastolic pressure was significantly 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.
KW - Cardioplegia
KW - Isolated rabbit heart
KW - Myocardial protection
KW - Nisoldipin
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U2 - 10.1177/107424849700200406
DO - 10.1177/107424849700200406
M3 - Article
AN - SCOPUS:0030831407
SN - 1074-2484
VL - 2
SP - 285
EP - 290
JO - Journal of Cardiovascular Pharmacology and Therapeutics
JF - Journal of Cardiovascular Pharmacology and Therapeutics
IS - 4
ER -