OBJECTIVE: Lidocaine exhibits a cardioplegic action via acute inhibition of sodium influx into the myocardial cells. In terms of the cardiac function and calcium dynamics in the myocardial cells, we investigated the myocardial protective effect of addition of FC43 of Perfluorochemicals, which has an excellent oxygen transport function to meet the myocardial oxygen demand, on lidocaine-induced cardioplegia. METHODS: Isolated rat hearts were perfused with Langendorff mode and were divided to three experimental groups. During of preservation, these hearts were perfused continuously with the next three solution, potassium chloride was added to Krebs-Henseleit bicarbonate buffer to make potassium concentration of 20 mM in the first group (Group A), 2 mM lidocaine was added to Krebs-Henseleit bicarbonate buffer in the second group (Group B), and 2 mM lidocaine and 20% FC43 were added to Krebs-Henseleit bicarbonate buffer in the third group (Group C). After 60 minutes of continuous perfusion, the cardiac function and the intracellular calcium concentration in Groups A and B during cardioplegia were measured. Furthermore, after 360 minutes of continuous coronary perfusion, the cardiac function were measured in Group B and Group C. RESULTS AND CONCLUSIONS: Lidocaine cardioplegia showed a good recovery of cardiac function, because lidocaine induced prompt cardiac arrest by blocking sodium influx and inhibited the intracellular calcium overload by the following inhibition of sodium-calcium channels. Moreover, our results suggested that combining Perfluorochemicals with lidocaine produced a more effective myocardial-preservation that meets the myocardial oxygen demand during long-term cardiac arrest.
OBJECTIVE:Lidocaine exhibits a cardioplegic action via acute inhibition of sodium influx into the myocardial cells. In terms of the cardiac function and calcium dynamics in the myocardial cells, we investigated the myocardial protective effect of addition of FC43 of Perfluorochemicals, which has an excellent oxygen transport function to meet the myocardial oxygen demand, on lidocaine-induced cardioplegia. METHODS: Isolated rat hearts were perfused with Langendorff mode and were divided to three experimental groups. During of preservation, these hearts were perfused continuously with the next three solution, potassium chloride was added to Krebs-Henseleit bicarbonate buffer to make potassium concentration of 20 mM in the first group (Group A), 2 mM lidocaine was added to Krebs-Henseleit bicarbonate buffer in the second group (Group B), and 2 mM lidocaine and 20% FC43 were added to Krebs-Henseleit bicarbonate buffer in the third group (Group C). After 60 minutes of continuous perfusion, the cardiac function and the intracellular calcium concentration in Groups A and B during cardioplegia were measured. Furthermore, after 360 minutes of continuous coronary perfusion, the cardiac function were measured in Group B and Group C. RESULTS AND CONCLUSIONS:Lidocaine cardioplegia showed a good recovery of cardiac function, because lidocaine induced prompt cardiac arrest by blocking sodium influx and inhibited the intracellular calcium overload by the following inhibition of sodium-calcium channels. Moreover, our results suggested that combining Perfluorochemicals with lidocaine produced a more effective myocardial-preservation that meets the myocardial oxygen demand during long-term cardiac arrest.
Authors: H J Bretschneider; G Hübner; D Knoll; B Lohr; H Nordbeck; P G Spieckermann Journal: J Cardiovasc Surg (Torino) Date: 1975 May-Jun Impact factor: 1.888