Volatile cardioplegia: fast normothermic cardiac arrest induction and recovery with halothane in isolated rat hearts.

To study the effect of halothane as a cardioplegic agent, ten Wistar rats were anesthetized by ether inhalation and their hearts were perfused in a Langendorff system with Krebs-Henseleit solution (36 degrees C; 90 cm H2O pressure). After a 15-min period for stabilization the control values for heart rate, force(T), dT/dt and coronary flow were recorded and a halothane-enriched solution (same temperature and pressure) was perfused until cardiac arrest was obtained. The same Krebs-Henseleit solution was reperfused again and the parameters studied were recorded after 1, 3, 5, 10, 20 and 30 min. Cardiac arrest occurred in all hearts during the first two min of perfusion with halothane-bubbled solution. One minute after reperfusion without halothane, the following parameters reported in terms of control values were obtained: 90.5% of control heart rate(266.9 +/- 43.4 to 231.5 +/- 71.0 bpm), 20.2% of the force (1.83 +/- 0.28 to 0.37 +/- 0.25 g), 19.8% of dT/dt (46.0 +/- 7.0 to 9.3 +/- 6.0 g/s) and 90.8% of coronary flow (9.9 +/- 1.5 to 9.4 +/- 1.5 ml/min). After 3 min of perfusion they changed to 99.0% heart rate (261.0 +/- 48.2), 98.9% force (1.81 +/- 0.33), 98.6 dT/dt (45.0 +/- 8.2) and 94.8% coronary flow (9.3 +/- 1.4). At 5 min 100.8% (267.0 +/- 40.6) heart rate, 105.0% (1.92 +/- 0.29) force and 104.4% (48.2 +/- 7.2) dT/dt were recorded and maintained without significant differences (P > 0.01) until the end of the experiment. These data demonstrate that volatile cardioplegia with halothane is an effective technique for fast induction of and prompt recovery from normothermic cardiac arrest of the rat heart.

Volatile cardioplegia: fast normothermic cardiac arrest induction and recovery with halothane in isolated rat hearts

To study the effect of halothane as a cardioplegic agent, ten Wistar rats were anesthetized by ether inhalation and their hearts were perfused in a Langgendorff system with Krebs-Henseleit solution (36 graus Celsius; 90 cm H2O pressure). After a 15-min period for stabilization the control values for heart rate, force (T), dT/dt and coronary flow were recorded and a halothane-enriched solution (same temperature and pressure) was perfused until cardiac arrest was obtained. The same Krebs-Henseleit solution was reperfused again and the parameters studied were recorded after 1,3,5,10,20 and 30 min. Cardiac arrest occurred in all hearts during the first two min of perfusion with halothanebubbled solution. One minute after reperfusion without halothane, the following parameters reported in terms of control values were obtained: 90.5 percent of control heart rate (266.9 + 43.4 to 231.5 + 71.0 bpm), 20.2 percent of the force (1.83 + 0.28 to 0.37 + 0.25 g), 19.8 percent of dT/dt (46.0 + 7.0 to 9.3 + 6.0 g/s) and 90.8 percent of coronary flow (9.9 + 1.5 to 9.4 + 1.5 ml/min). After 3 min of perfusion they changed to 99.0 percent heart rate (261.0 + 48.2), 98.9 percent force (1.81 + 0.33), 98.6 dT/dt (45.0 + 8.2) and 94.8 percent coronary flow (9.3 + 1.4). At 5 min 100.8 percent (267.0 + 40.6) heart rate, 105.0 percent (1.92 + 0.29) force and 104.4 percent (48.2 + 7.2) dT/dt were recorded and maintained without significant differences (P>0.01) until the end of the experiment. These data demonstrate that volatile cardioplegia with halothane is an effective technique for fast induction of and prompt recovery from normothermic cardiac arrest of the rat heart.

[Effect of diazepam on myocardial contraction and on the response to dopamine. Study in isolated rat hearts]. / Efeito do diazepam na contratilidade miocárdica e na resposta à dopamina. Estudo em corações isolados de ratos.

PURPOSE: The myocardial contractility variations and the cardiac rate were studied in isolated hearts of rats with injection of diazepam, dopamine and the association of both. METHODS: In all animals, after anesthesia, the hearts were removed and perfused with Krebs-Henseleit solution enriched by 95% O2 under a constant pressure of 90 cm H2O, until complete stabilization, for control value recordings. The following groups were studied: I) ten hearts: after stabilization the control values were recorded and dopamine (3 micrograms/ml) injected; IIA and IIB): also ten hearts were used and submitted to 50 micrograms and 100 micrograms of diazepam injections respectively. III) ten hearts studied with 50 micrograms of diazepam and 3 micrograms/ml of dopamine injection in a sequential form. RESULTS: Myocardial contractility arose in group I, from 37 g.seg-1 (control mean-value) to 70 and 53 g.seg-1 (1st and 3rd min); p < 0.001. In the groups IIA and IIB the dT/dt fell considerably in relation to the control: 35 g.seg-1 to 24 and 30 g.seg-1 (1st and 3rd min)--group IIA; p < 0.001 -32 g.seg-1 to 22 and 25 g.seg-1 (1st and 3rd min)--group IIB; p < 0.001. In the group III, a partial inhibition of the inotropic effects of dopamine by the injection of diazepam was observed. Heart rate follows fully the dT/dt variations in the groups IIA, IIB and III. CONCLUSION: Diazepam presents inotropic and chronotropic negative effects with the 50 micrograms as well as with 100 micrograms injection and the chronotropic and inotropic effect of dopamine (3 micrograms) injection was partially inhibited by the previous injection (50 micrograms) of diazepam.