Effects of isoflurane and halothane on the calcium ion-tension curve in rat myocardium.

In order to clarify the interaction of volatile anesthetics and extracellular calcium ion on the myocardial contraction, effects of both isoflurane (1.0%) and halothane (0.5%) on the extracellular calcium ion concentration ([Ca(2+)](O))-tension curve were studied. Increasing [Ca(2+)](O) enhanced the myocardial contraction response, and the maximal response was obtained at [Ca(2+)](O) of 3.0 mM. Halothane depressed the maximal value of the tension development in response to increasing [Ca(2+)](O), while isoflurane did not ( P < 0.01). The probit response of the developed tension to the changes in [Ca(2+)](O) indicated that isoflurane increased the median effective concentration (EC(50)) of [Ca(2+)](O) significantly from 0.484 +/- 0.051 (mean +/- SEM) to 0.870 +/- 0.056 mM ( P = 0.001), but halothane did not ( P = 0.018). Therefore, 1.0% isoflurane was concluded to move the [Ca(2+)](O)-tension curve to the right, while a downwards shift occurred with 0.5% halothane.

Frequency- and length-dependent tension development in rat heart muscles exposed to isoflurane and halothane.

Using 22 isolated rat ventricular muscle preparations, we investigated whether or not the increase in preload and/or contraction frequency may counteract the negative inotropy of both isoflurane (2.0%) and halothane (1.0%). Increases in preload from 94% of Lmax (the length where muscles produce the maximal tension) to Lmax did not alter significantly the percent decrements in tension development caused by either isoflurane or halothane. The increases in contraction frequency from 0.1 to 0.6 Hz augmented the depressant effect of isoflurane significantly ( P < 0.001), while the depressant effect of halothane was not altered at these contraction frequencies. Small but significant counteraction occurred in the depressant effects of halothane at 0.8 and 1.6 Hz ( P = 0.002). These changes in intracellular mechanism(s), resulted from the increase in contraction frequency, interacted with the two anesthetics on tension development, while these may not be the case for the increase in preload.

Circulatory effects of atracurium in patients with cardiovascular disease.

Atracurium 0.4 mg kg-1, which was sufficient to produce neuromuscular blockade sufficient for intubation, was administered as divided bolus doses to 40 patients with severe cardiovascular disease. Little haemodynamic change occurred. A transient reduction in arterial pressure was noted in one patient. Atracurium was found to be safe and effective, and administration in small bolus doses separated by 30 s may reduce the likelihood of significant circulatory changes.

Cardiocirculatory effects of prolonged administration of isoflurane in normocarbic human volunteers.

Effects of the prolonged administration of isoflurane on haemodynamics were studied in 17 healthy volunteers under normocarbic conditions. The anaesthetic was administered for 90 min at a constant alveolar concentration. Cardiac index was unchanged in the presence of decrease stroke volume index and increased heart rate. The mean arterial pressure decreased with parallel reductions in total peripheral resistance. Left ventricular work decreased. The left ventricular ejection time index increased marginally but significantly. Isoflurane caused no change in the pump performance of the heart but depressed the muscle performance.

Cardio-circulatory effects of enflurane anesthesia in health and disease.

The circulatory effects of enflurane (Ethrane) were studied in 10 unmedicated volunteers during anesthesia over a period of 90 min or more. Cardiac output did not change significantly at a mean alveolar concentration of 2.3 vol.%. Heart rate was increased in all cases. Enflurane causes negative inotropic activity in the heart muscle but has little influence on the pump performance of the heart.

Cardiac performance during prolonged halothane anaesthesia in the cat. Isolated heart muscle study.

The contractile response of papillary muscles, isolated from normal cats, to prolonged administration of halothane at minimum alveolar anaesthetic concentration (MAC) was studied. Average values of maximal velocity of shortening (Vmax) and maximal developed force (Fm) obtained in 12 muscles during the 1st, 2nd and 3rd hour of exposure to halothane anaesthesia were significantly less than those obtained during the control period and after recovery from halothane. There were no significant differences in values over a 3-h period. When post-extra-systolic potentiation was induced by paired electric stimulation, average values of Vmax and Fm increased significantly. We conclude that prolonged administration of halothane at a constant concentration resulted in a sustained depression of myocardial contractility without tissue tolerance. The myocardium depressed by halothane, however, still retains the ability to respond to additional inotropic stimulation.