Search

Pentobarbitone, 20 mg X kg-1 IV followed by infusion of 25 mg X kg-1 X hr-1, produced a progressive decrease in mean arterial pressure in dogs from 113 +/- 17 mmHg (SD) after one hour of infusion to 82 +/- 21 mmHg after 3.5 hours and to 49 +/- 22 mmHg after 5.5 hours. EEG silence occurred at 3.6 +/- 0.6 hours. In dogs similarly treated with pentobarbitone, a two hour infusion of dopamine 5 micrograms X kg-1 X min-1 beginning at the time of EEG silence prevented the further decrease in pressure and restored pressure to 87 +/- 18 mmHg. The mechanism for this effect of dopamine was an increase in cardiac output as systemic vascular resistance was unaffected by dopamine. The cardiac output increase was mainly the result of an increase in stroke volume as heart rate increased only slightly. Since reduced stroke volume was the main reason why pentobarbitone lowered blood pressure, the effect of dopamine on stroke volume and thus on blood pressure makes it an appropriate antagonist to the cardiovascular effects of toxic doses of pentobarbitone.

The effect of age on the arrhythmogenicity of epinephrine during halothane anaesthesia was studied in pigs of two different age groups. At a stable alveolar concentration of 0.84 volumes per cent halothane, ventricular arrhythmias could not be elicited in one- to three-day-old pigs by a 100 micrograms X kg-1 infusion of epinephrine. PVCs were produced in 50- to 55-day-old pigs at a mean epinephrine dose of 9.55 micrograms X kg-1. Heart rate, systolic blood pressure, and rate-pressure product were significantly higher before and during the epinephrine infusion in the 50- to 55-day-old pigs. It is concluded that there is an age dependent effect upon epinephrine induced arrhythmias during halothane anaesthesia in pigs.

Left-ventricular function was evaluated in 11 open-chest dogs under pentobarbital anesthesia. Ventricular performance was altered by infusing or withdrawing crossmatched blood, and simultaneous recordings obtained of left-atrial pressure, leftventricular pressure, aortic flow, and aortic pressure. From these recording were obtained the stroke volume, stroke work, peak ventricular power, and the maximal rate of change of aortic flow and ventricular pressure. The derived variables were plotted versus end diastolic pressure to provide ventricular-function curves. The curves were obtained during a control state, during norepinephrine infusion, and subsequent to aortic constriction at the level of the coronary ostia. Studies were done in the heart-rate paced and nonpaced animal; the data were presented in terms of per cent change from control values. Peak power and stroke work provided the more classical type of ventricular-function curves and it is suggested that these provide the most useful information. Pressure-derivative curves were the most widely separated. Similar studies were repeated in seven animals in which afterload was controlled at 100 mm Hg. Curve shape was somewhat altered but overall changes were comparable.