Effect of Lidocaine on the Asphyxial Responses in the Mature Fetal Lamb

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Abstract
The effects of lidocaine on the fetal circulatory responses to asphyxia were evaluated in chronically instrumented pregnant sheep. Twenty-six preparations were studied. Animals were assigned to one of three groups. The animals in group I (N = 10) did not hve umbilical cord occluders placed. Lidocaine at 0.1 mg .cntdot. kg-1 .cntdot. min-1 was infused to the mother for 180 min. The animals in group II (N = 11) had an umbilical cord occluder, which was inflated to induce fetal asphyxia (PaO2 15 mmHg) for 90 min. Occlusion was then maintained for an additional 180 min while lidocaine at 0.1 mg .cntdot. kg-1 min-1 was infused. The animals in group III (N = 5) also had an umbilical cord occluder inflated for 90 min. While occlusion was maintained for an additional 180 min, saline was infused, in place of lidocaine. The infusion rate of lidocaine of 0.1 mg .cntdot. kg-1 .cntdot. min-1 over 180 min resulted in a steady-state arterial lidocaine blood concentration in the mother of approximately 2.15 .mu.g/ml. Fetal circulatory responses to asphyxia were evaluated before and after maternal infusion of lidocaine or normal saline. Measurements included heart rate, blood pressure, arterial pH, and blood gases. Cardiac output and organ blood flow were determined using the radio-labelled microsphere technique. In general, arterial and tissue lidocaine concentrations in asphyxiated fetuses were higher than those in the nonasphyxiated ones, the differences being significant in the brain, heart, liver, and adrenal glands. Ninety minutes of asphyxia resulted in a decrease in fetal heart rate, while the blood pressure and cardiac output did not change significantly. At the same time, there was a significant increase in blood flow to the fetal brain, heart, and adrenals. These fetal responses were not altered after a further 180 min of asphyxia during which either lidocaine or normal saline was infused to the mother. It is concluded that lidocaine, in moderate concentrations, does not alter fetal responses to asphyxia, although placental transfer of the drug is enhanced by fetal acidosis.