Hypoxia in fetal lambs: a study with (1)H-MNR spectroscopy of cerebrospinal fluid.

In fetal lambs, severe hypoxia (SH) will lead to brain damage. Mild hypoxia (MH) is thought to be relatively safe for the fetal brain because compensating mechanisms are activated. We questioned whether MH, leading to mild acidosis, induces changes in cerebral metabolism. Metabolites in cerebrospinal fluid (CSF) samples, as analyzed by proton magnetic resonance spectroscopy, were studied in two groups of seven anesthetized near-term fetal lambs. In group I, SH leading to acidosis with an arterial pH <7.1 was achieved. In group II, MH with an intended pH of 7.23--7.27 was reached [start of MH (SMH)], and maintained during 2 h [end of MH (EMH)]. During SH, choline levels in CSF, a possible indicator of cell membrane damage, were increased. Both during SH and at EMH, CSF levels of lactic acid, alanine, phenylalanine, tyrosine, lysine, branched chain amino acids, and hypoxanthine were increased compared with control values and with SMH, respectively. At EMH, the hypoxanthine CSF-to-blood ratio was increased as compared with SMH. These results indicate that prolonged MH leads to energy degradation in the fetal lamb brain and may not be as safe as assumed.

Transmission pulse oximetry in the fetal lamb: is there a universal calibration?

Transmission pulse oximetry is widely used for oxygen monitoring. The use of pulse oximeters is steadily expanding toward situations with low arterial oxygen saturation (Sao2) values. Therefore, we evaluated transmission pulse oximetry in the unanesthetized fetal lamb at low Sao2 levels. In seven fetal lambs, fetal hypoxemia was induced by occlusion of the maternal common iliac artery, four days after the instrumentation of the animal. Two Nellcor prototype transmission Y-sensors (light emitting diodes: 660 and 890 nm) were applied, one around a forelimb muscle and one around a skinfold in the neck, and were connected to Nellcor pulse oximeters. The pulse oximeter was calibrated for the skin measurements. Pulse oximeter saturation readings (Spo2) were compared with sample Sao2 values, over an Sao2 range of 13 to 63%. For the neck sensor the SD of the difference was 5.0% (n = 101). For the muscle sensor the mean difference was 19.5% and the SD of the difference was 5.9% (n = 206). Regression analysis showed a different calibration line for the muscle sensor with the equation: Spo2 = 0.92 x Sao2 + 21.90. Continuous recordings were obtained both from the forelimb muscle and from the neck, but the recordings from the neck showed a substantial loss of signal during the hypoxemia period. We conclude that transmission pulse oximetry is less accurate below an Sao2 of 70% in fetal lambs than above 70% Sao2. At these low levels of Sao2, pulse oximeters may need to be constructed with different calibration lines for various application positions of the body.

The ductus arteriosus, pre- and post-ductal oxygen saturation measurements in fetal lambs.

In the fetus, the arterial oxygen saturation (SaO2) in the ascending aorta is higher than in the descending aorta. We questioned whether this difference over the ductus arteriosus (delta SaO2) would change during hypoxaemia. Therefore, six chronically instrumented fetal lambs (119-126 days of gestation) were studied, by changing the inspired oxygen (FIO2) via a tracheal tube to the ewe. The SaO2 was measured intermittently every 15 min with blood samples obtained from the ascending and descending aorta, and continuously with 2 pulse oximeters at both sides of the ductus arteriosus. delta SaO2 was at a level of 3.4-5.3% and had a tendency to decrease at preductal SaO2 levels of 10-20% and at pH levels below 7.25. The precision of the pulse oximeters, expressed as standard deviation of the differences between sample SaO2 and pulse oximeter SaO2, was around 5.0% for the individual calibration curves. This precision was not enough to show details of the course of delta SaO2 between the blood samples. Our results show that there is no change in delta SaO2 across the ductus arteriosus.

Chronic hyperglycemia and insulin concentrations in fetal lambs.

Insulin concentrations were measured in 20 chronically instrumented fetuses of 10 sheep with alloxan-induced chronic hyperglycemia and 10 control sheep to examine if the hyperglycemia resulted in high fetal insulin concentration. Additionally, in six neonatal lambs of three chronically hyperglycemic ewes and three control sheep, insulin concentrations were measured after intravenous glucose injection. After a 2-month period of significant maternal hyperglycemia, no relationship between concentrations of fetal glucose and insulin could be detected. The mean fetal glucose concentration was 3.5 +/- 0.5 mmol/L in the hyperglycemic group and 0.6 +/- 0.1 mmol/L in the control group. Mean fetal insulin levels were 12.5 +/- 1.4 and 10.7 +/- 1.3 microU/ml, respectively. The neonatal lambs of the hyperglycemic and control ewes showed comparable concentrations of glucose and insulin after infusion of glucose. It is presumed that persistent high glucose levels depress the insulin secreting capacity of the fetal pancreas.