Fetal breathing, sleep state, and cardiovascular responses to graded hypoxia in sheep

Abstract

Graded isocapnic hypoxemia was produced in unanesthetized fetal sheep by varying the inspired O2 concentration (21, 12, 10.5, and 9%) of the ewe. This produced corresponding mean preductal arterial O2 tension (PaO2) values of 25.2 +/- 1.1 (control), 20.1 +/- 1.0 (mild hypoxia), 17.8 +/- 0.9 (moderate hypoxia), and 16.8 +/- 1.4 Torr (severe hypoxia). These were associated with mean arterial O2 contents (CaO2) of 7.18 +/- 0.44, 5.19 +/- 0.34, 4.24 +/- 0.33, and 3.27 +/- 0.20 ml/dl, respectively. The most severe hypoxia was associated with metabolic acidosis and fetal bradycardia. Hypoxia did not reduce significantly the incidence of low-voltage electrocortical activity. The incidence of breathing and rapid eye movements was not affected by mild hypoxia; however, the incidence of both was significantly reduced during moderate and severe hypoxia. It is concluded that 1) acute reductions in the mean PaO2 of 5.9 +/- 0.6 Torr and CaO2 of 2.00 +/- 0.23 ml/dl are critical in that greater reductions inhibit fetal eye and breathing activity and 2) hypoxia probably inhibits eye and breathing movements by altering sleep state.

Impact of chronic hypoxemia on blood flow to the brain, heart, and adrenal gland in the late-gestation IUGR sheep fetus

“…In acutely hypoxemic sheep fetuses, there is a decrease in the incidence of FBMs (41,42). However, our data show that there was no difference in incidence or amplitude of FBMs between control and chronically hypoxemic PR fetuses.…”

The role of CO2 and central chemoreception in the control of breathing in the fetus and the neonate

“…Central chemoreceptors appear to be present within days after birth in the rabbit (Wennergren et al 1983) and piglet (Wolsink et al 1991) suggesting their previous presence in the fetus. Decreasing Pa O 2 inhibits rather than stimulates fetal breathing (Koos et al 1987; Jansen et al 1991), the inhibition likely originating from a region in the upper lateral pons (Johnston et al 1989; Johnston et al 1993). Moreover, denervation of the carotid bodies does not alter fetal breathing, fetal state, or the stimulating effect of CO 2 (Koos et al 1987; Moore et al 1989).…”

“…Decreasing Pa O 2 inhibits rather than stimulates fetal breathing (Koos et al 1987; Jansen et al 1991), the inhibition likely originating from a region in the upper lateral pons (Johnston et al 1989; Johnston et al 1993). Moreover, denervation of the carotid bodies does not alter fetal breathing, fetal state, or the stimulating effect of CO 2 (Koos et al 1987; Moore et al 1989). In addition, alteration of bicarbonate concentrations in the CSF can stimulate or depress fetal breathing in the chronically instrumented lamb (Hohimer et al 1983).…”

Changes in fetal lamb arterial blood gas and acid-base status with advancing gestation

“…This suggests that with this degree of hypoxemia, the increased plasma lactate concentration is coming from fetal sources. From the studies of Koos and colleagues (38,39), this could include the fetal brain. However, given the increase in fetal cerebral perfusion that occurs with hypoxemia (58), increased lactate production from other tissues in which perfusion is not increased, such as the carcass, seems more likely.…”