Methane production and energy partition of cattle in the tropics.

The aim of this experiment was to determine CH4 production and energy partition for a range of diets fed to Bos indicus cattle. Six Brahman cattle were fed on three different diets in a replicated Latin square experiment over three periods. The diets were (1) long-chopped Angleton grass (Dicanthium aristatum) hay ad libitum (DM digestibility (DMD) 41 (SE 2)%; 4 g N/kg), (2) long-chopped Rhodes grass (Chloris gayana) hay ad libitum (DMD 60 (SE 1)%; 14 g N/kg) or (3) 2 kg long-chopped lucerne (Medicago sativa) hay/d plus a high-grain diet (ad libitum) (DMD 70 (SE 1)%; 31 g N/kg). CH4 production was measured using confinement-type respiration chambers. Metabolizable energy intake (MJ/d) of cattle fed on Angleton grass (18.4 (SE 2.0)) was lower (P < 0.01) than that for Rhodes grass (54.9 (SE 2.1)), which was lower (P <0.01) than that for the high-grain diet (76.7 (SE 5.8)). CH4 production (g/d) for cattle fed on Rhodes grass (257 (SE 14)) was higher (P < 0.01) than that for cattle fed on both the high-grain diet (160 (SE 24)) and Angleton grass (113 (SE 16)). CH4 conversion rate (MJ CH4 produced per 100 MJ gross energy intake) was not significantly different between cattle fed on Angleton (10.4 (SE 1.1)) and Rhodes (11.4 (SE 0.3)) grass, but was higher (P < 0.01) than for cattle fed on the high-grain diet (6.7 (SE 0.7)). CH4 production (g/kg live-weight gain) was associated (P < 0.001) with both live-weight gain and feed:gain ratio. We conclude that the relationships between CH4 production, energy utilization and live-weight change of cattle fed on tropical forages differ from those of cattle fed on diets based on temperate forages.

Arousal and cardiorespiratory responses to airflow obstruction in sleeping lambs: effects of sleep state, age, and repeated obstruction.

We studied the effects of postnatal age on arousal and cardiorespiratory responses to airflow obstruction in sleeping lambs: we also determined the influence of sleep states and repeated airflow obstruction. Sixteen lambs were chronically prepared for monitoring sleep states, arterial O2 saturation (SaO2), heart rate (HR), and intrapleural pressure (Pp1) and were studied from 2-29 days after birth. Obstruction of respiratory airflow by facemask occlusion led to arterial desaturation, augmentation of respiratory efforts, bradycardia, and arousal. Lambs aroused more rapidly and with less desaturation in non-rapid eye movement (NREM) sleep (7 +/- 1 second and 7 +/- 1%, respectively) than in rapid eye movement (REM) sleep (18 +/- 2 seconds and 22 +/- 2%), and cardiac slowing was less in NREM than in REM sleep. In REM sleep only, the arousal latency and desaturation at arousal were affected by postnatal age; arousal responses occurred most rapidly in the youngest (< or = 6 days) and oldest (> or = 13 days) age groups and were delayed at 7-12 days. Repeated episodes of airflow obstruction led to reduced arousability in REM sleep only. We conclude that arousal from REM. but not NREM, sleep in response to the obstruction of respiratory airflow is transiently depressed during early postnatal development and that repeated obstructions and arousals also lead to depressed arousal from REM sleep.

Effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume in sheep.

OBJECTIVE: Our purpose was to determine the effects of prolonged hypoxemia on fetal renal function and amniotic fluid volume and composition. STUDY DESIGN: Twelve pregnant ewes underwent surgery at 115 +/- 2 days after mating (term approximately 147 days) for the implantation of fetal vascular, bladder, and amniotic sac catheters. At 125 +/- 1 days seven fetuses were studied during 6 days of hypoxemia and five control fetuses were studied over six days of normoxemia. Index values of fetal renal function and amniotic fluid volume were measured. RESULTS: During hypoxemia fetal SaO2 and PaO2 were reduced from 60.9% +/- 1.6% and 21.9 +/- 0.6 mm Hg to 29.6% +/- 3.8% and 14.9 +/- 0.8 mm Hg, respectively. Fetal hypoxemia was associated with a transient acidemia (arterial pH 7.29 +/- 0.02) at 4 hours. There were no sustained alterations in fetal urine production (9.5 +/- 0.8 ml/hr/kg) or glomerular filtration rate (1.3 +/- 0.1 ml/min/kg) during hypoxemia. In control fetuses the amniotic fluid volume increased over 7 days, from 717 +/- 169 ml to 1031 +/- 147 ml, whereas in the hypoxemic fetuses it did not change (741 +/- 68 ml) over the same period. CONCLUSION: During prolonged fetal hypoxemia in the absence of acidemia, fetal urine production is maintained, whereas the normal gestational increase in amniotic fluid volume is prevented, raising the possibility that intramembranous reabsorption of amniotic fluid is increased by hypoxemia.

Cerebral oxygen delivery is reduced during the acidaemia associated with prolonged hypoxaemia in the immature ovine fetus.

Our aim was to determine the effects of 12 h of hypoxaemia on cerebral blood flow (CBF) and cerebral O2 delivery in ovine fetuses at 0.6 gestation. During fetal hypoxaemia, induced by reduced uterine blood flow, fetal SaO2 and PaO2 were reduced (p < 0.01) from control values of 77.0 +/- 1.6% and 27.3 +/- 1.0 mm Hg, respectively, to 28.4 +/- 3.4% and 15.6 +/- 0.6 mm Hg; fetal pHa decreased from control values of 7.37 +/- 0.01 to 7.20 +/- 0.02 at 3 h, but returned to control values before 12 h. CBF (ml/min/100 g) was 2.0- to 2.6-fold higher (p < 0.01) than control values during hypoxaemia, but only 1.7-fold higher (p < 0.01) at 3 h when pHa was lowest. Cerebral O2 delivery (ml/min/100 g) was lower (p < 0.01) than control values of 3.15 +/- 0.29 at 1.5h (2.09 +/- 0.36) and 3h (1.84 +/- 0.22) of hypoxaemia and higher 1 h after hypoxaemia had ceased (3.81 +/- 0.22, p < 0.01). We conclude that the ovine fetus at 0.6 gestation is unable to sustain increased CBF and hence maintain cerebral O2 delivery during the first 6 h of hypoxaemia, a time which coincides with acidaemia; in contrast, at 6 and 12 h of hypoxaemia, when pHa was normal, cerebral O2 delivery was similar to control values. Reduced cerebral O2 delivery during the early, acidaemic, stages of hypoxaemia may lead to impaired neural development.

Development of ventilatory responsiveness to progressive hypoxia and hypercapnia in low-birth-weight lambs.

Our aim was to determine the effects of low birth weight on ventilatory responses to progressive hypoxia and hypercapnia during early postnatal life. Seven low-birth-weight (2.7 +/- 0.3 kg) and five normal-birth-weight (4.8 +/- 0.2 kg) lambs, all born at term, underwent weekly rebreathing tests during wakefulness while arterial PO2, PCO2, and pH were measured. Hypoxic ventilatory responsiveness (HOVR; percent increase in ventilation when arterial PO2 fell to 605 of resting values) increased in normal lambs from 86.6 +/- 7.1% at week 1 to 227.4 +/- 24.9% at week 6. In low-birth-weight lambs, HOVR was not significantly different at week 1 (60.1 +/- 18.7%) from that of normal lambs but did not increase with postnatal age (56.6 +/- 19.3% at week 6). HOVR of all lambs at 6 wk was significantly correlated with birth weight (r2 = 0.8). Hypercapnic ventilatory responsiveness (gradient of ventilation vs. arterial PCO2) did not change with age and was not significantly different between groups [84.7 +/- 7.5 (low-birth-weight lambs) vs. 89.4 +/- 6.6 ml.min-1.kg-1.mmHg-1 (normal lambs)]. We conclude that intrauterine conditions that impair fetal growth lead to the failure of HOVR to increase with age.

Influence of sedation on arousal and cardiorespiratory responses to airflow obstruction in sleeping lambs.

Our aim was to determine the effects of two commonly used sedatives, promethazine and diazepam, on arousal and cardiorespiratory responses to airflow obstruction in sleeping lambs. In eight lambs fitted with obstructable rubber face masks, we recorded electrocortical, electroocular, and electromyographic activities to identify sleep-wake states; intrapleural pressure, heart rate, and percentage O2 saturation (Sao2) were also recorded. In each lamb, arousal and respiratory responses were measured after tidal airflow was obstructed during rapid eye movement (REM) and nonREM sleep. Each lamb was studied, on different days, when unsedated and after being mildly sedated with either promethazine or diazepam. Seven of the lambs were studied while sleeping after being sedated with promethazine (1.6 +/- 0.07 mg/kg, orally with milk) and six were studied after sedation with diazepam (0.31 +/- 0.03 mg/kg, intramuscularly). In unsedated lambs, airflow obstruction led to augmentation of respiratory efforts, bradycardia, hypoxemia, and arousal; in REM sleep, arousal was delayed and occurred at lower Sao2 (16 +/- 3 s; 75.3 +/- 3%) compared with nonREM sleep (8 +/- 1 s; 90 +/- 1%). Sedation increased the arousal latency in both REM and nonREM sleep and caused arousal to occur at lower Sao2; in some sedated lambs Sao2 fell to less than 30% before arousal. The augmentation of inspiratory and expiratory efforts immediately before arousal was increased after sedation. We conclude that promethazine and diazepam depress arousal responses in sleeping lambs leading to profound hypoxia, and that this may be due to impaired sensitivity to augmented respiratory efforts and other physiologic changes during airflow obstruction.

Role of nitric oxide in the regulation of cerebral blood flow in the ovine foetus.

1. Our aim was to determine the role of nitric oxide (NO) in regulating cerebral blood flow (CBF) in foetal sheep under conditions of both hypoxaemia and normoxaemia. 2. Aseptic surgery was performed on 11 pregnant sheep at 125 +/- 1.1 days of gestational age (g.a.) when foetal vascular catheters were implanted for the measurement of CBF using coloured microspheres. Additionally, each ewe was prepared for one of two procedures for inducing foetal hypoxaemia; either an adjustable clamp was placed around the maternal common internal iliac artery to reduce uterine blood flow, or a catheter was implanted into the maternal trachea for insufflation of N2. At 131 +/- 0.3 days g.a., in control foetuses (n = 5), CBF and cerebral vascular resistance (CVR) were measured under basal (normoxaemic) conditions and after 3h of hypoxaemia. In other foetuses (n = 6) CBF and CVR were measured under basal conditions and after 3 h of hypoxaemia; in these foetuses NO synthesis was inhibited with N-nitro-L-arginine (NOLA) between 2-3 h of hypoxaemia. 3. In the hypoxaemia experiments foetal SaO2 and PaO2 were reduced (P < 0.05) in both control and NOLA-treated foetuses, from normoxaemic values of 69.5 +/- 2.1% and 23.8 +/- 1.0 mmHg, respectively, to 29.3 +/- 1.0% and 14.6 +/- 0.4 mmHg during the period of hypoxaemia. In control foetuses, CBF (mL/min) was increased by 82.7% during hypoxaemia; in NOLA-treated foetuses CBF increased by 55.3%, which was less (P < 0.05) than in control foetuses. In control foetuses CVR (mmHg)/ mL/min) was reduced by 43.5% during hypoxaemia, whereas in NOLA-treated foetuses there was no significant change. 4. In five of the 11 foetuses, the role of NO in regulating CBF under basal (normoxaemic) conditions was determined at 132 +/- 0.3 days g.a. Cerebral blood flow and CVR did not significantly change from basal values after NOLA-treatment. 5. We conclude that in foetal sheep NO plays an important role in regulating cerebral vascular tone and hence CBF during hypoxaemia, but its contribution during normoxaemia is less apparent.

Prematurity alters hypoxic and hypercapnic ventilatory responses in developing lambs.

We have determined the effects of preterm birth on the postnatal development of ventilatory responses to progressive hypoxia and hypercapnia in awake lambs. Hypoxic and hypercapnic rebreathing tests were performed at weekly intervals in 5 preterm (born at 135 +/- 0.5 d) and 5 term (born at 146 +/- 0.2 d) lambs up to 6-7 weeks after birth. Term lambs were also studied at 25 weeks after birth. During rebreathing tests, we measured arterial PO2 and PCO2 and related them to minute ventilation (VI). Owing to variability in resting PAO2, hypoxic sensitivity was defined as the percentage increase in VI when PaO2 fell to 60% of resting values. Hypoxic sensitivities of preterm lambs did not change with age (68.9 +/- 24.4%), whereas values for term lambs more than doubled over the first 6 weeks (day 2, 73.9 +/- 15.8%; week 6, 227.4 +/- 24.9%) but returned to early postnatal values by week 25 (87.0 +/- 21.2%). Hypercapnic sensitivities (ml min-1 kg-1 mmHg CO2(-1) of preterm lambs were lower than those of term lambs between day 2 and week 2, but reached values in term lambs thereafter. We conclude that preterm birth abolishes the normal postnatal maturation of hypoxic ventilatory sensitivity, and temporarily depresses hypercapnic sensitivity.

Acidaemia enhances the inhibitory effect of hypoxia on fetal lung liquid secretion in sheep.

Previous studies have shown that moderate fetal asphyxia reduces the secretion rate of fetal lung liquid. The present aim was to determine the relative effects of the individual components of asphyxia (hypoxia, hypercapnia and acidaemia) on lung liquid secretion in fetal sheep. Fetal hyperoxia was also studied to determine the extent to which lung liquid secretion is restricted by the relatively low fetal blood PO2. As each manipulation of fetal blood gas tensions and pH treatment produced alterations in more than one aspect of blood composition, data from all treatment groups were combined and a multiple analysis of variance was performed to determine the separate effects of PaO2, PaCO2, SaO2 and pHa. Lung liquid secretion rate was significantly reduced when mean PaO2 values were below 24.5 mmHg (range 12.9-24.3 mmHg). When PaO2 values below 24.5 mmHg occurred in combination with pHa values below 7.275 (range 6.934-7.268) the secretion rates were further reduced. Alterations in pHa alone or in PaCO2 had no significant effect. These results indicate that hypoxia is the principal factor responsible for the inhibition of lung liquid secretion during asphyxia and that acidaemia enhances this inhibition.

Alterations in fetal urine production during prolonged hypoxaemia induced by reduced uterine blood flow in sheep: mechanisms.

1. Our aim was to identify mechanisms whereby prolonged fetal hypoxaemia alters renal function and urine production in fetal sheep. 2. Fetal hypoxaemia was induced for 24 h by reducing uterine blood flow at 129.0 +/- 2.1 days of gestation (term 145-147 days), causing a reduction in fetal arterial O2 saturation (SaO2) from 52.5 +/- 2.3 to 22.0 +/- 1.3% (P < 0.05). This hypoxaemia was initially associated with a mild acidaemia (pH 7.23 +/- 0.03). 3. The glomerular filtration rate (GFR) increased from a control value of 1.8 +/- 0.3 mL/min per kg to a maximal value of 2.8 +/- 0.6 mL/min per kg (P < 0.05) at 4-5 h of hypoxaemia, returning to control levels by 6-9 h of hypoxaemia. After 4 h of hypoxaemia renal blood flow was no different to control values (144 +/- 8 mL/min per 100 g kidney weight) but after 24 h of hypoxaemia it had increased to 190 +/- 8 mL/min per 100 g kidney weight (P < 0.05). Fractional reabsorption of Na+ in the proximal tubules decreased from a control value of 81.5 +/- 2.2 to 65.2 +/- 3.9% at 2-3 h of hypoxaemia (P < 0.05) and remained reduced (68.5 +/- 3.1%) at the end of hypoxaemia (P < 0.05). Fetal mean arterial pressure transiently increased (P < 0.05) but returned to control values by 4-5 h of hypoxaemia. Fetal renal vascular resistance was not significantly altered during hypoxaemia. Fetal urine production increased from a control value of 12.3 +/- 2.1 mL/h per kg to a maximal value of 19.1 +/- 4.2 mL/h per kg at 4-5 h of hypoxaemia (P < 0.05) and returned to control by 24 h of hypoxaemia. 4. Our results indicated that prolonged fetal hypoxaemia leads to the inhibition of Na+ reabsorption in the proximal portion of the renal tubules. Changes in GFR induced by hypoxaemia were similar to those in fetal urine production and were not associated with changes in renal blood flow. We conclude that prolonged fetal hypoxaemia affects renal haemodynamics and the reabsorptive capacity of the renal tubules, resulting in a diuresis.

Postnatal development of responses to airflow obstruction.

1. Obstruction of the upper airway could be an initiating factor in the Sudden Infant Death Syndrome (SIDS). Responses to upper airway obstruction include augmentation of respiratory efforts, active dilation of the upper airway and electrocortical arousal. Vulnerable individuals may fail to mount these responses effectively. 2. Respiratory and arousal responses to obstruction of the upper airway have been investigated in newborn lambs. In conscious lambs, nasal obstruction causes a profound augmentation of inspiratory efforts, mild asphyxiation and eventual formation of an oral airway. The ability to establish an oral airway involves both chemoreception and mechanoreception and improves with age. 3. In sleeping lambs, obstruction of tidal airflow leads to progressive hypoxaemia, augmentation of inspiratory efforts, bradycardia and arousal. Arousal occurs earlier and with less hypoxaemia and bradycardia in non-REM sleep than in REM sleep. Arousal occurs after inspiratory efforts have increased to the same extent during both sleep states, suggesting that mechanoreception, or a sense of inspiratory effort, is important in initiating arousal. 4. Obstruction of nasal tubes tends to cause arousal from sleep earlier, and with less hypoxaemia and less augmentation of inspiratory effort, than when a more compliant face mask is obstructed. This supports the suggestion that mechanoreception, which may be involved in the perception of inspiratory effort, is a determinant of arousal. 5. With increasing postnatal age, lambs become less arousable in response to airflow obstruction when in REM sleep. This suggests that lambs may become progressively more vulnerable to the effects of airway obstruction during the immediate newborn period.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory responses to progressive hypoxia and hypercapnia in developing sheep.

We aimed to determine the time course of postnatal development of ventilatory responsiveness to progressive hypoxia and hypercapnia. Eight lambs underwent hypoxic and hypercapnic rebreathing tests at weekly intervals from soon after birth to 6 weeks of age. Six mature ewes were also studied. During the tests blood samples were collected at intervals from the aorta so that arterial PO2 (PaO2) and PCO2 (PaCO2) could be related to ventilation. Hypoxic sensitivity was defined as the percentage increase in minute ventilation when PaO2 fell from control values (104.7 +/- 6.9 mmHg) to 50 mmHg. When measured in this way, hypoxic sensitivity increased significantly from 64.2 +/- 19.3% (mean +/- SE) in the newborn (2.3 +/- 0.4 days) to 150.4 +/- 14.0% at 3-4 weeks (25.1 +/- 0.6 days, P = 0.05). The hypoxic sensitivity of ewes (66.3 +/- 16.8%) was greatly reduced compared to 6-week-old lambs (140.3 +/- 18.9%, P < 0.05). Hypercapnic sensitivity (ml.min-1.kg-1.mmHg CO2(-1)) did not change significantly with age. We conclude that hypoxic sensitivity increases during the first 3-4 postnatal weeks and declines between infancy and adulthood. In contrast hypercapnic sensitivity does not change with age, although tidal volume and breathing frequency contributions to ventilatory responses change with advancing postnatal age.

Cerebral blood flow is increased throughout 12 h of hypoxaemia in the mid-gestation ovine fetus.

The changes in regional cerebral blood flow (CBF) in response to prolonged hypoxaemia were measured using coloured microspheres in the 0.6-gestation ovine fetus (n = 5). Fetal hypoxaemia was induced for 12 h by reducing maternal uterine blood flow with an adjustable clamp. CBF (mL min-1 100 g-1) was increased (P < 0.05) from control values (38.7 +/- 3.5) to 105.6 +/- 5.6 at 6 h of hypoxaemia, and to 121.9 +/- 23.1 at 12 h of hypoxaemia. One hour after fetal hypoxaemia had ceased, CBF (54.0 +/- 3.3) had decreased (P < 0.05) towards control values indicating incomplete cardiovascular recovery. Cerebral vascular resistance at 6 h and 12 h of hypoxaemia was lower (P < 0.05) than control values, and returned to control values 1 h after fetal hypoxaemia had ceased. Cerebral oxygen delivery at 6 h and 12 h of hypoxaemia was not significantly different from control values, but was higher (P < 0.05) 1 h after hypoxaemia had ceased. It is concluded that CBF is sufficiently increased during prolonged hypoxaemia in the mid-gestation fetus to maintain cerebral oxygen delivery.

Measurement of lung diffusing capacity and functional residual capacity in lambs during the first postnatal month.

The diffusing capacity of the lung for carbon monoxide (DLCO) is an important index of lung function but is not easily measured in spontaneously breathing animals with small lung volumes. Our aim was to devise a simple rebreathing method that would allow us to make serial measurements of DLCO in spontaneously breathing lambs during their first month after birth. By adding He to the rebreathing gas mixture, we were also able to measure functional residual capacity (FRC), enabling us to normalize DLCO with respect to FRC. We have compared FRC measured by the rebreathing technique with that measured by a closed-circuit helium dilution method (FRCcc). Using the rebreathing method we found highly significant positive correlations between DLCO and body weight (r = 0.70, P < 0.001) and between FRC and body weight (r = 0.79, P < 0.001). There was no significant change in DLCO/FRC over the first postnatal month; the mean value was 8.1 +/- 0.6 mL/min/mmHg/mL. Rebreathing FRC was highly correlated with FRCcc (r = 0.88, P < 0.001), but was lower than FRCcc by about 18%. In normal lambs DLCO and FRC, but not DLCO/FRC, increased during the first month after birth, suggesting that the increase in DLCO parallels lung growth. We conclude that the modified rebreathing method is suitable for measuring DLCO in small uncooperative spontaneously breathing animals.

The effects of twenty-four hours of reduced uterine blood flow on fetal fluid balance in sheep.

OBJECTIVE: Our aim was to determine the effects of a sustained reduction in uteroplacental perfusion, leading to fetal hypoxia, on determinants of amniotic fluid volume in sheep. STUDY DESIGN: Surgery was performed on five pregnant ewes 110 to 116 days after mating. At 127.3 +/- 2.2 days uterine blood flow was reduced for 24 hours, which reduced fetal SaO2 from 61.9% +/- 1.2% to 24.9% +/- 0.8%. RESULTS: Fetal urine production was increased from a control value of 193.0 +/- 24.0 ml/kg per 24 hours to 279.3 +/- 30.0 ml/kg per 24 hours during periods of reduced uterine blood flow and remained above control values for up to 48 hours after the reduced uterine blood flow period. A substantial loss of fetal water and electrolytes occurred through urine, which was associated with changes in the composition of fetal plasma and fetal tracheal, fetal swallowed, and amniotic fluids. Fetal swallowing was reduced throughout the reduced uterine blood flow period from a control value of 200.8 +/- 56.0 ml/kg per 24 hours to 32.7 +/- 8.4 ml/kg per 24 hours and returned to control levels after the cessation of the reduced uterine blood flow. CONCLUSION: We conclude that 24 hours of reduced uterine blood flow causes major changes in fetal renal function and fetal swallowing that, in spite of an expected reduction in lung liquid production, would increase the flow of fluid and electrolytes from the fetus into the amniotic sac.

Swallowing and urine flow responses of ovine fetuses to 24 h of hypoxia.

The aim of this study was to determine the effects of 24 h of hypoxia on fetal swallowing and urine flow rates. The study design included successive 24-h control, hypoxia, and recovery periods. To induce hypoxia, we infused nitrogen into the trachea of late-gestation pregnant sheep. During hypoxia, there were decreases in fetal arterial oxygen saturation [from 62.7 +/- 2.2 to 30.9 +/- 2.9% (SE)] and PO2 (from 21.1 +/- 1.0 to 14.1 +/- 0.9 mmHg) (n = 7). Fetal arterial pH decreased maximally by 0.04 +/- 0.01 at 6 h and returned to control thereafter. Fetal swallowing decreased from 13.4 +/- 2.1 to 0.6 +/- 0.2 ml.h-1.kg fetal wt-1 with the onset of hypoxia and gradually increased, but only to one-half control levels, during the last 12 h of hypoxia. Fetal urine flow gradually decreased from 9.6 +/- 1.6 ml.h-1.kg-1 to a minimum of 5.3 +/- 0.5 ml.h-1.kg-1 at 2-3 h of hypoxia and returned to control thereafter. During the first hour of the recovery period, fetal swallowing transiently increased to twice control levels before returning to control. This was followed by a delayed, transient increase in urine flow to 63% above control levels at 2-6 h after hypoxia. We conclude that the fetal swallowing and urine flow responses to prolonged hypoxia in the absence of acidemia are distinctly different from the initial inhibitory responses, in that swallowing partially and urine flow fully recovers from the initial suppression.

Maternal undernutrition during mid-pregnancy in sheep. Placental size and its relationship to calcium transfer during late pregnancy.

The aim of the present experiment was to determine the relationship between placental and fetal weight after placental growth had been retarded by maternal undernutrition. Placental weight and fetal weight were measured in single-lamb-bearing ewes which were well-fed throughout pregnancy, or severely undernourished between the 30th and 96th day of pregnancy. Placental transfer of calcium and whole-body metabolism of both glucose and Ca were measured during late pregnancy. The change in fleece-adjusted live weight between the 30th and 96th day of pregnancy was 99 (SE 9.8) and -146 (SE 9.6) g/d for the well-fed and undernourished ewes respectively. The condition score of well-fed ewes did not significantly change between the 96th (2.9 (SE 0.08)) and 140th (3.0(SE 0.13)) day of pregnancy, while it increased from 1.6 (SE 0.15) to 2.3 (SE 0.11) for the previously undernourished group. Undernutrition caused an increase (P less than 0.01) in placental weight measured on the 96th (21%) and 140th (30%) day of pregnancy. In contrast fetal growth was not significantly affected by maternal undernutrition. While the voluntary dry matter intakes (g/d) of previously undernourished ewes after the 97th day of pregnancy were higher than for their well-fed counterparts, there was no significant difference between whole-body glucose or Ca metabolism, or the placental transfer of Ca measured during late pregnancy. This experiment confirms earlier reports of an increase in placental weight as a result of maternal undernutrition during mid-pregnancy; but the factors causing and the functional significance of this response have not been identified. Contrary to earlier proposals, placental weight per se did not limit fetal growth during late pregnancy. It is hypothesized that a combination of factors originating from maternal, placental and fetal sources act together to regulate growth of the fetus.