Transcutaneous measurement of carbon dioxide tension: effect of sleep state in term infants

Transcutaneous measurement of carbon dioxide tension (tcPO2) was used to assess the effect of sleep state on arterial carbon dioxide tension (PaCO2) in infants. Initially, tcPCO2 was correlated with PaCO2 in 50 sick preterm and term neonates with indwelling arterial lines. At a skin electrode temperature of 42 degrees C, the correlation coefficient between tcPCO2 and PaCO2 was .95. In eight healthy term infants there was a small but significant decrease in tcPCO2 of 2 +/- 1 mm Hg (P less than .001) during active as compared to quiet sleep. This decrease in tcPCO2 was accompanied by a significant decrease in transcutaneous oxygen tension (tcPO2) of 5 +/- 4 mm Hg (P less than .02) as has been previously described. The simultaneous decrease of both tcPCO2 and tcPO2 appears to indicate ventilation/perfusion inequalities in these infants during active sleep. These findings illustrate that tcPCO2 can accurately predict PaCO2 in infants and that this is a useful technique for studying neonatal respiratory control during various stages of sleep.     

The effect of energy intake and expenditure on the recovery of 13CO2 in the parenterally fed neonate during a 4-hour primed constant infusion of NAH13CO3

The use of 13CO2 excretion to measure the oxidation of 13CO2 labeled substrates is increasing as it is both noninvasive and lacks the radiation exposure associated with the use of 14C. No standards are available for 13CO2 recovery in breath from the bicarbonate pool in the neonate. A primed constant infusion of NaH13CO3 over 4 h was used with open circuit indirect calorimetry in 15 appropriate for gestational age newborn infants (gestational age 28-39 wk; postnatal age 2-52 days), on varying amounts of intravenous feeding (37-114 kcal X kg-1 X day-1). Following a bolus of 6.9 mumol X kg-1 of NaH13CO3, a maintenance infusion of 4.6 mumol X kg-1 X h-1 was started. The 13C enrichment in breath rose rapidly to reach a plateau by 90 min with less than 5% variation of the plateau. Recovery of the tracer in breath ranged from 69.6-83.5% and was significantly correlated with 1) energy intake (37-114 kcal X kg-1 X day-1); 2) metabolic rate (34.6-56.1 kcal X kg-1 X day-1); 3) VCO2 (4.86-7.43 ml X kg X -1 X min-1). There was no correlation with the level of protein or fat intake. We provide an equation that can be used to calculate the correction factor when doing constant infusion substrate oxidation studies with a 13C label in neonates.     

Effects of intravenous glucose loading on oxygen consumption, carbon dioxide production, and resting energy expenditure in infants with bronchopulmonary dysplasia

To determine the effects of intravenous glucose loading on basal oxygen consumption, resting energy expenditure, and basal carbon dioxide production in infants with bronchopulmonary dysplasia who were still oxygen dependent, we administered intravenous glucose loads of 4 and 12 mg/kg-1/min-1 on 2 consecutive days, under identical experimental conditions, to six infants with bronchopulmonary dysplasia and six healthy control subjects. Infants were not fed for 9 hours before and during the 4- to 6-hour study periods; the intravenous glucose infusion, along with an amino acid mixture (2 gm.kg-1.24 hr-1), was started at the beginning of the fasting period. Oxygen consumption and carbon dioxide production and resting energy expenditure were measured by a flow-through indirect calorimetry technique under basal conditions. Infants with oxygen-dependent bronchopulmonary dysplasia had significantly higher basal oxygen consumption and resting energy expenditure than did control infants and significantly higher basal carbon dioxide production during the high glucose infusion. With glucose loading, infants with bronchopulmonary dysplasia had a significant rise in basal oxygen consumption (7.91 +/- 0.91 ml.kg-1.min-1 to 9.65 +/- 1.35 ml.kg-1.min-1, p less than 0.05), basal carbon dioxide production (5.93 +/- 0.72 ml.kg-1.min-1 to 7.10 +/- 1.04 ml.kg-1.min-1), and resting energy expenditure (53.8 +/- 5.75 kcal.kg-1.24 hr-1 to 65.3 +/- 7.0 kcal.kg-1.24 hr-1, all p values less than 0.05). Control infants had no significant changes with intravenous glucose loading. We conclude that intravenous glucose loading in infants with bronchopulmonary dysplasia resulted in a net increase in resting energy expenditure, which should be taken into account in assessing their energy intake during nutritional management. The risk of pulmonary stress caused by an increase in basal oxygen consumption and carbon dioxide production resulting from glucose load should also be considered.     

Histamine provocation in young, awake children with bronchial asthma, using a fall in oxygenation as the only indicator of a bronchial reaction

Bronchial provocation with histamine was performed in 11 boys and 6 girls, age range 2.7-7.4 y, with unspecific respiratory symptoms or bronchial asthma, using a fall in oxygenation as the only indicator of a bronchial reaction. In addition to transcutaneous oxygen tension (tcPO2), transcutaneous carbon dioxide tension (tcPCO2) was continuously monitored during the provocation procedure in order to identify possible changes in ventilation. A fall of 20% or more in the tcPO2 below a "floating" baseline value, defined as the highest tcPO2 value between the inhalations of histamine up to that point, was regarded as indicating a significant bronchial reaction. One child was excluded from the study because of an "early, false-positive" reaction due to hyperventilation during the inhalation, verified by a decrease in the tcPCO2 followed by a compensatory period of hypoventilation, resulting in a fall of more than 15% in the tcPO2 after the inhalation of saline. In the vast majority of the children, however, the tcPO2 values remained stable during the first dose stages of saline and histamine, with either a gradual fall immediately before or a distinct fall in conjunction with the reaction. The mean reaction concentration was significantly lower in the group of children with clinical asthma, 0.74 mg/ml, compared with the group of children with unspecific respiratory symptoms, 2.00 mg/ml (p = 0.03). In conclusion, a 20% fall in the tcPO2 can be used as the only indicator of a bronchial reaction during bronchial provocation tests in young, awake children. Changes in ventilation evaluated by monitoring tcPCO2, makes it possible to distinguish between a fall in oxygen tension due to an early, "false" reaction as a result of hypoventilation and a "true" bronchial reaction.     

Energy expenditure in premature newborns with bronchopulmonary dysplasia.

Five premature newborns (birth weight, mean +/- SD, 960 +/- 145 g; gestational age 28 +/- 1 weeks) with bronchopulmonary dysplasia (BPD) according to the criteria of Bancalari, and 6 controls (birth weight 1,320 +/- 210 g; gestational age 30 +/- 2 weeks) were studied for energy expenditure (EE) by indirect calorimetry. The measurement of total EE was performed when the intake of the infants in both groups was the same and when the respiratory condition had stabilized (control group: postnatal age 31 +/- 6 days, 1,950 +/- 200 g; BPD group: postnatal age 105 +/- 45, postnatal weight 2,440 +/- 380). The BPD group had a higher VO2 (11.15 vs. 8.04 ml/kg/min, p less than 0.01), VCO2 (9.13 vs. 7.74 ml/kg/min, p less than 0.02) and total EE (76 vs. 61 kcal/kg/day, p less than 0.02). The highest values were encountered in the 3 more severely ill infants: mean VO2 11.03 ml/kg/min, mean EE 82 kcal/kg/min. In these cases, administration of medium chain triglycerides limits the increase in VCO2 and lowers the respiratory quotient (0.87 vs. 0.96 in controls.     

Transcutaneous oxygen and carbon dioxide levels and a clinical symptom scale for monitoring the acute asthmatic state in infants and young children

Measurement of transcutaneous PO2 and PCO2 in addition to a clinical symptom grading system was used to monitor the acute asthmatic attack in children under two years of age. tcPO2 was lowered already at signs of mild obstruction and decreased in parallel with clinical deterioration. tcPCO2 was almost unchanged at mild to moderate obstructive symptoms. With clinical deterioration tcPCO2 rose steadily. An increase of the oxygen concentration to 30-40% in the inspired air increased tcPO2, on the average by 70%, but did not change the tcPCO2, level. Continuous recording of tcPO2 and tcPCO2 as well as the clinical grading system are valuable tools when monitoring severely obstructive infants and young children.     

In utero ventilation augments the left ventricular response to isoproterenol and volume loading in fetal sheep

In its normal circulatory environment, the fetal left ventricle can maximally increase output less than 2-fold, in contrast to the nearly 3-fold increase that occurs at birth. Several studies have attributed this finding to fetal myocardial "immaturity," and speculated that there is a rapid maturation of the myocardium in the perinatal period. We investigated the importance of the circulatory environment itself, rather than myocardial immaturity, by measuring left ventricular output (LVO) during in utero oxygen ventilation and isoproterenol infusion. We studied seven near-term fetal sheep greater than or equal to 2 d after placement of intravascular catheters, an endotracheal tube, and an electromagnetic flow transducer around the ascending aorta. We measured hemodynamic variables in the presence and absence of all combinations of oxygen ventilation, isoproterenol infusion, and volume infusion. Baseline LVO was normal (133 +/- 27 mL.kg-1.min-1). Individually, oxygen ventilation (136 +/- 11 mL.kg-1.min-1, p less than 0.001) and isoproterenol (48 +/- 11 mL.kg-1.min-1, p less than 0.05) increased LVO significantly; volume infusion did not. Their cumulative effect increased LVO nearly 3-fold (to 387 +/- 98 mL.kg-1.min-1), similar to levels seen in the newborn lamb. Mean left atrial pressure increased above right during oxygen ventilation (from 0.05 +/- 0.54 kPa to 0.82 +/- 0.39 kPa, p less than or equal to 0.0001). We conclude that the previously observed limitation in maximal LVO in the near-term fetus is primarily caused by its circulatory environment rather than relative myocardial immaturity, and speculate that a prominent Starling response is uncovered by decreases in left ventricular afterload and right ventricular constraint.     

Spectral analysis of impedance respirogram in newborn infants

Respiratory rate (RR), transthoracic electric impedance (TEZ) and transcutaneous PO2 and PCO2 were monitored during the 5 first postnatal days in 54 neonates on three separate occasions. There was no difference in the overall RR between the term and healthy preterm babies on different days of recordings but RR of the babies with RDS (who were all ventilated) was lower on day 1 (p less than 0.01). When the power spectrum of the TEZ respirogram was computed and the spectral density was divided into low-frequency (LF, less than 0.20 Hz) and high-frequency (HF, greater than 0.20 Hz) areas, the LF/HF ratio of healthy preterm babies was greater than that of term babies on day 1 (p less than 0.01). The preterm babies with RDS did not differ from the term babies in this respect. The LF/HF ratio was negatively correlated with gestational age and it had a positive correlation to PtcO2 (p less than 0.05) and PtcCO2 (p less than 0.01) (R2 = 0.07). The result evidences that the control of respiration changes in relation to maturity and the LF/HF ratio is a quantitative indicator of respiratory variability reflecting this development.     

Effect of formula carbohydrate concentration on tolerance and macronutrient absorption in infants with severe, chronic diarrhea

To determine how the carbohydrate (CHO) content of "semielemental" formulas affects tolerance and macronutrient absorption, we enrolled 12 infants with severe diarrhea in two successive metabolic balance studies. The infants received, in random order, one of two isocaloric formulas that differed mainly in their CHO and fat concentrations. No significant differences were found between the two feeding periods for peak breath hydrogen levels and fecal osmolality. The low-CHO formula was tolerated better than the high-CHO formula, as indicated by a significantly lower stool output (mean +/- SD 387 +/- 230 vs 764 +/- 443 gm, respectively; p less than 0.05), and higher fecal pH (5.9 +/- 0.7 vs 4.9 +/- 0.5; p less than 0.05). Macronutrient absorption was greater during the ingestion of the low-CHO formula, as indicated by a significantly higher coefficient of fat absorption (p less than 0.005) and lower total fecal energy (mean +/- SD for high- vs low-CHO formula, 372 +/- 205 vs 207 +/- 102 kcal; p less than 0.05), which resulted from a lower CHO excretion (p less than 0.05). A correlation coefficient between the energy derived from CHO in feces and the total stool output was significant for both the high-CHO formula (r = 0.83; p less than 0.001) and the low-CHO formula (r = 0.7; p = 0.01). The CHO concentration of the special infant formula that we tested had an overriding effect on stool output and on fat and energy absorption.     

Cardiorespiratory response to exercise after the Fontan procedure for tricuspid atresia

Noninvasive exercise testing was used to assess gas exchange in 13 patients age 6-25 yr who had undergone Fontan procedures for tricuspid atresia, five of whom had preexisting Glenn shunts. The results were compared to 28 age- and sex-matched controls. Oxygen saturation was measured by ear oximetry at rest and after exercise. Ventilation, oxygen consumption (VO2), carbon dioxide production (VCO2), and heart rate were measured during progressive exercise. The ventilatory equivalents for oxygen (VE/VO2) and carbon dioxide (VE/VCO2), mixed expired pCO2 (PECO2) end-tidal pCO2 (PETCO2), and dead space to tidal volume ratio (VD/VT) were determined during steady state exercise on a cycle ergometer. Heart rate was higher for VO2 by 15% (p less than 0.02) and ventilation was higher for both VO2 (by 37%, p less than 0.001) and VCO2 (by 27%, p less than 0.002) in the patients than the controls. Mean VE/VO2 was 35.4 +/- 7.8 (SD) compared to 25.8 +/- 3.1 (p less than 0.001) and mean VE/VCO2 was 41.7 +/- 9.0 compared to 31.6 +/- 4.3 (p less than 0.001). Mean PECO2 was 21.4 +/- 4.4 torr with controls at 27.9 +/- 3.8 (p less than 0.001) and mean PETCO2 was 33.0 +/- 5.3 torr compared to 40.0 +/- 3.3 (p less than 0.001). The patients had a mean oxygen saturation of 92 +/- 5% at rest and abnormal saturation after exercise (87 +/- 9, p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of arterial glucose infusion above the celiac axis in the neonatal lamb

Refractory hypoglycemia has been reported in an infant receiving glucose infusion via an umbilical artery catheter (UAC) above the celiac axis. To prove the hypothesis that hypoglycemia resulted from direct glucose infusion to the pancreas, 15 term spontaneously delivered lambs were infused with 5.3 +/- 0.1 mg X kg-1 min-1 of glucose via an arterial catheter. In 9 glucose was infused below the celiac, and the glucose production rate (GPR) was derived. After a recovery period, the study was repeated with glucose infused above the celiac. During glucose infusion above the celiac, the plasma glucose concentration was lower than when the infusion was given below the celiac (140 +/- 6 vs. 175 +/- 11 mg/dl, p less than 0.01). There was also a fall in the average GPR (3.7 +/- 0.5 vs. 5.5 +/- 0.8 mg X kg-1 min-1, p less than 0.05). In 6 lambs the study was performed in the reverse sequence (high then low infusion) and no differences were noted in the parameters measured. However, there was a marked heterogeneity in the paired GPR in these lambs. We conclude that direct glucose infusion above the celiac increases glucose delivery to the pancreas. This produces increased insulin delivery to the portal system resulting in suppressed GPR and reduction in plasma glucose concentration. These changes may account for refractory hypoglycemia in infants clinically when glucose is infused above the celiac through a UAC.     

Cardiovascular responses to alpha-melanocyte stimulating hormone during the perinatal period in sheep

To determine the effects of alpha-melanocyte stimulating hormone (alpha MSH) on the circulation of undisturbed fetal sheep and young lambs and to explore possible mechanisms of actions, we examined the responses of ascending aortic blood flow, heart rate, stroke volume, and arterial blood pressure to a single intravenous injection of alpha MSH, ACTH, cortisol and to alpha MSH after beta-adrenergic blockade. We also measured cardiac output and organ blood flows before and after alpha MSH injection by the radionuclide labeled microsphere technique. alpha MSH increased ascending aortic blood flow from 249 +/- 23 to 327 +/- 30 ml X min-1 X kg-1 (P less than 0.001), heart rate from 111 +/- 10 to 126 +/- 11 min-1, (P less than 0.001) and stroke volume from 2.32 +/- 0.21 to 2.75 +/- 0.20 ml X kg-1, (P less than 0.001) in 10 young lambs 15-30-day-old. alpha MSH decreased mean systemic arterial blood pressure from 42.6 +/- 1.7 to 39.3 +/- 1.6 mmHg (P less than 0.001) in fetal sheep and min-1, (P less than 0.001) and stroke volume from 2.32 +/- 0.21 to 2.75 +/- 0.20 ml X kg-1, (P less than 0.001) in 10 young lambs 15-30-days-old. alpha MSH decreased mean systemic arterial blood pressure from 42.6 +/- 1.7 to 39.3 +/- 1.6 mmHg (P less than 0.001) in fetal sheep and from 77.5 +/- 4.5 to 72.7 +/- 4.3 mmHg (P less than 0.001) in young lambs. In six additional young lambs (20-35-day-old) cardiac output, measured by microspheres, increased with alpha MSH from 216 +/- 20 to 261 +/- 19 ml X min-1 X kg-1 (P less than 0.001). alpha MSH also increased blood flow to the myocardium from 104 +/- 22 to 151 +/- 26 ml X min-1 X 100 g-1 (P less than 0.001), to the adrenals from 195 +/- 38 to 243 +/- 41 ml X min-1 X 100 g-1, (P less than 0.05), and to the lungs from 157 +/- 31 to 468 +/- 81 ml X min-1 X 100 g-1 (P less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)     

Small preterm infants (less than or equal to 1500 g) have only a sustained decrease in ventilation in response to hypoxia.

The classic "biphasic" ventilatory response to 15% O2 was previously observed in preterm infants who were large compared with those in the intensive care nursery today. We hypothesized that in the smaller infant (less than or equal to 1500 g) the response might be closer to that of the fetus, with no initial increase in ventilation. Thus, we studied 14 healthy preterm infants less than or equal to 1500 g [birth weight 1200 +/- 63 g (mean +/- SEM); gestational age 29 +/- 0.4 wk; postnatal age 17 +/- 3 d] during rapid eye movement and quiet sleep. Ventilation was measured using a nosepiece and a flow-through system. Sleep states were defined using EEG, electro-oculogram, and body movements. After a control period in 21% O2 (3 min), infants breathed 15% O2 for 5 min. In rapid eye movement sleep, minute ventilation decreased from 0.186 +/- 0.020 (control) to 0.178 +/- 0.021 (30 s), to 0.171 +/- 0.017 (1 min; p = 0.03), to 0.145 +/- 0.016 (3 min; p = 0.002), and to 0.129 +/- 0.011 l.min-1.kg-1 (5 min; p = 0.004). In quiet sleep, it decreased from 0.173 +/- 0.019 (control) to 0.164 +/- 0.019 (30 s), to 0.166 +/- 0.019 (1 min), to 0.148 +/- 0.013 (3 min; p = 0.03), and to 0.146 +/- 0.012 l.min-1.kg-1 (5 min; p = 0.04).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effect of alpha-adrenergic blockade on the pulmonary vascular response to dopamine in neonatal lambs

The effect of alpha-adrenergic blockade by phentolamine on the pulmonary vascular response to dopamine was studied in chronically prepared newborn lambs. Dopamine was administered at doses of 2.7 micrograms . kg-1 . min-1, 27 micrograms . kg-1 . min-1 and 270 micrograms . kg-1 . min-1 with and without alpha-adrenergic blockade. Dopamine infusion at 270 micrograms . kg-1 . min-1 caused a rise in the mean pulmonary artery pressure from 22 +/- 3.2 mmHg (mean +/- S.E.) at baseline to 36 +/- 4.1 mmHg (P less than 0.001). This rise was unaffected by alpha-adrenergic blockade. Dopamine infusion alone did not change pulmonary blood flow, but, in the presence of alpha-adrenergic blockade, pulmonary blood flow rose from 190 +/- 12 ml . min-1 . kg-1 at baseline to 280 +/- 13 ml . min-1 . kg-1 at the maximum dopamine infusion rate (P less than 0.001). Pulmonary vascular resistance was the same before and after alpha-adrenergic blockade and did not change from the baseline value during dopamine infusion.     

Fetal lamb ventricles respond differently to filling and arterial pressures and to in utero ventilation

Right and left ventricular function were investigated in 12 fetal lambs (127-140 days gestation) instrumented with electromagnetic flow sensors on the ascending aorta and the main pulmonary artery, and with vascular catheters. Nine fetuses were equipped with a postductal aortic occluder and the trachea was cannulated in eight. Control arterial blood values were pH 7.36 +/- 0.02 (SD), PCO2 49.3 +/- 2.3 torr, PO2 18.4 +/- 1.7 torr, and hematocrit 37.3 +/- 4.4%. Biventricular function curves relating stroke volume to mean right and left atrial pressure were generated by rapid withdrawal and reinfusion of fetal blood. Both function curves were composed of steep ascending and plateau limbs that intersected at a breakpoint. Stroke volumes at the breakpoints were 0.94 +/- 0.19 ml.kg-1 and 0.63 +/- 0.15 ml.kg-1 for right and left ventricle, respectively (p less than 0.001). During postductal aortic occlusion, arterial pressure increased by 19.3 +/- 7.9 torr while right ventricular stroke volume decreased by approximately 48% and left ventricular stroke volume decreased by approximately 9%. In utero ventilation increased arterial pressure, heart rate, PO2, and oxygen content. Right atrial pressure increased from 3.9 +/- 1.3 to 5.8 +/- 2.9 torr (p less than 0.05); left atrial pressure from 3.5 +/- 1.5 to 10.0 +/- 4.4 torr (p less than 0.05). Aortic flow nearly doubled (112 +/- 29 to 211 +/- 35 ml.min-1.kg-1) (p less than 0.05), and the left ventricular function curve shifted upward. The right ventricular function curve was shifted downward during ventilation. We conclude that the fetal ventricles differ significantly in their outputs, response to changes in arterial pressure, and to the onset of in utero ventilation.     

Ontogeny of glucose homeostasis in low birth weight infants

Suppression of the endogenous glucose production rate (Ra) is the adult response to glucose infusion. Persistent Ra (greater than or equal to 1 mg.kg-1min-1 or less than 80% decrease in basal Ra) in response to glucose infusion is evidence of a transitional homeostatic state in the neonate during the first days after birth. To determine whether postnatal development produces an adultlike response, Ra was measured in 11 infants (birth weight 1716 +/- 48 g, gestational age 33 +/- 0.3 weeks) at 2 to 5 weeks of age. In these paired studies, 4 micrograms.kg-1min-1 D-(U-13C)glucose tracer was infused by prime constant infusion to determine Ra, during infusion of either saline solution or glucose, the latter at a rate of 5.3 +/- 0.2 mg.kg-1min-1 (mean +/- SEM). When the results of the saline infusion turnover period were compared with those of the glucose infusion turnover period, plasma glucose concentration increased significantly, from 88 +/- 3 mg/dL to 101 +/- 4 mg/dL (P less than 0.001). Plasma insulin concentration remained unchanged (12 +/- 5 microU/mL vs 8 +/- 3 microU/mL). Ra was heterogenous during glucose infusion, and persistent Ra was present in six of 11 infants. Of the five infants who had decreased Ra during glucose infusion, three received glucose at a rate exceeding basal Ra. Of the remaining six infants who evidenced persistent Ra during glucose infusion, three received glucose at a rate equal to or in excess of basal Ra. We conclude that glucose homeostasis in low birth weight infants is transitional throughout the neonatal period.     

Lateral positioning of the stable ventilated very-low-birth-weight infant. Effect on transcutaneous oxygen and carbon dioxide

Eighteen stable very-low-birth-weight (VLBW) mechanically ventilated infants with chronic lung disease were studied to examine the effects of right and left lateral positioning in contrast to supine positioning on transcutaneous (tc) oxygen (tcPO2) and carbon dioxide measurements (tcPCO2). The neonates were studied at a median postnatal age of 31 days (range, 17 to 57 days) and had median birth weights and gestational ages of 975 g (range, 570 to 1360 g) and 27.5 weeks (range, 24 to 30 weeks), respectively. Median fraction of inspiratory oxygen was 0.32 (range, 0.23 to 0.40). The sequence of study positions was randomly determined. Sleep state as well as tcPO2 and tcPCO2 were recorded every 30 s for five minutes. A significant difference in mean tcPO2 or tcPCO2 was not detected for any of the positions. Lateral positioning may facilitate the development of midline behavior in VLBW infants. Care givers are often reluctant to position infants in side lying, however, because of concerns that ventilation or oxygenation might be compromised. We conclude that placing the stable VLBW mechanically ventilated infant in a side-lying position has no deleterious effects on oxygenation and ventilation, as measured by tcPO2 and tcPCO2, and therefore should be encouraged.     

Effect of tilting on oxygenation in newborn infants.

Transcutaneous (tc) PO2 in newborn infants increased on head up tilting (median increase 0.5 kPa at term, 1.0 kPa preterm). Head down tilting was associated with an equivalent fall in tcPO2. There was no change in tcPCO2. Tilting of infants mechanically ventilated for respiratory distress syndrome or surgery produced no consistent change in PO2.     

Enhancement of lung conditioning by acetylcholine in the prevention of respiratory distress syndrome in the preterm fetal lamb

We exposed 128- to 130-day-gestation fetal lambs by cesarean section leaving the umbilical cord and placenta undisturbed, and we then treated the lungs with pulmonary conditioning (i.e., repeated prolonged inflations to 35 cm H2O, followed by a continuous positive airway pressure of 15 cm H2O). To investigate the added effect of pulmonary vasodilation upon the increase of total compliance and pulmonary oxygen uptake, we also administered acetylcholine intravenously at a rate of 80 micrograms min-1. Eleven of 13 lambs met the endpoint criteria of either compliance (0.5 ml [cm H2O]-1 kg-1; 1 animal), or pulmonary oxygen uptake (6 ml kg-1 min-1; 6 animals), or both (4 animals), and were delivered within 0.6 +/- 0.3 h. This time was significantly (p less than 0.05) shorter than previously seen in similar studies without the infusion of a vasodilator; all animals so delivered survived 24 h of mechanical ventilation in excellent health. We suggest that pharmacologic pulmonary vasodilation, in addition to deep sustained pulmonary insufflation and distension, is an effective and rapid means of transforming stiff immature lungs into lungs that can sustain normal ventilation and gas exchange.     

Cerebral blood flow and O2 metabolism after asphyxia in neonatal lambs

A neonatal lamb model has been developed to examine the regulation of cerebral blood flow (CBF) and oxygen metabolism during the critical period after an asphyxial insult. Nine newborn lambs had control measurements and timed measurements after asphyxia of CBF (radioactive microsphere technique), arterial and cerebral venous (sagittal sinus) blood gases and oxygen contents performed. Immediately after resuscitation from asphyxia, there was a marked increase in CBF compared to control (239 +/- 22 versus 82 +/- 7 ml X 100 g-1 X min-1, mean +/- SEM; p less than 0.01). Cerebral oxygen delivery (CBF X arterial O2 content) increased from 12.87 +/- 1.20 to 37.40 +/- 3.40 ml X 100 g-1 X min-1 (p less than 0.01), while cerebral O2 consumption was significantly decreased compared to control (4.75 +/- 0.42 to 3.42 +/- 0.46 ml X 100 g-1 X min-1, p less than 0.05). Cerebral fractional O2 extraction, the relationship between oxygen uptake and delivery fell from 0.38 +/- 0.03 to 0.09 +/- 0.02; p less than 0.01. This reactive hyperemia was followed in all animals by a period of hypoperfusion. CBF (52 +/- 4 ml X 100 g-1 X min-1), O2 delivery (7.94 +/- 0.50 ml X 100 g-1 X min-1), and cerebral O2 consumption (3.34 +/- 0.24 ml X 100 g-1 X min-1) were all significantly depressed when compared to control. These data demonstrate important changes in CBF and O2 metabolism after neonatal asphyxia that may be important to the pathogenesis of brain injury.