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While 24 newborn infants (ages, 2 to 48 hours; gestational ages, 24 to 42 weeks) breathed various concentrations of oxygen, the PO2 values on their unheated skin surface were measured by an unheated microcathode electrode for transcutaneous PO2 monitoring. In infants with arterial PO2 values in the range of 50 to 100 torr and with similar skin temperatures, the mean surface PO2 of unheated skin was inversely related to birth weight: 27.2 torr in infants weighing less than 1,500 gm, 14.3 torr in infants weighing 1,500 to 2,500gm, and 2.9 torr in infants weighing more than 2,500 gm. In the smallest infants, the skin surface PO2 was significantly related to arterial PO2: it was about one third of arterial PO2 as estimated by a second electrode for transcutaneous PO2 monitoring heated to 44 degrees C. Phototherapy, crying, or blood transfusion increased the surface PO2 of unheated skin, but not the tcPO2 measured at 44 degrees C. These findings suggest that blood flow to the skin in excess of its metabolic needs due to immature control of cutaneous circulation, along with low resistance to oxygen diffusion, determines the high oxygen permeability of skin in premature infants.

Ophthalmic artery blood flow velocity (OA-BFV, cm/s), cerebral blood flow velocity (C-BFV, cm/s), and cardiac output (ml/min) were measured by pulsed Doppler sonography in 15 healthy term and 10 well preterm (26-35 wk) infants in the first week of life. OA-BFV did not increase with increasing gestational age (preterm: peak systolic BFV 29 +/- 5 cm/s, mean BFV 7.2 +/- 1.5 cm/s; term: peak systolic BFV 27 +/- 5 cm/s, mean BFV 6.6 +/- 1.3 cm/s), unlike C-BFV (preterm: peak systolic BFV 34 +/- 8 cm/s, mean BFV 9.4 +/- 2.3 cm/s; term: peak systolic BFV 43 +/- 9 cm/s, p less than 0.05; mean BFV 11 +/- 3.0 cm/s, p less than 0.05) and cardiac output (preterm 329 +/- 128 ml/min, term 732 +/- 112 ml/min; p less than 0.001). The ratio of OA-BFV/C-BFV was significantly higher in preterm than in term infants (p less than 0.01). In preterm infants, but not in term infants, there was a positive linear correlation of OA-BFV to C-BFV (r = 0.88). We conclude that it is possible to measure opthalmic artery blood flow velocity in neonates by pulsed Doppler sonography. Gestational age has different effects on OA-BFV and on C-BFV. Although it is a point of discussion if blood flow velocities are reflecting absolute blood flow, Doppler assessment of OA-BFV could be a tool for monitoring risk factors for retinopathy of prematurity.

Red cell mass (RCM) was estimated using 125I-labelled human serum albumin in 128 premature infants born after 26 to 36 weeks gestation. Infants of three different gestational periods (26--29, 30--32, and 33--36 weeks) with respiratory distress (RD) averaged lower one-minute Apgar scores and lower RCM than infants without RD (P less than 0.05). The incidence of RD was significantly (P less than 0.05) higher in infants with Apgar scores below 6 and in infants with RCM of less than 35 ml/kg than in the infants with greater values. The highest incidence of RD and the highest mortality rate were found in the infants with low Apgar scores and low RCM values. Prematures with similar Apgar scores showed a higher incidence of RD when RCM was low, and infants with similar RCM showed a higher incidence of RD when Apgar scores were low. Our results suggest that both birth asphyxia and deficiency of red cell mass interfere with postnatal cardio-respiratory adaptation. In high-risk premature infants, erythrocytes should be transfused when the venous haematocrit is below 0.459

To determine the influence of heart rate (HR) on systolic time intervals (STI) in neonates, serial measurements of right ventricular (RVSTI) and left ventricular systolic time intervals (LVSTI) were made on 30 healthy term newborn infants at age 4-8 h, 24-30 h, eight days, and four weeks. STI was related to HR and age. Age-related changes were similar to previously reported results. The preejection periods (RPEP and LPEP) significantly shortened with increasing age, whereas the right and left ventricular ejection times (RVET and LVET) were unrelated to age. RPEP was unrelated to HR, but tended to be prolonged in restless infants. With increasing HR, RVET decreased and RPEP/RVET increased in all age groups, but less at four weeks. A rise in HR of 50/min resulted in an increase of RPEP/RVET by 26% of the mean value at age 4-8 h and by 20% at four weeks. In 14 infants, RVSTI was recorded during a change in HR. In all these infants, RPEP and RPEP/RVET increased with increasing HR. We conclude that HR-related changes of RVSTI in neonates are different from those in older subjects. It should be considered that in neonates elevated values of RPEP/RVET, suggesting increased pulmonary vascular resistance, may be caused by high HR and unrest.

The Hypoxic-Ischemic Encephalopathy (HIE) is a severe illness of the unborn, respectively of the newborn. About 90 percent of the causes occur in utero, about 10 percent after birth. The risk for HIE arises from anatomical and pathophysiological particularities: little overlapping between the great cerebral arteries, poor periventricular vascularisation, and a loss of the autoregulation of cerebral blood flow during asphyxia. Most important is the early detection of intrauterine asphyxia. After birth the general measures include: thermoneutral temperature, oxygenation, normal pCO2, regular blood pressure monitoring, glucose infusion, therapy of convulsions and of an inherent brain edema. After birth the five most common clinical settings in which HIE occurs, are: postpartum asphyxia, PFC, septic shock, pneumothorax and apneas. Therapeutic measures (e.g. volume therapy) have to be prompt but subtle, to prevent ischemia, avoiding overtherapy with its risk of intracranial hemorrhage.

Four devices for transcutaneous PO2 (tcPO2) monitoring have been applied simultaneously in 16 infants. Both during a maximal change in PaO2 and during physiological PO2 variations, the in vivo response time of the electrodes did not show the differences observed in vitro. We compared A, a prototype of the electrode by Huck, Lübbers and Huch (25 micrometer Telfon membrane) ; B, the commercial version of A by Hellige--Draeger (25 micrometer Telfon); C, the Radiometer TCM I oxygen monitor (25 micrometer polypropylene); and D, the Roche macrocathode electrode (6 micrometer Mylar), at 44 degree C. In vitro the 50% response times were 2.9 (A), 4.4 (B), 3.7 (C), and 7.4 (D) sec. The rates of tcPO2 changes at the midpoint of the response curves were 3.8(A) 2.0 (B), 3.0 (C), and 1.7 (D) kPa/sec. In vivo during a sudden change from hyperoxemia (FIO2 1.0) to normoxaemia the respective rates were 0.6 (A), 0.8 (B), 1.1 (C), and 1.0(D) kPa/sec. The in vivo 50% response times were 53.3 (A), 51.1 (B), 46.2 (C) and 45.3 (d) kPa/sec. The in vivo 50% response time were 53.3 (A), 51.1 (B), 46.2 (C), and 45.3 (d) kPa/sec. The in vivo 50% resonse time were 53.3 (A), 51.1 (B), 46.2 (C), and 45.3 (D) sec. The lag time between PaO2 and tcPO2 was about one third of this overall response time. The response to more physiological variations of PaO2 (periodic breathing) was not different among the tested electrodes in terms of damping and of delay of the tcPO2 deflections. In a steady state the correlation of tcPO2 44 degree C vs PaO2 was close (r = 0.98) with all devices up to 6.1 kPa (456 torr).

In order to obtain the still lacking reference data of individual plasma steroids in the immediate postnatal period needed for the assessment of adrenocortical function in various neonatal maladaptation syndromes, aldosterone (A), corticosterone, deoxycorticosterone (DOC), progesterone (P), 17-hydroxyprogesterone (17-OHP), cortisol, and cortisone were simultaneously followed in the same human newborn in a single 250-500 microliters peripheral plasma sample obtained at constant times during the first week of life using a mechanized Sephadex LH-20 multicolumn chromatography and standardized RIAs. Mean concentrations in 12 spontaneously delivered full term newborns of either sex and in paired umbilical (UV) and peripheral maternal (MV) venous plasma are given in the table. Besides significant maternoumbilical gradients in each steroid, DOC, P, 17-OHP, and cortisone, originating predominantly from the fetoplacental unit, disappear rapidly with steadily increasing half-lives. A, corticosterone, and cortisol, however, remain elevated in comparison with later infancy, with the exception of a marked "glucocorticoid dip" in cortisol and corticosterone levels between 2 and 12 h after birth.

A patient with a cerebro-hepato-renal syndrome was investigated. The visceral manifestations were those of the Zellweger syndrome (ZS); however, the child exhibited muscular hypertonia and survived into the 2nd year of life. Ultramicroscopically, hepatocytes were lacking peroxisomes, but, contrary to findings in one patient with ZS [2], contained smooth endoplasmic reticulum. No catalase was found by histochemistry or spectroscopy. Mitochondria showed normal succinate and glutamate respiration, and normal coupling of respiration to the phosphorylation potential. The cytochrome (cyt) content was diminished to one-third with an abnormally inversed redox pattern of the respiratory chain in the controlled state, cyt b being 5%, cyt c 23% reduced. The oxygen affinity of cyt a3 was normal. These findings exclude a defect in the nonheme iron protein region of the respiratory chain as described in ZS [2], but point to a functional abnormality of cyt b in out patient.

We evaluated adrenocortical steroid concentrations at birth and during postnatal adaptation (2 h until 7 days) in 10 vaginally delivered term small-for-gestational-age (SGA) infants and 12 term appropriate-for-gestational age infants. Plasma aldosterone, 11-deoxycorticosterone, corticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, and cortisone were longitudinally measured by specific RIA after Sephadex LH-20 chromatography. Mean aldosterone was significantly higher in SGA than in appropriate-for-gestational-age infants (2 h to 7 days; p less than 0.001). In SGA infants, cortisone and cortisol levels were significantly lower in umbilical artery (p less than 0.05), and all glucocorticoid levels were significantly lower 12 h after birth (p less than 0.05). Thereafter (24 h to 7 days), only 11-deoxycortisol levels remained significantly lower in SGA; corticosterone and cortisol levels were even higher (p less than 0.05) in SGA 24 h after birth. The data suggest that SGA infants maintain high aldosterone levels throughout the 1st wk of life. Low cortisol and cortisone levels in umbilical artery as well as low glucocorticoid levels at 2 h and/or 12 h compared to term appropriate-for-gestational-age infants may reflect either a less stressful postnatal adaptation or, more likely, a reduced adrenocortical synthesis in term SGA infants.

In 107 infants aged 3 hours to 9 months, hemoglobin concentration, 2,3-DPG concentration and GOT activity in red cells, and reticulocyte count were determined in order to evaluate whether the previously observed decrease in red cell 2,3-DPG [1] during the first 30-40 days of life related to red cell ageing. A significant positive correlation of 2,3-DPG vs. GOT, an indicator of red cell age, is found. The decrease in 2,3-DPG over a period of 25-30 days is finally followed by a sharp rise in reticulocyte count, suggesting that an alteration in blood oxygen affinity might trigger the onset of erythropoiesis in normal infants in this age group.

Peripheral blood flow and systolic blood pressure (strain-gauge plethysmograph), blood volume (Evans blue) and whole blood viscosity (cone-plate viscometer) have been measured in 66 premature and full-term infants 6 to 144h of age. Blood flow and blood volume were moderately decreased in the infants with respiratory distress. Highly significant (P less than 0.001) correlations were found between blood flow and blood volume (r = 0.77), blood pressure and blood volume (r = 0.50), peripheral resistance and blood volume (r = -0.44), blood flow and blood pressure (r = 0.50), blood flow and peripheral resistance (r = -0.67), peripheral resistance and blood viscosity (r = 0.45), and blood viscosity and haematocrit (r = 0.86). There was no correlation between peripheral blood flow and blood viscosity. However, at given blood volume, peripheral blood flow decreased with increasing blood viscosity. These results indicate that in newborn infants peripheral blood flow, blood pressure and peripheral resistance are influenced by blood volume, but also depend on blood viscosity.

We studied the effect of hypotension and of electrode temperature (41 degrees C to 44 degrees C) on the relation of skin surface PCO2 (Roche prototype) to arterial PCO2 in 24 sick neonates of 690 to 3,500 gm with systolic blood pressures of 5 to 70 mm Hg. PsCO2 closely correlated with PaCO2. The standard error of estimating PaCO2 from PsCO2 was 3.02 torr at 44 degrees C, 3.20 torr at 43 degrees C, and 3.57 torr at 41 degrees C. The pH (6.89 to 7.61), body temperature (33.5 to 38.1 degrees C), hematocrit (0.28 to 0.65), scleredema, or treatment with tolazoline did not affect the relation of PsCO2 to PaCO2. PsCO2 grossly exceeded the predicted value at systolic blood pressures below 15 mm Hg, irrespective of electrode temperature.

The maternal adrenal cortex seems to be involved in the adaptation to pregnancy. To study in detail adrenocortical secretion during pregnancy, we measured plasma aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, and cortisone simultaneously by RIA after extraction and automated Sephadex LH-20 chromatography of 10 normal pregnant women longitudinally throughout pregnancy at weeks 8-10, 14-17, 21-24, 28-32, and 38 as well as at the time of admission to the delivery room. The mean plasma progesterone and 17-hydroxy-progesterone concentrations increased from 37.2 +/- 6.5 (+/- SE) and 8.2 +/- 1.0 nmol/L, respectively, in early gestation to maximum levels of 138.0 +/- 25.7 and 22.8 +/- 2.2 nmol/L at week 38 (P less than 0.01). Plasma glucocorticoid levels rose 2- to 3-fold (P less than 0.01) from weeks 8-10 (corticosterone, 18.5 +/- 5.4; 11-deoxycortisol, 1.9 +/- 0.2; cortisone, 24.2 +/- 4.2; cortisol, 195.5 +/- 37.6 nmol/L) to week 38 (corticosterone, 42.9 +/- 11.2; 11-deoxycortisol, 4.6 +/- 0.5; cortisone, 71.5 +/- 13.6; cortisol, 420 +/- 63 nmol/L). Similarly, plasma mineralocorticoid levels increased 5- to 7-fold (P less than 0.01) from weeks 8-10 (11-deoxycorticosterone, 0.69 +/- 0.12; aldosterone, 0.41 +/- 0.08 nmol/L) to maximum levels at week 38 (5.3 +/- 0.9 and 2.1 +/- 0.3 nmol/L, respectively). At the time of admission to the delivery room, plasma 11-deoxycortisol, corticosterone, and cortisol concentrations were higher (P less than 0.02) than at 38 weeks, but plasma progestin and mineralocorticoid concentrations were not. We conclude that the source of the elevated maternal corticosteroid levels in pregnancy in addition to the estrogen-mediated rise in corticosteroid-binding globulin is the maternal adrenal cortex itself. The peak glucocorticoid levels at admission to the delivery room reflect increased maternal and fetal stress with the onset of labor.

Weight, extracellular volume (ECV; distribution volume of sucrose) and renal function were studied in 13 preterm infants at birth (age 6 h (2-12); median, range) and again when postnatal weight loss exceeded 5% of birth weight (age 84 (64-97) h). Gestational age was 28 (26-32) weeks, and birthweight was 1,170 g (810-1,455). The infants were nursed in incubators and mechanically ventilated. Fluid therapy allowed a weight loss of up to 10% of birthweight. Body weight decreased significantly from 1,101 +/- 202 g at birth to 1,016 +/- 198 g at day 3 and ECV from 499 +/- 155 ml to 413 +/- 118 ml. Mean weight loss of 85 +/- 50 g was the same as mean ECV loss of 86 +/- 48 ml, suggesting that postnatal weight loss is water loss from the ECV. Weight loss was preceded by a marked increase in diuresis, exceeding fluid intake on day 2. Creatinine clearance did not change. The increased urine output led to a significant increase of sodium excretion without inducing hyponatremia but resulted in an isotonic reduction of ECV.

Report on a further hemoglobin M variant, discovered in a boy with congenital cyanosis. Chemical analysis of hemoglobin structure revealed indentity with HbM Saskatoon (= beta63 His leads to Tyr). The abnormal hemoglobin is characterized by normal oxygen transport function. The observed slight constant hemolysis is thought to be due to increased instability of the abnormal hemoglobin molecule. In addition to the hemoglobin anomaly, the activity of NADH-methemoglobin reductase was reduced by approximately 40% of normal. None of the parents presented with an abnormal hemoglobin, indicating that the occurrence of hemoglobin M Erlangen is most likely the result of a new mutation.

In preterm infants, plasma and red blood cells display several specific properties (eg, RBC size, plasma composition) that could influence blood flow behavior. Hemorheologic properties of blood from 20 preterm infants (24 to 36 weeks of gestation), ten full-term neonates, and ten adults were studied by means of a cone-plate viscometer adapted with a Couette-type chamber allowing viscometry at a wide range of shear rates (1.15 to 230/s). Blood viscosity (at given hematocrit of 60%), plasma viscosity, and RBC aggregation were very low in the smallest preterm infants, increased with gestational age, and reached the highest values in the adults. Whole blood viscosity increased directly with increasing plasma viscosity, plasma fibrinogen, and total plasma protein concentration, with the strongest correlations at the lowest shear rate of 1.15/s. The viscosity of RBCs suspended in a nonaggregating buffer solution was similar in all groups, thereby indicating that RBC deformability is similar in preterm infants, full-term neonates, and adults. Because mixing of neonatal and adult blood components occurs in most small preterm infants as a result of the transfusion of adult blood products, viscosities of cross suspensions (neonatal RBCs in adult plasma and adult RBCs in neonatal plasma) were measured. The exchange of neonatal plasma for adult plasma increased blood viscosity values in the neonates to adult values. On the other hand, the exchange of neonatal RBCs for adult RBCs did not affect blood viscosity. These results indicate that viscosity of blood with given hematocrit is lower in preterm infants than in term neonates and adults as a result of low plasma viscosity and low RBC aggregation, and that neonatal RBCs do not possess specific properties that influence blood viscosity.

For continuous PO2 monitoring as a valuable diagnostic tool in intensive care of newborn infants two methods are available, namely transcutaneous and intravascular monitoring. Both methods have advantages and limitations, but they are rather complementary than competing. The necessity of these new methods and the clinical implications are described.

Plasma levels of aldosterone, corticosterone, 11-deoxycorticosterone, progesterone, 17-hydroxyprogesterone, 11-deoxycortisol, cortisol, and cortisone were measured simultaneously by a micromethod of multisteroid analysis in eight vaginally delivered premature infants (PI) of 33-36 wk gestation with uneventful peri- and postnatal course. Mean concentrations (ng/ml) in umbilical arterial and in peripheral venous or capillary plasma sampled longitudinally at age 2 h to 7 days were compared with the same kind of data obtained from a group of 12 term infants (TI) who served as controls. Mean aldosterone was two to five times higher in PI than in TI (umbilical artery, 2 h to 7 days; p less than 0.05), whereas 11-deoxycorticosterone was lower in PI from 2 h (p less than 0.01) until 7 days (NS). Corticosterone was significantly higher in PI than TI at 6 and 24 h after birth, whereas cortisol was slightly lower (NS) in PI in umbilical artery and 2 h after birth, but higher (p less than 0.02) at 6 h, showing less variation in PI than in TI. 17-Hydroxyprogesterone levels in PI were two to three times higher (p less than 0.02) during 6 h until 7 days after birth. The data suggest that PI are able to maintain high aldosterone levels in the early neonatal period. Higher levels of the active glucocorticoids (cortisol and corticosterone) seen after delivery point to a more stressful extrauterine adaptation of PI. Furthermore, the data demonstrate that the adrenal cortex is fully functioning in premature infants (33-36 wk gestation) as well as in term infants.