Serum myoglobin and myocardial infarction (author's transl)

The serum myoglobin level was determined in 45 healthy persons and 64 patients of whom 43 had a recent proven myocardial infarct. The normal myoglobin value was found to ae 43.7 +/- 16.0 ng/ml. All the patients with myocardial infarct who had been transferred to our Coronary Care Unit showed raised serum myoglobin levels already 4 hours after symptoms commenced, the maximum being reached after 10 hours. 20 hours after myocardial infarction normal values were once again registered. Pathological serum myoglobin levels were also found without infarction after skeletal muscle damage in the course of resuscitation measures, or after operations or in renal failure. The value of the serum myoglobin concentration in the diagnosis of myocardial infarction lies in the early elevation of this parameter, but it is unspecific and the method is relatively laborious.     

Dynamics of changes in the levels of myoglobin and anti-myoglobin autoantibodies in the blood serum of patients with myocardial infarction

The mean level of myoglobin and autoantibodies to myoglobin in the blood of healthy donors was 77.57 +/- 8.17 ng/ml and 18.01 +/- 1.85 micrograms/ml respectively. The level of myoglobin in the blood of patients with primary transmural myocardial infarction was rapidly increased, reaching its maximum in 9-12 h and returning to normal in 9 days. The mean level of autoantibodies was decreased in the first 66 h and got back to normal by the 6th day of disease. In primary large focal nontransmural myocardial infarction the concentration of myoglobin in the blood of patients was also increased, reaching its maximum in 3-9 h and returning to normal by the end of the 2nd day after onset of an angina attack. A decrease in the level of autoantibodies to myoglobin was observed up to the 18th day of disease. The peculiarity of repeated large focal nontransmural myocardial infarction was a two-peak curve of changes in a MG level with maximum levels in 9-12 and 21-24 h after onset of a pain attack. Final normalization of the level of myoglobin in the blood of patients of this group occurred in 69 h. The concentration of autoantibodies to myoglobin was more than once decreased up to the 6th day of disease. The results obtained showed that groups of examinees differed in the time course of changes in the level of myoglobin and autoantibodies to myoglobin. Such differences can be used for diagnostic purposes.     

Development of a rapid microparticle-enhanced nephelometric immunoassay for serum myoglobin in acute myocardial infarction.

A microparticle-enhanced nephelometric immunoassay was developed for myoglobin quantitation in human serum. It uses rabbit antimyoglobin serum and hydrophilic polyacrylic microparticles covalently coated with baboon myoglobin in a competitive immunoagglutination system. The level of microparticle agglutination is assessed with a specially designed nephelometer. This sensitive (45 ng/ml of myoglobin detected in serum) and accurate (coefficients of variation from 3.0% to 8.2% in precision study and linear recovery of myoglobin in overloaded sera) immunoassay was evaluated with human sera from patients suffering from acute myocardial infarction. Myoglobin levels in patient's serum on admission appeared to be correlated with clinical and biological parameters assessed in emergency wards and later. This new, rapid, and easy microparticle-enhanced nephelometric immunoassay could thus be useful in emergency conditions for the early quantitation of serum myoglobin.     

Risk stratification of chest pain patients in the emergency department by a nurse utilizing a point of care protocol.

OBJECTIVE: Risk stratification of patients with ischaemic type chest pain assessed in the emergency department utilizing a point of care (POC) protocol. METHODS: Patient demographics, cardiac biomarkers, management and follow-up at 6 months were reviewed for patients seen over 20 months. RESULTS: Out of 546 patients, 351 (64%) were admitted. The diagnoses after admission were confirmed as acute myocardial infarction in 59 patients and unstable angina, (cTroponin T<0.09 ng/ml) in 92 patients. The c-statistic of the receiver operating curves for myocardial infarction (myocardial infarction, cTroponinT at 12 h >0.09 ng/ml) as determined by the POC assay was cTroponin I=0.884, CK-MB=0.883, myoglobin=0.845 and beta-type natriuretic peptide (BNP)=0.755. The c-statistic for the same sample assessed by the hospital laboratory was cTroponin T=0.893: for CK-MB within 12 h of admission it was 0.918; the 12 h cTroponin T was 0.982 and within 24 h of admission NT pro-BNP was 0.789. POC BNP in patients admitted was 68 ng/l (median) vs. 24 ng/l (median) for those not admitted, (P<0.001). POC BNP for patients admitted with unstable angina (12 h cTroponin T <0.09 ng/ml) was 47 ng/l (median, P<0.001). At 6 months, 14 patients had died; five during admission, two within 30 days and seven up to 6 months. During admission two died from heart failure, two with respiratory tract infection and one from carcinoma. Of those not admitted one had died from asbestosis. CONCLUSION: Risk stratification by a specialist nurse utilizing a POC protocol is an appropriate means of assessing patients with chest pain.     

Myoglobin stratifies short-term risk in acute major pulmonary embolism

BACKGROUND: Concentrations of cardiac troponins can be elevated in acute pulmonary embolism (APE) indicating myocardial injury. Although concentration of myoglobin (MYO) increases after myocardial damage, even before detectable rise of cardiac troponin levels occurs, MYO was not evaluated in APE. Therefore, we assessed prevalence and prognostic significance of myoglobin in major APE. METHODS: We studied 46 patients (30 women, aged 61.9+/-17.8 years) with major APE defined with right ventricular dilatation. On admission serum myoglobin, and cardiac troponin T (cTnT) were measured. Serum MYO concentrations >58 ng/ml for women, and >72 ng/ml for men were considered abnormal. CTnT>0.01 ng/ml was regarded to indicate myocardial injury. RESULTS: MYO levels exceeding sex specific norms were found in 21/46 (45.7%) of patients, while detectable cTnT was found in 24/46 (52.1%) of patients. Seven patients died during hospitalization. Elevated MYO significantly predicted in-hospital mortality (OR 25, 95% CI 1.3-474.2), while increased cTnT concentration did not affect the survival. Among clinical and echocardiographic variables only older age indicated worse prognosis (OR 1.6, 95% CI 1.06-2.41). CONCLUSIONS: Myoglobin levels are elevated in serum on admission in almost half of patients with major APE. Elevated myoglobin level, marker of myocardial injury, is a powerful predictor of increased risk of fatal outcome in major pulmonary embolism.     

Measurement of serum myoglobin by a turbidimetric latex agglutination method.

We evaluated an immunoturbidimetric quantitation for serum myoglobin by the latex agglutination method using an automated biochemical analyzer. This method is rapid, specific, accurate, precise, and has wide dynamic range. The total assay time is 10 min and is performed at 37 degrees C with continuous monitoring at 570 nm. The assay results were compared with radioisotopic immunoassay results and showed a good correlation coefficient, r = 0.99; Y = 0.98 x + 9.3; N = 79. Sera from healthy adults has a myoglobin concentration in the range of 15-80 ng/ml(N = 362). Sex- and age-related differences were observed. The serum myoglobin levels in males and elderly people showed higher concentration than in females and younger people. The peak elevation of serum myoglobin compared with other cardiac markers was observed within 6 hours after onset of chest pain as well as the CK-isoform ratio (MM3/MM1). All of the serum from 21 patients with definite acute myocardial infarction showed increased serum myoglobin levels (100-1200 ng/ml) upon admission and within 6 hours. The results suggest that assays for serum myoglobin levels are helpful in the early diagnosis of acute myocardial necrosis.     

The serum selenium concentration of patients with acute myocardial infarction

Serum selenium concentration was determined in 49 patients with acute myocardial infarction within 4 hours after the beginning of the symptoms. The mean serum selenium concentration of the patients was significantly lower than that of healthy controls (55 +/- 15 micrograms/l vs. 78 +/- 11 micrograms/l). Among the 49 patients with acute myocardial infarction 20 (41%) had serum selenium concentration below the 95% percentile of the healthy control group. It is concluded that the low serum selenium concentration was present in these patients before the acute event and was not a consequence of the myocardial infarction. No relationship was found in this study between the serum selenium concentration and the severity of myocardial infarction if the number of coronary vessels occluded is taken as the criterion of severity. Serum selenium concentration was similar in patients with 1 or more coronary vessels occluded. Patients with anterior or posterior myocardial infarction had similar serum selenium concentrations. A positive correlation was observed between serum selenium concentration and total serum creatine kinase (CK) activity and serum myoglobin (MB). The serum selenium concentration correlated negatively with the ratio CK-MB/total CK activity, which can be interpreted as minor injury of mitochondria during infarction in patients with normal serum selenium concentration.     

Clinical significance of measurement of plasma annexin V concentration of patients in the emergency room

Annexin V, a calcium-binding protein, is widely present in various organs and tissues. In the present study, plasma annexin V concentration was measured in 158 patients who were brought to the emergency room, including 25 patients suffering from acute myocardial infarction (AMI), 14 with cerebrovascular disease, 11 with trauma of the extremities, 11 with severe trauma associated with visceral damage, and 35 with witnessed cardiac arrest. Annexin V concentration in normal healthy individuals (n=110) was 1.9+/-0.7 ng/ml. Annexin V concentration in AMI and cardiac arrest patients was 11.0+/-4.9 and 15.3+/-7.9 ng/ml, respectively, being significantly higher than that in patients with cerebrovascular disease (5.4+/-2.7 ng/ml). The value in severe trauma patients was 15.9+/-9.4 ng/ml, being significantly higher than that in patients with trauma of the extremities (5.6+/-1.2 ng/ml). Annexin V concentrations in the cardiac arrest and AMI patients who survived more than 24 h after admission were lower than those in patients who died within 24 h after the onset of symptoms. Annexin V content in the lungs and myocardium in normal rats was extremely high in comparison to that in brain and skeletal muscle. These results suggest that the high levels of plasma annexin V in patients with AMI, cardiac arrest and severe trauma reflect the severity of damage of the myocardium and/or other visceral organs, and measurement of plasma annexin V concentration may help to assess the prognosis of patients brought to the emergency room.     

Rapid and sensitive radioimmunoassays for human myoglobin

A radioimmunoassay for quantitation of serum myoglobin in healthy individuals and patients with different diseases is described. Purified myoglobin was labelled by an 125I-labelled ester (N-succinimidyl 3-(-4 hydroxy, 5-[125I]iodophenyl) propionate), a commercially available antiserum was used, and the antigen-antibody complex was precipitated with polyethylene glycol 6000. The rapid assay can be performed within 1 h at 37 degrees C with a detection limit of 45 micrograms/l. Prolonged incubation at 4 degrees C for 18 or 72 h gives a detection limit of 6 and 2 micrograms/l, respectively. The mean coefficient of variation of the routine assay was 11%. In healthy human subjects a significant difference in mean serum myoglobin concentration was found between 43 women (34 +/- 17 micrograms/l) and 51 mean 47 +/- 15 micrograms/l). In twenty patients admitted to hospital with the clinical diagnosis acute myocardial infarction, the serum myoglobin concentration profiles were in close agreement with the final diagnosis. In three patients with myocardial infarction serum samples were taken every 2 h after the acute episode, and serum myoglobin levels were compared with the levels of creatine kinase, lactate dehydrogenase, aspartate aminotransferase and creatine kinase isoenzyme-MB.     

Semi-quantitative estimation of serum myoglobin by a rapid latex agglutination method: an emergency screening test for acute myocardial infarction

The present study reports the evaluation of a new latex agglutination test for serum myoglobin (SMb). The time of agglutination of the latex particles coated with antibodies to myoglobin was measured in 172 serum specimens with known concentration of myoglobin quantitated by a radioimmunoassay (RIA), collected from myocardial infarction (MI) patients, subjects suffering from various diseases, and normal controls. Myoglobin levels in the samples were found to decrease exponentially with time of agglutination. Agglutination occurring within 1 min (result coded as + + + +) corresponded to 761 +/- 366 micrograms/l of myoglobin; between 1 and 2 min (+ + +), to 285 +/- 101 micrograms/l; between 2 and 3 min (+ +), to 85 +/- 47 micrograms/l; between 3 and 4 min (+), to 51 +/- 38 micrograms/l; and after more than 4 min (-), to 31 +/- 16 micrograms/l. Blood samples were serially drawn from 24 MI patients with short hospitalization delays; the rapid agglutination which was obtained in the specimens taken upon admission (20 results coded as + + + + and four as + + +) actually corresponded to markedly increased SMb levels. In contrast, serum creatine kinase (CK) activities were still less than 150 U/l in four patients (16.6%); CK-MB was less than 5 U/l in five cases (20.8%). Positive agglutinations for SMb were also obtained 4 and 8 h following admission in all subjects, confirming that the latex test is an early and very sensitive indicator for MI.(ABSTRACT TRUNCATED AT 250 WORDS)     

Diagnosis and risk stratification of patients with anginal pain and non-diagnostic electrocardiograms

Patients with acute chest pain suggestive of myocardial ischaemia, and normal or non-diagnostic electrocardiograms, form a difficult subgroup for diagnosis and early risk stratification. We prospectively evaluated the role of troponin T (cTnT), troponin I (cTnI), CKMB mass and myoglobin, in the diagnosis and risk stratification of 214 patients with acute chest pain of < or = 24 h and non-diagnostic or normal ECGs admitted directly to the Cardiac Unit of the Royal Victoria Hospital Belfast from the Mobile Coronary Care Unit or the Accident/Emergency Department. This was a single-centre prospective study, and follow-up (3 months) was complete for all patients. Blood was assessed for quantitative cTnT, cTnI, CKMB mass and myoglobin, and qualitative cTnT on admission and at 12 h. Diagnosis of index event and incidence of new cardiac events (death, non-fatal myocardial infarction, revascularization, or readmission for unstable angina) over 3 months were assessed. Based on standard criteria, myocardial infarction occurred in 37/214 (17%), and unstable angina in 72/214 (34%). At 12 h from admission, cardiac troponins had higher sensitivity for the diagnosis of acute coronary syndromes (myocardial infarction and unstable angina) than conventional markers (cTnI 48%, cTnT 38%, CKMB mass 30% or myoglobin 27%). At 3 months, a new cardiac event had occurred in 42/214 (20%). Significantly higher event rates occurred when any of the biochemical markers was elevated, but the statistical significance was highest for patients with elevated cTnI (p < 0.0001). Whilst gender, history of ischaemic heart disease (IHD), stress test response, cTnT, cTnI, CKMB mass and myoglobin were univariate predictors, cTnI at 12 h and stress test response were the only two independent significant predictors for a subsequent cardiac event at 3 months. Raised cTnI at 12 h after admission had the highest sensitivity for the diagnosis of acute coronary syndromes, and was independently associated with a 2-3 times increased risk of future cardiac events within 3 months among patients with acute chest pain suggestive of myocardial ischaemia but with normal or non-diagnostic ECGs.     

The significance of measuring plasma leptin in acute myocardial infarction

We measured leptin concentrations in patients with acute myocardial infarction (AMI, n = 21) and in 15 age-matched controls, and compared leptin concentrations with levels of other myocardial enzymes and indicators of AMI. Blood was sampled immediately after hospital admission and at 1 h, 2 h, 3 h, 6 h and 9 h, then every 12 h until 5 days post-admission. Patients were stratified into three groups according to peak leptin concentrations: hypoleptinaemia (< 3 ng/ml); normoleptinaemia (> or = 3 - < 15 ng/ml) and hyperleptinaemia (> or = 15 ng/ml). Hypoleptinaemic AMI patients had significantly increased concentrations of plasma lactate dehydrogenase compared with normoleptinaemic patients. No significant differences in other serum markers were noted between hyperleptinaemic and normoleptinaemic AMI patients. A significant negative correlation was found between the peak concentrations of leptin and interleukin 6. Leptin may play a role in the regulation of the development of cardiac damage in patients with AMI.     

Prognostic implications of myocardial necrosis triad markers' concentration measured at admission in patients with suspected acute coronary syndrome

The aim of the study was to analyze the prognostic implications of 3 myocardial necrosis markers measured at admission in short-term observation of patients with suspected acute coronary syndrome. The study group consisted of 336 consecutive patients whose concentration of cardiac troponin I, creatine kinase-MB fraction, and myoglobin were measured at admission. All patients referred due to chest pain and suspected acute coronary syndrome and were followed up for 30 days. The patients who died had statistically higher concentration of cardiac troponin I (8.7 +/- 17.2 vs 0.9 +/- 3.2 ng/mL; P = .0006), myoglobin (215.2 +/- 181.5 vs 109.7 +/- 151.5 ng/mL; P = .003), and creatine kinase-MB (21.9 +/- 30.7 vs 8.8 +/- 25.9 ng/mL; P = .005), compared to patients who stayed alive. There was statistically significant increase in 30-day all-cause mortality with increasing numbers of positive markers-0.6% for patients with nonpositive marker, 3.4% for patients with 1 positive marker, and 11.5% for patients with at least 2 positive markers (P = .001 for trend).     

Radioimmunoassay for Measurement of Thyroglobulin in Human Serum

A specific and reproducible double antibody radioimmunoassay for the measurement of thyroglobulin (HTg) in human serum has been developed. Since antithyroglobulin autoantibodies combine with the [(131)I] HTg tracer, antibody-positive sera were rejected for measurement. Specificity is demonstrated in that thyroid analogous such as thyroxine (T(4)), triiodothyronine (T(2)) monoiodotyrosine (MIT) and diiodotyrosine (DIT) did not crossreact. Sera previously reacted with anti-HTg-Sepharose contained no immunoassayable HTg. Finally, sera obtained from patients after total thyroid ablation for thyroid carcinoma did not contain demonstrable HTg. The sensitivity of the assay is 1.6 ng/ml, and HTg was detectable in 74% of 95 normal subjects. The mean concentration was 5.1 ng/ml +/-0.49 SEM (range <1.6-20.7 ng/ml). Day to day variation in HTg levels is large in some euthyroid subjects and nearly absent in others. HTg was detectable in 90% of the sera obtained in 23 pregnant women at delivery in whom a mean concentration of 10.1 ng/ml +/-1.3 SEM was observed. The mean level for the corresponding newborn infants at birth was 29.3 ng/ml +/-4.7 SEM a value significantly higher than the mean maternal HTg concentration (P <0.01). A group of 17 thyrotoxic individuals all had elevated HTg levels; the mean for this group was 344.8 ng/ml +/-90.7 SEM. In the acute phase of subacute thyroiditis HTg was also elevated in all of 12 patients, and the mean for this group was 136.8 ng/ml +/-74.6 SEM.     

S-100ao protein in serum during acute myocardial infarction

Concentrations in serum of S100ao protein (alpha alpha form of S-100 protein, which is present at high concentrations in heart muscle) were successively measured by enzyme immunoassay in 21 patients with acute myocardial infarction (AMI) and six with angina pectoris (ANP). Results were compared with measurements of creatine kinase isoenzyme MB (CK-MB) concentrations in the same specimens. Mean S100ao concentrations in sera from 100 healthy adults were 0.12 (SD 0.08) microgram/L. In patients with AMI, S100ao concentrations were 4.74 +/- 5.27 micrograms/L at admission, peaked 8 h after admission (23.5 +/- 27.7 micrograms/L), then decreased gradually. Among nine AMI patients who were admitted within an hour after their attack, eight showed abnormally high concentrations of S100ao in serum (greater than 0.5 microgram/L), whereas only four showed abnormally high CK-MB concentrations (greater than 5 micrograms/L) in sera at the time of admission. Serum S100ao concentrations remained within the normal range in all six patients with ANP; however, serum CK-MB concentrations were increased in two of them. Therefore, serum S100ao is useful not only for detection of AMI but also for differentiating AMI from ANP.     

Determination of triiodothyronine concentration in human serum

A simplified method has been described for the measurement of triiodothyronine (T3) in human serum. The sensitivity was sufficient for determinations on hypothyroid as well as normal and thyrotoxic sera. The values obtained have been in reasonable agreement with a double isotope derivative assay.The normal T3 concentration in human serum approximates 0.2 mug/100 ml; the mean +/-SD of 31 normal sera was 220 +/-27 ng/100 ml. Elevations were observed in sera from 40 patients with thyrotoxicosis (752 +/-282 ng/100 ml), and diminutions were found in sera from 10 hypothyroid patients (98+/-48 ng/100 ml).In rare instances thyrotoxicosis may be due to elevated serum T3 with normal thyroxine (T4) concentration. The incidence of this condition remains to be determined.In approximately half the cases with low serum T4 after (131)I therapy, the eumetabolic state may be maintained by normal or elevated T3 concentration.From these data and kinetic studies indicating a rapid turnover it may be inferred that T3 rather than T4 may be the more important hormone in health and in disease.     

Serum levels of endostatin, vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF) in patients with acute myocardial infarction undergoing early reperfusion therapy

Angiogenesis is controlled by anti-angiogenic factors as well as by angiogenic factors, such as VEGF (vascular endothelial growth factor) and HGF (hepatocyte growth factor). Endostatin, a potent endogenous angiogenesis inhibitor, is known to inhibit endothelial proliferation and suppress tumour growth. However, to date, little is known about the pathophysiology of endostatin in ischaemia/reperfusion. To investigate the mechanisms of angiogenesis induced by myocardial ischaemia/reperfusion in more detail, we studied the circulating levels of endostatin, VEGF and HGF in 17 patients with acute myocardial infarction, who underwent early reperfusion therapy. In all patients, serum endostatin, VEGF and HGF levels before reperfusion were increased significantly compared with those in 17 control subjects (endostatin, 49.2+/-11.7 ng/ml, but not detectable in controls; VEGF, 685.6+/-150.3 pg/ml compared with 173.7+/-33.6 pg/ml; HGF, 3638+/-1285 pg/ml compared with 59+/-13 pg/ml; values are means+/-S.E.M.). After reperfusion, the serum endostatin and VEGF levels decreased significantly, but still remained higher than those in control subjects (endostatin, 19.6+/-7.0 ng/ml; VEGF, 284.2+/-90.2 pg/ml). In contrast, serum HGF levels increased significantly (15 146+/-2230 pg/ml) after reperfusion. These data indicated that serum levels of endostatin changed in parallel with those of VEGF in response to myocardial ischaemia/reperfusion, and the marked increase in serum HGF levels after reperfusion seemed to be, at least in part, due to heparin administration. Our data offer a possible anti-endostatin therapy in patients with acute myocardial infarction to facilitate collateral vessel formation.     

心脏型脂肪酸结合蛋白在急性心肌梗死早期诊断中的临床应用价值

目的 探讨心脏型脂肪酸结合蛋白（H-FABP）在急性心肌梗死（acute myocardial infarction,AMI）早期诊断中的意义.方法 收集AMI 患者32例,另选择健康体检人员50例作为对照.AMI 患者入院后0～2 h、2～4 h、4～6 h检测血清H-FABP、cTnI、CK-MB,体检人员仅采血检测血清H-FABP.结果 入院后0～2 h、2～4 h、4～6 h,患者血清H-FABP的检测灵敏性、特异性均高于cTnI和CK-MB,差异有统计学意义（P＜0.05）.50例体检人员血清H-FABP平均浓度为（4.81±1.37）ng/mL;入院后0～2 h、2～4 h、4～6 h,患者血清H-FABP的平均浓度分别为（52.78±2.40）ng/mL、（85.49±1.88）ng/mL及（91.21±1.46）ng/mL.结论 将H-FABP检测用于AMI的早期诊断具有较高的临床应用价值.     

Measurement of human ventricular myosin light chain-1 by monoclonal solid-phase enzyme immunoassay in patients with acute myocardial infarction

A monoclonal solid-phase enzyme immunoassay has been developed for the detection of human serum ventricular myosin light chain-1. Cross-reactivity of this with human skeletal muscle myosin was observed, but the enzyme immunoassay with the sera of patients with acute myocardial infarction gave similar results with radioimmunoassay. The human ventricular myosin light chain-1 levels in the healthy subjects were 0.2-6.6 ng/ml in males and 0.2-4.1 ng/ml in females. Within-run and between-run precision (CVs) of the assays was on the order of 2.3-4.7% and 4.3-8.7, respectively. Sensitivity of the assay was 1.0 ng/ml, and working range was 5-100 ng/ml. In all patients with define acute myocardial infarction, serum ventricular myosin light chain-1 levels increased three- to ten-fold the upper reference range within 6 hr after the onset of chest pains. Two types of subtrend were discovered: its levels remain elevated for 3-4 days and its levels increased and then decreased 1-2 days after the initial rise but became elevated again for the next 4-7 days after the onset of chest pain, which is in contrast to the case with all conventionally used biochemical cardiac markers.     

Serum Triiodothyronine and Thyroxine in the Neonate and the Acute Increases in These Hormones Following Delivery

Low triiodothyronine (T(3)) and high normal thyroxine (T(4)) concentrations are present in cord sera from full term infants. To examine this phenomenon further, radioimmunoassay of T(3) and T(4) was carried out in paired maternal and cord sera as well as capillary sera from neonates at different intervals after delivery. Free T(3) and free T(4) concentrations were also estiamted in cord and maternal sera by equilibrium dialysis. In 12 paired specimens, the T(3) concentration in cord sera was significantly lower than the maternal level (51+/-4 vs. 161+/-11 ng/100 ml, mean +/-SE). Mean free T(3) concentration was also lower in the cord samples (0.15+/-0.02 vs. 0.31+/-0.04 ng/100 ml). whereas total and free T(4) concentrations were not significantly different. Umbilical vein and artery samples from 11 neonates did not differ significantly in their T(3) and T(4) concentrations. In seven infants the mean T(3) concentration increased from 51+/-3 ng/100 ml at delivery to 79+/-13 at 15 min and 191+/-16 at 90 min. In four other infants the mean T(3) concentration at 24 and 48 h was not significantly different from the 90 min value of the previous group. Less pronounced changes were observed for T(4) which increased from 12.3+/-2.0 mug/100 ml (mean +/-SE) at delivery to 14.1+/-1.9 at 90 min and appeared to have reached a plateau at approximately twice the cord value by 24-48 h after delivery.The maternal-fetal gradient observed for free T(3) is further evidence of the autonomy of the fetal thyroidpituitary axis. The time course of the abrupt increase in serum T(3) in the neonate suggests that it results from the earlier acute increase in serum TSH which occurs shortly after birth. This suggests that the neonatal thyroid contains significant quantities of T(3). Therefore, unavailability of thyroidal T(3) does not appear to explain the low total and free T(3) concentrations present in the sera of newborns.