ABSTRACT:The aim of the study was to evaluate the impact of clinical severity and placental weight upon fetal lactacidemia in intrauterine growth restricted (IUGR) pregnancies. Seventy pregnancies complicated by IUGR were compared with 70 normal (appropriate for gestational age, AGA) pregnancies at the time of elective cesarean section. IUGR pregnancies were divided according to clinical severity in three groups: Group 1 had normal fetal heart rate (FHR) and normal pulsatility index of the umbilical artery (PI); Group 2 had normal FHR and abnormal PI; and Group 3 had abnormal FHR and PI. No cases with severe lactacidemia had placental weights Ն250 g. Forty-four fetuses had placental weight Ͻ250 g: Twenty-four had severe lactacidemia and all were Group 2 and 3, whereas 20 had normal umbilical artery lac (lactate) (and small placentas) regardless of the clinical severity. Gestational age, fetal and placental weights, F/P ratios, uv (umbilical vein) and ua lac and ua oxygen content and pH were significantly decreased in fetuses with small placentas and high lactate. There was a significant relationship between fetal and placental weight in AGA and IUGR. However, IUGR fetuses with placental weight Ն250 g exhibited an F/P ratio significantly lower than that in AGA fetuses suggesting that IUGR may be due to a reduction of placental function per gram of tissue. (Pediatr Res 59: 570-574, 2006) L actate represents the end product of anaerobic metabolism of glucose. However, many experimental as well as studies in human pregnancies both in vivo (1-3) and in vitro (4,5) have shown that lactate is produced within the placenta and delivered into both the maternal and umbilical circulation where it serves as source of carbon for fetal growth. This has been clearly demonstrated by studies in pregnant sheep where fetal utilization of lactate at term is three times higher than the umbilical uptake (approximately 4 mg/kg/min) in the welloxygenated fetus (6). The fetal liver is the organ with the highest lactate consumption and liver lactate uptake almost equals umbilical uptake: lactate is then used for oxidation and synthesis of fatty acid and glycogen (7). In human pregnancies, fetal lactate concentration is higher than maternal (2,3). Many clinical studies at the time of delivery (i.e. under non-steady stressed conditions) have shown that umbilical venous and arterial lactate concentrations as well as the umbilical venoarterial concentration difference correlate with Apgar scores both at 1= and 5= (8,9). In clinical studies performed at the time of spontaneous delivery, lactate concentrations have been shown to represent a much more reliable marker of fetal acidosis compared with pH measurements (10,11). However, difficulties in sample management have limited its widespread clinical application. Recently the characteristics of L-lactic acid transport across the human placental syncytiotrophoblast have been described (12,13) as has been done for human erythrocytes (14), hepatocytes (15), intestinal brush border membrane (16,17)...