Intrauterine growth restriction improves cerebral O2 utilization during hypercapnic hypoxia in newborn piglets.
Data are scant regarding the capacity of cerebrovascular regulation during asphyxia for prevention of brain oxygen deficit in intrauterine growth-restricted (IUGR) newborns. We tested the hypothesis that IUGR improves the ability of neonates to withstand critical periods of severe asphyxia by optimizing brain oxygen supply. Studies were conducted to examine the effects of IUGR on cerebral blood flow (CBF) regulation and oxygen consumption (cerebral metabolic rate for oxygen, CMRO(2)) at different stages of asphyxia (hypercapnic hypoxaemia) in comparison to pure hypoxia (normocapnic hypoxaemia). We used 1-day-old anaesthetized and ventilated piglets. Animals were divided into normal weight (NW) piglets (n = 47; aged 11-26 h, body weight 1481 +/- 121 g) and IUGR piglets (n = 48; aged 13-28 h, body weight 806 +/- 42 g) according to their birth weight. Different stages of hypoxaemia were induced for 1 h by appropriate lowering of the inspired fraction of oxygen (moderate hypoxia: = 31-34 mmHg; severe hypoxia: = 20-22 mmHg). Fourteen NW and 16 IUGR piglets received additionally 9% CO(2) in the breathing gas, so that a of 74-80 mmHg resulted (hypoxia/hypercapnia groups). Eight NW and nine IUGR animals served as untreated controls. Furthermore, affinity of haemoglobin for oxygen was measured under hypoxic and asphyxic conditions. During asphyxia cerebral oxygen extraction was markedly increased in IUGR animals (P < 0.05). This resulted in a significantly diminished CMRO(2)-related increase of CBF at gradually reduced arterial oxygen content (P < 0.05). Therefore, an enhanced effectivity in oxygen availability appeared in newborn IUGR piglets under graded asphyxia by improved cerebral oxygen utilization (P < 0.05). This was not supported by related O(2) affinity of haemoglobin. Thus, IUGR newborns are more capable to ensure brain O(2) demand during asphyxia (hypercapnic hypoxia) than NW neonates.
Bauer
Reinhard
R
Institute of Molecular Cell Biology, Center for Molecular Biomedicine, and Department of Neuropaediatrics, Children's Hospital, Friedrich Schiller University, D-07740 Jena, Germany. reinhard.bauer@mti.uni-jena.de
Walter
Bernd
B
Brandl
Ulrich
U
D000222:Adaptation, Physiological; D000818:Animals; D000831:Animals, Newborn; D001724:Birth Weight; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D004195:Disease Models, Animal; D005317:Fetal Growth Retardation / Q000378:metabolism* / Q000503:physiopathology; D006454:Hemoglobins / Q000378:metabolism; D006935:Hypercapnia / Q000378:metabolism* / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism* / Q000503:physiopathology; D010100:Oxygen / Q000097:blood / Q000378:metabolism*; D010101:Oxygen Consumption; D013552:Swine
D006454:Hemoglobins; D010100:Oxygen
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