Pressure-passivity of cerebral blood flow velocity in preterm infants in the first week of life

Pressure-passivity of cerebral blood flow velocity in preterm infants in the first week of life

58 The only significant difference between the three groups was a higher Raw in the ventilated infants at 6 months only (**P ...

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58 The only significant difference between the three groups was a higher Raw in the ventilated infants at 6 months only (**P
infants results in a temporary role played by prematurity.

The influence of postnatal age on the Hering-Breuer reflex in healthy infants. P.S. Rabbettea, and J. Stocksb, aRespiratory and Anaesthetic Unit, Institute of Child Health, London Neonatal Medicine, Homerton Hospital, London (U.K.)

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K.L. Costeloeb and bDept. of

One of the most important adaptations to extrauterine life that must occur after birth is the establishment of a regular pattern of breathing. The Hering-Breuer reflex (HBR) is a vagally mediated reflex known to contribute to the regulation of breathing in neonates. However, its persistence beyond the first week of life remains a point of controversy. The aim of this study was to use the airway occlusion technique to perform sequential measurements of the HBR during the first 6 to 8 weeks of life. In this study the strength of the HBR during tidal breathing was assessed from the relative increase in expiratory time (TE) following brief end inspiratory airway occlusions as compared to TE during spontaneous breathing. Studies were performed in 31 healthy, fullterm Caucasian infants during the first 2 days of life and repeated between 5 to 8 weeks of age. All measurements were performed during behaviourally assessed quiet sleep. The mean increase in TE following airway occlusion was 91.9% (SD. 31.5%, range 38-158%) at approximately 2 days, and 89.8% (S.D. 30.7%, range &175%) at approximately 6 weeks. These findings demonstrate that the activity of the HBR during tidal breathing persists beyond the neonatal period, and that there is no significant change in its strength during the first 6 weeks of life in healthy infants. This study was funded by the Foundation for the Study of Infant Deaths.

Pressure-passivity of cerebral blood flow velocity in preterm infants in the fust week of life. S. Bignall and R.P.A. Rivers, Department of Paediatrics, St. Mary’s Hospital, South WharfRoad, London W2 INY (U.K.) Pressure-passivity of cerebral blood flow velocity (CBFV), defined as the direct transmission of beat-bybeat blood pressure (BP) changes to CBFV, has been identified in preterm infants at risk from brain injury [ 11. We investigated pressure-passivity of CBFV in 10 preterm infants with normal cranial ultrasound scans during the first week of life in order to establish the effects of postnatal age on pressure-passivity. A duplex Doppler system was used to insonate the middle cerebral arteries; aortic BP and respiratory phase were recorded simultaneously for digital analysis. Beat-by-beat relationships between BP and CBFV in the middle cerebral arteries revealed that the ratio of the coefficient of variation over 20 beats (cv%) in CBFV to cv% in BP fell with postnatal age in the first week (P = 0.003). Mean percent change in CBFV per mmHg change in the same direction in BP was 4,7U/o/mmHg and this fell with postnatal age (P < 0.01) but was not related to Pace, levels. The mean regression coefficient for beat-by-beat, time averaged mean values with postnatal age (P = 0.01). Patterns of interaction between BP, which indicated that respiration could affect CBFV independently these must be distinguished before direct “pressure-passivity” of

of CBFV against BP fell significantly CBFV and respiration were identified of respiratory effects on BP, and that CBFV can be established.

Pressure-passive states of CBFV are not the sole determinants of identifiable brain injury in preterm infants, but the fall in pressure-passivity during the first postnatal week is in keeping with the observed incidence of the lesions. 1

Perlman,

J.M., McMenamin,

J.B. and Volpe, J.J. (1983): N. Engl. J. Med., 309, 20&209.

pulmonary production of tumour necrosis factor-alpha (TNF) in ventilated preterm infants. S.H. Murch, T.T. MacDonald, C.B.S. Wood and K.L. Costeloe, Academic Departments of Child Health and Paediatric Gastroenterology, Homerton and St. Bartholomew’s Hospital, London (U.K.) TNF is well known as a mediator of cachexia and tissue-damage. has recently been demonstrated Distress Syndrome (ARDS).

and it is thought

to contribute

Its local production to the pathogenesis

by alveolar macrophages of Adult Respiratory