660 It is of interest to speculate on the aetiology of apnoeic attacks in otherwise normal preterm infants. There are
probably two main mechanisms for the control of breathing at this time, the respiratory centre in the brainstem and a peripheral reflex system mediated by the pulmonary stretch receptors.10 If in the immature infant the central mechanism is not yet fully active, the peripheral mechanism may temporarily assume greater importance. C.P.A.P. probably acts through this peripheral system driving breathing, making it regular, and abolishing apnoeic attacks. It is unlikely that the effect of C.P.A.P. is due to a rise in Pao2 for in neither of the 2 cases in which continuous Pao2 recordings were obtained was hypoxia present, except during apnoeic attacks. Furthermore there was no difference between the Pao2 during C.P.A.P. and that recorded in between the apnoeic attacks before therapy. Requests for reprints should be addressed
to
Daily, W. 510.
Hb
PRODUCTION DURING NORMAL HUMAN DEVELOPMENT
After embryonic Hb production has ceased at about the 6th week of gestation HbF is the major hsemogtobin of intrauterine life. HbA is produced from as early as 8 weeks’ gestation and constitutes about 10% of the total Hb up to about 34 wk. At this time there is an increase in the rate of synthesis of p chains relative to y chains and at birth there are approximately equal numbers of 3 and Y chains
B.D.S.
REFERENCES 1.
mia. HbF synthesis persists into adult life in some gene tic anaemias, and its production is apparently reactivated in normal pregnancy and in several hxmatological disorders. We suggest that the production of HbF in manB of these conditions is confined to a unique cell line which has retained the ability to synthesise I chains, and that the persistence or apparent reactivation of HbF is due to differential selection of these cells.
J., Klaus, M., Meyer, H. B. P. Pediatrics, Springfield, 1969, 43,
2. Illingworth, R. S. Archs Dis. Childh. 1957, 32, 328. 3. Francis-Williams, J., Davis, P. A. Dev. Med. Child Neurol. 1974, 16, 709. 4. Fitzhardinge, P. M., Ramsay, M. ibid. 1973, 15, 447. 5. Tizard, J. P. M. Pediatrics, Springfield, 1964, 34, 771. 6. Lucey, J. F. ibid. 1975, 55, 584. 7. Dunn, P. M. Proc. R. Soc. Med. 1974, 67, 245. 8. Speidel, B. D., Dunn, P. M. Lancet, 1975, i, 302. 9. Cross, K. W., Klaus, M., Tooley, W. H., Weisser, K. J. Physiol. 1960, 151, 551. 10. Olinsky, A., Bryan, M. H., Bryan, A. C. J. appl. Physiol. 1974, 36, 426.
Hypothesis
being produced.1 After birth y-chain synthesis rapidly declines and in normal adults HbF constitutes only about 0-5-1% of the total haemoglobin. HbF is a mixture of two molecular species, OC2 Yz (136Gty) and
probably two main mechanisms for the control of breathing at this time, the respiratory centre in the brainstem and a peripheral reflex system mediated by the pulmonary stretch receptors.10 If in the immature infant the central mechanism is not yet fully active, the peripheral mechanism may temporarily assume greater importance. C.P.A.P. probably acts through this peripheral system driving breathing, making it regular, and abolishing apnoeic attacks. It is unlikely that the effect of C.P.A.P. is due to a rise in Pao2 for in neither of the 2 cases in which continuous Pao2 recordings were obtained was hypoxia present, except during apnoeic attacks. Furthermore there was no difference between the Pao2 during C.P.A.P. and that recorded in between the apnoeic attacks before therapy. Requests for reprints should be addressed
to
Daily, W. 510.
Hb
PRODUCTION DURING NORMAL HUMAN DEVELOPMENT
After embryonic Hb production has ceased at about the 6th week of gestation HbF is the major hsemogtobin of intrauterine life. HbA is produced from as early as 8 weeks’ gestation and constitutes about 10% of the total Hb up to about 34 wk. At this time there is an increase in the rate of synthesis of p chains relative to y chains and at birth there are approximately equal numbers of 3 and Y chains
B.D.S.
REFERENCES 1.
mia. HbF synthesis persists into adult life in some gene tic anaemias, and its production is apparently reactivated in normal pregnancy and in several hxmatological disorders. We suggest that the production of HbF in manB of these conditions is confined to a unique cell line which has retained the ability to synthesise I chains, and that the persistence or apparent reactivation of HbF is due to differential selection of these cells.
J., Klaus, M., Meyer, H. B. P. Pediatrics, Springfield, 1969, 43,
2. Illingworth, R. S. Archs Dis. Childh. 1957, 32, 328. 3. Francis-Williams, J., Davis, P. A. Dev. Med. Child Neurol. 1974, 16, 709. 4. Fitzhardinge, P. M., Ramsay, M. ibid. 1973, 15, 447. 5. Tizard, J. P. M. Pediatrics, Springfield, 1964, 34, 771. 6. Lucey, J. F. ibid. 1975, 55, 584. 7. Dunn, P. M. Proc. R. Soc. Med. 1974, 67, 245. 8. Speidel, B. D., Dunn, P. M. Lancet, 1975, i, 302. 9. Cross, K. W., Klaus, M., Tooley, W. H., Weisser, K. J. Physiol. 1960, 151, 551. 10. Olinsky, A., Bryan, M. H., Bryan, A. C. J. appl. Physiol. 1974, 36, 426.
Hypothesis
being produced.1 After birth y-chain synthesis rapidly declines and in normal adults HbF constitutes only about 0-5-1% of the total haemoglobin. HbF is a mixture of two molecular species, OC2 Yz (136Gty) and
