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TRANSFUSION OF FRESH BLOOD IN THE NEWBORN
352 diet. It is possible to forecast the presence or absence of Western diseases (C.V.D., diverticulosis, cholecystitis, peptic ulcer, varicose veins, caries of the teeth, diabetes) simply by examining the diet of the people concerned. These are not " uncertain and improbable hypotheses "-
they
are
known facts.
The Surgery, Marshland Street, Terrington St. Clement, King’s Lynn, Norfolk.
above both the lower limits for assay and resting daytime levels for supine normotensive individuals,3 we suggest that interesting data may be revealed by including studies of night-time plasma and urine catecholamines in research into a wide variety of cardiovascular disorders and their responses to treatment. We thank Dr Richard Rondel, Dr R. W. D. Turner, Dr Ian Oswald, and Ciba-Geigy (U.K.) Limited.
GEORGE A. STANTON.
Department of Psychiatry, University of Edinburgh, VLASTA BĐŘEZINOVÁ. Edinburgh EH10 5HF. of Chemical Pathology Department (Research), St. Mary’s Hospital Medical School,
GROWTH HORMONE AND DIABETIC RETINOPATHY
SIR,-Iwould take issue with the interpretation of the results offered by Dr Passa and his colleagues (July 13, p. 72) who claim to have demonstrated a difference in the growth-hormone response of diabetics, without and with retinopathy, to moderate muscular exercise. The exerciseinduced increase in immunoreactive G.H. was 6-1 ng. per ml. (maximum level minus mean of two pre-exercise, basal levels) in diabetics without retinopathy and 8-6 ng. per ml. in those with retinopathy, an insignificant difference. It is in the " basal ". G.H. levels, upon which the approximately equal exercise-induced increments are imposed, that a difference appears to lie. While this basal difference may point to relatively higher levels of G.H. in diabetics with retinopathy than in those without there may be many reasons for this, not least the kidney disease and stress which accompanies severe proliferative retinopathy and visual impairment. There is also, surely, something wrong with a statistical analysis which asserts a significant G.H. rise in group lib but excludes one in group lia (see their table II and figure). Only careful prospective studies can establish that raised G.H. levels are a cause of microvascular disease in diabetics and not a consequence of it. Unit for Metabolic Medicine, H. KEEN. Guy’s Hospital, London SE1.
PLASMA-CATECHOLAMINES IN SLEEPING HYPERTENSIVES SIR,-It might be supposed that, during the state of rest that occurs in sleep, the plasma-catecholamines would be lower in hypertensives than the raised values reported to occur in them during the day.1 However, in pilot experiments we find that this is not so. Four patients with labile hypertension, aged between 43 and 56, spent a night in a comfortable bed and in a sound-attenuated room while a catheter from a forearm vein passed by an extension through the bedroom wall.2 The patients were all receiving debrisoquine. Every 20 minutes 10 ml. of blood was withdrawn and immediately centrifuged in a lithium-heparin tube. After 3 minutes the plasma was decanted and deep-frozen. Assays were carried out within a week by a method previously described.3 Ranges for catecholamines in plasma obtained during sleep for the four patients (expressed in g. per litre) were 009-1-91, 0-50-0-89, 0-49-0-95, and 0-30-0-86 for noradrenaline, and 001-018, 0-03-0-25, 0-04-0-28, and 0-01-0-21 for adrenaline. We could find no relation between the catecholamine values and the stages of rapid-eye-movement and nonrapid-eye-movement sleep. Since the values were well 1. De Quattro, V., Chan, S. Lancet, 1972, i, 806. 2. Ogunremi, O. O., Adamson, L., Brezinová, V., Hunter, W. M., MacLean, A. W., Oswald, I., Percy-Robb, I. W. Bri. med. J.
1973, ii, 202. 3. Carruthers, M., Taggart, P., Conway, N., Bates, D., Somerville, W. Lancet, 1970, ii, 62.
London W2 1PG.
MALCOLM CARRUTHERS.
TRANSFUSION OF FRESH BLOOD IN THE NEWBORN
SIR,-We have noted the comments of Dr Oberman (July 13, p. 102) concerning our policy of small fresh-blood transfusions for sick newborn infants in our special-care baby unit. However, we feel that Dr Oberman has misinterpreted our reasons for using small volumes of fresh blood instead of cross-matched prepared units of blood. These are: 1. It is very wasteful to breach a single 500 ml. unit of blood is the unit provided by the National Blood Transfusion Service in the U.K.) to supply only 5 or 10 ml. In our service infants with respiratory-distress syndrome receive a mean of four transfusions during their period of intensive care. If prepared units of blood were used this would mean wasting four pints of blood when only 30-40 ml. was required. 2. In most hospitals in the U.K. obtaining cross-matched blood, especially between 5 P.M. and 9 A.M., would often result in an unacceptable delay. For example, the hypotensive newborn infant may require a top-up transfusion within one hour of birth.
(which
We regard the speedy availability of small volumes of fresh blood as an overriding consideration. We believe our practice is acceptable since newborn infants’ serum so seldom contains high titres of alloantibodies. In keeping with experienced transfusionists4 we have always found it safe to give un-cross-matched transfusions of ABO and Rh-compatible blood provided there is no evidence of hsemolytic disease of the newborn. Dr Oberman’s objections are based on theoretical considerations. We have noted no sequela: from our practice of giving small freshblood transfusions to sick newborn infants, but if Dr Oberman has observed any complications we would be most interested to hear of them. Department of Pædiatrics, John Radcliffe Hospital, Headington, Oxford OX3 9DU.
J. D. BAUM N. R. C. ROBERTON V. Y. H. YU.
EFFECTS OF FEEDING ON BLOOD-GASES IN A NEWBORN INFANT
SIR,-We were interested to read the description by Wilkinson and Youof a fall in arterial Po2 after feeding in ill newborn infants. Wilkinson and Yu do not suggest a mechanism for this but perhaps some speculation may be permitted. In children, elastic recoil of the lungs increases as the child grows older, and it has been suggested that the increase in closing volume seen in younger children is a reflection of this.6 In very young children elastic recoil Mollinson, P. L. Blood Transfusion in Clinical Medicine; p. 445. Oxford, 1972. 5. Wilkinson, A., Yu, U. Y. H. Lancet, 1974, i, 1083. 6. Mansell, A., Bryan, C., Levison, H. 1. appl. Physiol. 1972, 33, 711. 4.
they
are
known facts.
The Surgery, Marshland Street, Terrington St. Clement, King’s Lynn, Norfolk.
above both the lower limits for assay and resting daytime levels for supine normotensive individuals,3 we suggest that interesting data may be revealed by including studies of night-time plasma and urine catecholamines in research into a wide variety of cardiovascular disorders and their responses to treatment. We thank Dr Richard Rondel, Dr R. W. D. Turner, Dr Ian Oswald, and Ciba-Geigy (U.K.) Limited.
GEORGE A. STANTON.
Department of Psychiatry, University of Edinburgh, VLASTA BĐŘEZINOVÁ. Edinburgh EH10 5HF. of Chemical Pathology Department (Research), St. Mary’s Hospital Medical School,
GROWTH HORMONE AND DIABETIC RETINOPATHY
SIR,-Iwould take issue with the interpretation of the results offered by Dr Passa and his colleagues (July 13, p. 72) who claim to have demonstrated a difference in the growth-hormone response of diabetics, without and with retinopathy, to moderate muscular exercise. The exerciseinduced increase in immunoreactive G.H. was 6-1 ng. per ml. (maximum level minus mean of two pre-exercise, basal levels) in diabetics without retinopathy and 8-6 ng. per ml. in those with retinopathy, an insignificant difference. It is in the " basal ". G.H. levels, upon which the approximately equal exercise-induced increments are imposed, that a difference appears to lie. While this basal difference may point to relatively higher levels of G.H. in diabetics with retinopathy than in those without there may be many reasons for this, not least the kidney disease and stress which accompanies severe proliferative retinopathy and visual impairment. There is also, surely, something wrong with a statistical analysis which asserts a significant G.H. rise in group lib but excludes one in group lia (see their table II and figure). Only careful prospective studies can establish that raised G.H. levels are a cause of microvascular disease in diabetics and not a consequence of it. Unit for Metabolic Medicine, H. KEEN. Guy’s Hospital, London SE1.
PLASMA-CATECHOLAMINES IN SLEEPING HYPERTENSIVES SIR,-It might be supposed that, during the state of rest that occurs in sleep, the plasma-catecholamines would be lower in hypertensives than the raised values reported to occur in them during the day.1 However, in pilot experiments we find that this is not so. Four patients with labile hypertension, aged between 43 and 56, spent a night in a comfortable bed and in a sound-attenuated room while a catheter from a forearm vein passed by an extension through the bedroom wall.2 The patients were all receiving debrisoquine. Every 20 minutes 10 ml. of blood was withdrawn and immediately centrifuged in a lithium-heparin tube. After 3 minutes the plasma was decanted and deep-frozen. Assays were carried out within a week by a method previously described.3 Ranges for catecholamines in plasma obtained during sleep for the four patients (expressed in g. per litre) were 009-1-91, 0-50-0-89, 0-49-0-95, and 0-30-0-86 for noradrenaline, and 001-018, 0-03-0-25, 0-04-0-28, and 0-01-0-21 for adrenaline. We could find no relation between the catecholamine values and the stages of rapid-eye-movement and nonrapid-eye-movement sleep. Since the values were well 1. De Quattro, V., Chan, S. Lancet, 1972, i, 806. 2. Ogunremi, O. O., Adamson, L., Brezinová, V., Hunter, W. M., MacLean, A. W., Oswald, I., Percy-Robb, I. W. Bri. med. J.
1973, ii, 202. 3. Carruthers, M., Taggart, P., Conway, N., Bates, D., Somerville, W. Lancet, 1970, ii, 62.
London W2 1PG.
MALCOLM CARRUTHERS.
TRANSFUSION OF FRESH BLOOD IN THE NEWBORN
SIR,-We have noted the comments of Dr Oberman (July 13, p. 102) concerning our policy of small fresh-blood transfusions for sick newborn infants in our special-care baby unit. However, we feel that Dr Oberman has misinterpreted our reasons for using small volumes of fresh blood instead of cross-matched prepared units of blood. These are: 1. It is very wasteful to breach a single 500 ml. unit of blood is the unit provided by the National Blood Transfusion Service in the U.K.) to supply only 5 or 10 ml. In our service infants with respiratory-distress syndrome receive a mean of four transfusions during their period of intensive care. If prepared units of blood were used this would mean wasting four pints of blood when only 30-40 ml. was required. 2. In most hospitals in the U.K. obtaining cross-matched blood, especially between 5 P.M. and 9 A.M., would often result in an unacceptable delay. For example, the hypotensive newborn infant may require a top-up transfusion within one hour of birth.
(which
We regard the speedy availability of small volumes of fresh blood as an overriding consideration. We believe our practice is acceptable since newborn infants’ serum so seldom contains high titres of alloantibodies. In keeping with experienced transfusionists4 we have always found it safe to give un-cross-matched transfusions of ABO and Rh-compatible blood provided there is no evidence of hsemolytic disease of the newborn. Dr Oberman’s objections are based on theoretical considerations. We have noted no sequela: from our practice of giving small freshblood transfusions to sick newborn infants, but if Dr Oberman has observed any complications we would be most interested to hear of them. Department of Pædiatrics, John Radcliffe Hospital, Headington, Oxford OX3 9DU.
J. D. BAUM N. R. C. ROBERTON V. Y. H. YU.
EFFECTS OF FEEDING ON BLOOD-GASES IN A NEWBORN INFANT
SIR,-We were interested to read the description by Wilkinson and Youof a fall in arterial Po2 after feeding in ill newborn infants. Wilkinson and Yu do not suggest a mechanism for this but perhaps some speculation may be permitted. In children, elastic recoil of the lungs increases as the child grows older, and it has been suggested that the increase in closing volume seen in younger children is a reflection of this.6 In very young children elastic recoil Mollinson, P. L. Blood Transfusion in Clinical Medicine; p. 445. Oxford, 1972. 5. Wilkinson, A., Yu, U. Y. H. Lancet, 1974, i, 1083. 6. Mansell, A., Bryan, C., Levison, H. 1. appl. Physiol. 1972, 33, 711. 4.