GROWTH HORMONE AND SOMATOMEDIN A IN GIRLS WITH ADOLESCENT IDIOPATHIC SCOLIOSIS

Abstract. Girls with adolescent idiopathic scoliosis are taller than nonscoliotic girls of the same age. This observation may be related to factors regulating longitudinal growth. Plasma growth hormone was determined in a group of scoliotic girls by double antibody radioimmunoassay under the following conditions: 1) Insulin induced hypoglycemia, 2) glucose tolerance test, 3) exercise. Somatomedin A was determined by a method based on the ability of serum to stimulate the incorporation of radioactive sulphate in embryonic chick cartilage. The results were compared with those obtained in a control group of healthy nonscoliotic girls of comparable age. After overnight fasting and after at least one hour's rest the basal growth hormone level was 9.8 ± 11.1 (±S.D.) ng/ml in the scoliotic girls ( n =48) and 2.2 ± 1.1 ng/ml in the controls ( n =15). This difference is significant. In the hypoglycemia test the peak growth hormone level tended to be higher in the scoliotic girls but the difference is not significant. In the exercise test the maximal value was reached at different times in the two groups: at 20 min after start of the exercise in the scoliotic girls ( n =14, 17.3±11.8 ng/ml) and at 40 min in the controls (n=9, 16.0±6.6 ng/ml). In the glucose tolerance test the growth hormone level was suppressed in both groups but the mean values tended to be higher during the first 120 min in the scoliotic girls. The serum somatomedin levels were higher in the group of scoliotic girls ( n =19, 1.13±0.17 U/ml) than in the controls ( n =14, 0.88±0.16 U/ml) and the difference is significant. The results obtained are difficult to interpret but suggest that growth hormone secretion is higher in girls with adolescent idiopathic scoliosis than in healthy girls of comparable age.     

Effects of sympathetic stimulation on cerebral and ocular blood flow Modification by hypertension,hypercapnia, acetazolamide,PGI2 and papaverine

The effect of unilateral, electrical stimulatio of the cervical sympathetic chain in rabbits anesthetized with pentobarbital sodium and vasodilated by hypercapnia, acetazolamide, papaverine or PGI₂ was investigated to determine to what extent the sympathetic nerves to the brain and the eye cause vasoconstriction and prevent overperfusion in previously vasodilated animals. Evans blue was given as a tracer for protein leakage. Blood flow determinations were made with the labelled microsphere method during normotension and acute arterial hypertension. Hypertension was induced by ligation of the thoracic aorta and in some animals metaraminol or angiotensin was also used. Acetazolamide caused a two to threefold increase in cerebral blood flow (CBF) and hypercapnia resulted in a fivefold increase. CBF was not markedly affected by papaverine or PGI₂. In the choroid plexus, the ciliary body and choroid, papaverine and hypercapnia caused significant blood flow increases on the control side. Sympathetic stimulation induced a 12 % blood flow reduction in the brain in normotensive, hypercapnic animals. Marked effects of sympathetic stimulation at normotension were obtained under all conditions in the eye. In the hypertensive state the CBF reduction during sympathetic stimulation was moderate, but highly significant in hypercapnic or papaverine-treated animals as well as in controls. Leakage of Evans blue was more frequently seen on the nonstimulated side of the brain. In the eye there was leakage only on the control side except in PGI₂-treated animals where 2 rabbits had bilateral leakage. The effect of sympathetic stimulation on the blood flow in the cerebrum and cerebellum in vasodilated animals seems to be small or absent if the blood pressure is normal. In the eye pronounced vasoconstriction occurs under these conditions. In acute arterial hypertension sympathetic stimulation protects both the cerebral and ocular barriers even under conditions of marked vasodilation.     

Effect of a new inhibitor of lipid peroxidation on kidney function after ischaemia-reperfusion. A study on rat and rabbit kidneys

Lipid peroxidation of mitochondrial and cell membrane structures is the final step in the oxygen radical-induced damage observed at reperfusion of kidneys after ischaemia. We compared the ability of an indeno-indol compound (code name H290/51) with that of α-tocopherol to inhibit lipid peroxidation in reoxygenated isolated rat renal tissue in vitro measured as production of TBARS (thiobarbituric acid reactive substances). H290/51 was 100 times more efficient than α-tocopherol. Treatment of rats in vivo with H290/51 in a dosage giving a plasma concentration of 500 nmol L^-1 inhibited TBARS production measured in vitro by 80%. Treatment of rabbits with H290/51 almost completely inhibited radical production at reperfusion after 60 min of ischaemia measured with spin trap technique using OXANOH (2-ethyl-3-hydroxy-2,4,4-trimethyloxazolidine) as a spin trap. Furthermore, such pretreatment significantly improved kidney function and survival of rabbits subjected to 60 min of ischaemia to the left kidney and contralateral nephrectomy. These studies stress the importance of inhibiting lipid peroxidation to prevent the ischaemia-reperfusion damage and furthermore suggest a role for treatment with antioxidants like H290/51 in clinical practice, e.g. at reconstructive renal surgery and transplantation.     

Acute and long-term effects of 17b-oestradiol on agonist-stimulated force in rat tail artery

The effects of 17β-oestradiol on the force responses to KCl and noradrenaline were investigated in rings of the rat tail artery. Incubation with 10 μm 17β-oestradiol for 100–295 min reduced the force amplitude after 5 min in high-K⁺ (140 mm ) to 10% of the control value. The inhibitory effect of the steroid was unaffected by the NO-synthase inhibitor l -NAME. Rings activated by an intermediate degree of depolarization (60 mm K⁺) were less affected by the steroid (58% of control force). The sustained force response to 1 μm noradrenaline was reduced in the presence of 17β-oestradiol to 60% of control value. Lower concentrations of 17β-oestradiol (0.1 and 1 μm ) were without acute effects on force development. However, long-term effects of 17β-oestradiol on vessel reactivity were found at these low concentrations. Rings were cultured for 3–7 days in the absence or in the presence of the steroid before they were stimulated with agonists. Cultured rings developed an increased sensitivity to noradrenaline compared with freshly prepared ones. Cocaine (30 μm) shifted the noradrenaline concentration–response curve to the left in freshly prepared rings while it had no effect in cultured ones, indicating that the increased sensitivity to noradrenaline in cultured rings depends on loss of noradrenaline uptake. Rings cultured for 7 days in the presence of 0.1 μm 17β-oestradiol developed a more pronounced supersensitivity to noradrenaline (EC₅₀ for noradrenaline was 0.13±0.03 μm in steroid exposed rings vs. 0.38±0.09 μm in control rings). Thus, prolonged treatment with 17β-oestradiol results in a potentiation of noradrenaline evoked force, in contrast to the acute effect of the steroid.     

Effects of aminoguanidine and L-NAME on histamine-induced blood pressure drop in the rat

Mean arterial blood pressure changes in response to i.v. administration of histamine were monitored in the anaesthetized rat in the absence or presence of the diamine oxidase (DAO) inhibitor aminoguanidine (AMG, 10 mg kg^?1). AMG prolonged the duration of the transient drop in blood pressure induced by a bolus injection of histamine (0.05 mg kg^?1) by 34%. In animals pretreated with AMG, no potentiation of the decrease in pressure in response to a 10 min infusion of histamine was observed. However, when infusion was stopped, the time needed for pressure recovery was twice as long in animals treated with AMG as in controls. Blood samples were taken prior to infusion and during the recovery phase and the quantities of histamine were determined by liquid chromatography. The prolonged recovery phase observed in animals pretreated with AMG was associated with five times higher levels of histamine. The duration of histamine-induced hypotension (0.01 mg kg^?1) was 50% shorter in the presence of the nitric oxide synthase inhibitor L -NAME (10 mg kg^?1). We suggest that DAO, through elimination of histamine from the bloodstream, is important for the recovery from histamine-induced hypotension, and that the duration of histamine-induced pressure drop is influenced by formation of nitric oxide.     

Growth in Infancy and Childhood in Girls with Turner's Syndrome

ABSTRACT. We describe spontaneous longitudinal growth in girls with Turner's syndrome (TS), using the infancy-childhood-puberty (ICP) growth model. Lenght/height during the first 12 years of life was studied in 58 Swedish girls with TS. Their mean length at birth was 47.8 cm (SDS –1.4) and mean height at 12.0 years of age 127.3 cm (SDS –3.0). A clear age-dependent subnormality was observed in the change in length-height SDS (ΔSDS). Mean ΔSDS values at ages 0.0 to 0.5 and 3.0 to 6.0 years were normal. In contrast, the mean ΔSDS at ages 0.5 to 3.0 and 6.0 to 12.0 years were subnormal. The onset of the childhood growth component (normally located between 0.5 and 1.0 year of age) was, on the average, delayed by 0.28 year. This accounts for the subnormality of ΔSDS at 0.5 to 3.0 years of age. About 50% of the variation in height at 12.0 years of age, as determined by a multiple linear regression analysis, was significantly explained by length at 0.5 year of age, age at the onset of the childhood component, and ΔSDS at 6.0 to 12.0 years of age.     

A Follow-up Study of Children with Neonatal Herpes Simplex Virus Infections with Particular Regard to Late Nervous Disturbances

Forty-five children with neonatal herpes simplex virus (HSV) infection, representing all known cases in the diagnostic records of four virological laboratories within a 15-year period, were followed up. Twelve children had died. Sixteen of the 33 survivors were healthy. Thirteen children had severe disabilities: all of them showed severe mental retardation; moreover, 11 were tetraplegic, one was hemiplegic with hydrocephalus and one had a pronounced behavioural abnormality. Four children had slight to moderate disabilities: one child was mildly mentally retarded and three, although mentally normal, had hemiplegia and delayed speech development, one of them having a learning disorder as well. Of these 17 neurologically impaired children 16 had ophthalmological abnormalities. EEG recordings were made in 29 patients in the neonatal period. They were markedly abnormal in 24 patients, 14 of whom had localized periodic complexes. An abnormal EEG was a bad prognostic sign. The neurological outcome was better in the HSV-l-infected children (10 cases) than in the HSV-2-infected ones (35 cases). Progressive or recurrent encephalitis was strongly suspected in two preterm children.