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Hemorheological factors play an important role in the pathogenesis of different cardiovascular diseases. In the present study the fundus picture and hemorheological parameters (plasma and whole blood viscosity *WBV* by capillary viscosimetry; fibrinogen level; red blood cell aggregation by Myrenne and LORCA aggregometers) of 33 hypertensive patients (23 females, 10 males; mean age: 55 years) and 30 diabetic patients (14 females, 16 males; mean age: 57 years) and healthy controls were examined. The fundus pictures showed different forms of retinopathy in both groups. All the measured hemorheological parameters of the examined patients were in the pathological range and were significantly higher than in healthy controls. In the group of hypertensive patients hematocrit (p < 0.05), plasma fibrinogen (p < 0.01), plasma viscosity (p < 0.01) and whole blood viscosity (p < 0.01) showed a significant increase. The hemorrheological factors showed a parallel deterioration with the severity of hypertension (measured BP values) and of fundus picture, namely their values were significantly (p < 0.01) higher in patients with stage III fundus picture (WBV at 90 1/s: 6.02 mPas), than stage I hypertension (WBV at 90 1/s: 4.51 mPas). In the diabetic group hematocrit (p < 0.01), plasma fibrinogen (p < 0.001), plasma viscosity (p < 0.01), "WBV" (p < 0.001), red blood cell aggregation (p < 0.05) showed a significant increase comparing to healthy controls. These results show that there is a correlation between hemorrheological parameters and fundus picture in hypertensive and diabetic patients, and this suggests that hemorrheological factors may play a role in the development of hypertensive and diabetic retinopathy.

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Hemorheological factors play an important role in the pathogenesis of different cardiovascular diseases. Diabetes mellitus resulting in micro- and macroangiopathies is one of the major risk factors for cardiovascular diseases. In our present study the hemorheological parameters (hematocrit, plasma fibrinogen level, plasma and whole blood viscosity, red blood cell aggregation) of 30 diabetic patients (mean age: 57 +/- 12 years) and 30 healthy volunteers (mean age: 31 +/- 10 years) were examined. The fundus appearance of patients showed diabetic retinopathy; non-proliferative stage in 22 cases, preproliferative or proliferative stage in 8 cases. The measured hemorheological parameters of the examined patients were in the pathological range and were significantly higher than those of healthy volunteers (hematocrit: p < 0.01; plasma fibrinogen: p < 0.001; plasma viscosity: p < 0.01; whole blood viscosity: p < 0.001; red blood cell aggregation: p < 0.01). In our study there was not significant difference in the hemorheologic variables of patients with different stages of retinopathy. Our results propose the importance of hemorheologic factors in the development of diabetic microangiopathy.

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Red blood cell (RBC) aggregation is an important component of whole blood viscosity, especially at low shear rates, and is the major cause of the non-Newtonian flow properties of normal blood. In different laboratories several methods are used to determine RBC aggregation, therefore the standardization of aggregation measurements is especially important for getting comparable results. Aggregation indices of 62 human blood samples were determined by two different methods; LORCA (Laser-assisted Optical Rotational Cell Analyzer) and Myrenne aggregometers and related to plasma fibrinogen concentration. Our results show closer correlation values between RBC aggregation and fibrinogen concentration, when RBC aggregation was measured by LORCA (p<0.001), although correlation could be revealed with Myrenne, when plasma fibrinogen level was less than 4.5 g/l. Correlation coefficient between aggregation indices measured by LORCA and Myrenne aggregometers was also closer below this fibrinogen level. In vitro examination of RBC aggregation in fibrinogen solutions showed that higher fibrinogen concentration results in higher RBC aggregation only up to a certain level similarly to that found in human whole blood samples. Our results show that plasma fibrinogen level has an important, concentration dependent effect on RBC aggregation in human blood, but above a certain level it may not cause further aggregate formation.

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Plasma zinc, copper, and selenium concentrations were determined in 129 full-term infants at birth and at the age of four months by electrothermal or hydride generation atomic absorption spectrometry. Of these, 49 infants were exclusively breast-fed (HM), 45 received various commercially available cow's milk formulae (F) and 35 infants were fed partially hydrolysed whey protein formula (PHF). The results were correlated with hematological, biochemical and somatic data. Plasma zinc values decreased from birth to the age of four months in all three groups (p < 0.001). The plasma Zn level of the babies fed PHF were similar to those of breast-fed infants, whereas in F-fed children the zinc values were significantly lower (PHF, 807 +/- 106; HM, 794 +/- 112; F, 725 +/- 111 micrograms l-1; all the measurements were performed at the age of four months). In infants fed PHF formula there was a negative correlation between plasma zinc and weight or height increments. In agreement with the literature, plasma copper and ceruloplasmin increased significantly within the first four months of life. The plasma copper content was similar in either feeding group. Plasma selenium was low at birth (40 +/- 9 micrograms l-1) and remained constant in breast-fed infants. In infants on PHF there was a steeper decline of plasma Se (20 +/- 6 micrograms l-1) than in infants fed cow's milk formula (29 +/- 9 micrograms l-1). Other parameters of the Se status showed a similar pattern. Despite the different zinc, copper, and selenium supply, plus presumedly different bioavailability, all the infants thrived.(ABSTRACT TRUNCATED AT 250 WORDS)

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Selenium and the selenium-dependent glutathione peroxidase (GSH-Px) were measured in healthy and diabetic children from Germany and Hungary. Hyperglycemia and hyperlipidemia are present in diabetes mellitus and they are associated with increased lipid peroxidation. The selenium content of erythrocytes, whole blood and plasma, as well as of plasma glutathione peroxidase activity, were found to be low in the healthy Hungarian children compared to the healthy Germans. Both groups of diabetics had significantly higher blood selenium (1.05 +/- 0.14 versus 0.86 +/- 0.1 mumol/L in Hungarians, 1.34 +/- 0.21 versus 1.12 +/- 0.22 mumol/L in Germans) and higher plasma selenium (0.89 +/- 0.15 versus 0.68 +/- 0.01 mumol/L in Hungarians and 1.01 +/- 0.2 versus 0.88 +/- 0.19 mumol/L in Germans) than the healthy children of the same countries. In all diabetic children the plasma glutathione peroxidase activity and triglycerides were higher and the plasma HDL-cholesterols (HDLC = high density lipoprotein-cholesterol) lower than those in healthy controls. The patients showed linear correlations between blood glucose and plasma glutathione peroxidase activity, as well as in erythrocyte glutathione peroxidase activity with triglycerides (TG) and an inverse correlation with HDL-cholesterol. Plasma selenium correlated only in healthy children with triglycerides, cholesterol and HDL-cholesterol. Irrespective of the geographical region diabetics had a higher selenium status than healthy children. In addition, we found correlations between selenium and lipoproteins in the reference group. The mode of glycation, oxidative procedures and the selenium binding to lipoproteins could explain the different associations in the healthy and diabetic children.

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A case of haemolytic uraemic syndrome in a three year old boy is described. The clinical course was complicated by hyperglycaemia, and biochemical assay of plasma showed an almost total lack of pancreatic insulin. Extensive necrosis of the exocrine and endocrine pancreas was found at necropsy. The possible pathological physiology of this complication and its prognostic importance are discussed.

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Pancreatic rudiments from 14-day fetal rats were cultured whole for 8 days in medium containing 5.5 or 16.5 mmol glucose/l (1G or 3G medium). Rudiments grown in 3G medium (3G cells) contained more DNA and insulin than those grown in 1G medium (1G cells) but there was no alteration in the insulin/DNA ratio or the fractional area of the rudiment occupied by insulin-containing cells. Morphometric analysis of ultrastructure revealed that the beta cells grown in 3G medium were smaller and had smaller nuclei than those grown in 1G medium. The size of exocrine cell nuclei in 1G or 3G medium was similar. Insulin granules occupied a greater proportion of the cytoplasmic volume in rudiments grown in 3G medium although the mean absolute volume of insulin granules per cell grown in 1G and 3G media was similar. Hence the residual cytoplasmic volume (cell--nucleus and granules) of 3G cells was less than that of 1G cells. Insulin granules from 3G cells had smaller granule sacs and cores than those from 1G cells. It is concluded that glucose stimulates the growth of rat fetal pancreas in vitro and has important effects on beta cell ultrastructure.

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Plasma adrenocorticotrophin (ACTH) and glucocorticoid concentrations were measured during and for 3 hours after exchange transfusion in four groups of infants. Transfusion with ACD blood via the umbilical artery were performed on 10 infants of 35--40 weeks gestation and 11 infants of 27 to 33 weeks gestation. Ten transfusions via the umbilical vein were performed with ACD blood and 9 with heparin blood on infants of 32 to 41 weeks gestation. In all four types of transfusion there was a significant washing out of ACTH and glucocorticoids from the baby. An associated rise of plasma ACTH and glucocorticoid levels indicated increased secretion in the larger infants transfused with ACD blood via the umbilical artery. Equivocal results were obtained in the other groups. After all types of transfusion plasma glucocorticoid levels remained relatively constant for one hour and then doubled and then doubled in the second and third hour. The results suggest that (a) exchange transfusion via the umbilical artery is more stressful than that via the umbilical vein, (b) the glucocorticoid response of premature infants to exchange transfusion is similar to that of mature ifants, (c) an unspecified stimulus, which is not solely hypoglycaemia nor the metabolic reaction to a citrate load, results in a rise in plasma glucocorticoid levels 2-3 hours after all types of transfusion.

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Nineteen exchange transfusions were performed via the umbilical artery using blood preserved with acid-citrate and dextrose in 8 infants of 34-40 weeks gestation (larger infants) and 9 very small infants of 26-33 weeks gestational age. The plasma glucose rise which was similar in both groups stimulated insulin secretion from the larger infants but not the very small infants. No significant differences occurred between the groups in the fall in mean free fatty acid levels or increase in growth hormone secretion. Following transfusion there was a sharp rise in mean plasma insulin concentration in the larger infants and a smaller rise in the very small infants. A highly significant positive correlation was found between the maximum posttransfusion plasma insulin and the birth weight of the infants. Plasma glucose levels of less than 30 mg/100 ml occurred in 2 larger and 5 very small infants during the first 3 hours after transfusion. One infant of birth weight 0.98 kg received four transfusions; in 2 where he received ACD blood via the umbilical artery or vein, insulin secretion was not stimulated but in the other 2 in which glucagon or arginine was added to the ACD donor blood, insulin secretion was stimulated. Feeding practice should take account of the fact that although very small infants secret less insulin than larger infants during exchange transfusion they are more likely to become hypoglycaemic in the immediate posttransfusion period.

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Insulin release was studied in vitro using pieces of pancreas from rabbits of between 24 days gestational age and 6 weeks postnatal age. When allowance was made for the fraction of pancreas which was endocrine, 16-5mM-glucose caused increasing stimulation of insulin release as development advanced and 3-3 mM-glucose caused a similar rate of secretion at all ages. Secretion was not significantly influenced by insulin destruction in the incubation medium. Glucagon (5 mug/ml) did not stimulate insulin secretion from 24-day foetal pancreas but did so postnatally. Theophylline (1 mmol/1) stimulated insulin release at all ages and was equipotent on 24-day foetal pancreas in 3-3 or 16-5 mM-glucose. The stimulation of insulin release from 24-day foetal pancreas by 1 mM-theophylline occurred in the absence of extracellular glucose, pyruvate, fumarate and glutamate and in the presence of mannoheptulose and 2-deoxyglucose (each 3 mg/ml). Adrenaline (1 mumol/1) and diazoxide (250 mug/ml) abolished or attenuated the stimulation of insulin release by glucose, leucine plus arginine or theophylline from 24-day foetal, 1 day and 6 weeks postnatal pancreas. The stimulation of insulin release from 6-week-old pancreas by 1mM-barium was blocked by adrenaline and diazoxide but the effect became less with increasing immaturity. The experimental results illustrate some of the ways in which insulin secretion by the rabbit beta cell changes as a function of development and draw attention to the importance of glucose and cyclic adenosine monophosphate in this process.

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Twenty exchange transfusions for hyperbilirubinaemia were performed via the umbilical vein or artery in 17 term and pre-term infants. Blood preserved with acid citrate and dextrose was used and the effect of the route of transfusion on plasma glucose, free fatty acid, insulin and growth hormone (GH) concentrations was measured during the transfusion and for 3 h afterwards. Infants transfused via the umbilical vein secreted more insulin than those transfused via the artery although both groups had similar rises in plasma glucose. After transfusion, glucose disappearance was faster and minimum plasma glucose levels were lower in infants transfused via the vein. This group had a smaller fall in plasma free fatty acids during transfusion, but otherwise plasma free fatty acid levels were similar in both groups. More GH was secreted by infants transfused via the artery resulting in higher plasma levels during and after transfusion.

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