Increase In Blood Glucose Concentration Research Articles

Microalbuminuria, insulin sensitivity and haemostatic factors in non-diabetic treated hypertensive men. Risk Factor Intervention Study Group.

To examine whether microalbuminuria in non-diabetic, treated hypertensive men is associated with insulin resistance and measures of endothelial function, thrombogenesis and fibrinolysis. Cross-sectional study. Outpatient clinic in city hospital. Ninety-two treated hypertensive men, aged 57-77 years, either with a serum cholesterol of > or = 6.5 mmol L-1 or smokers, or both. Patients with diabetes mellitus or overnight urinary albumin excretion of > 100 mg 12 h-1 were excluded. Overnight urinary albumin excretion, insulin-mediated glucose disposal (hyperinsulinaemic euglycaemic clamp), blood glucose and plasma insulin during oral glucose tolerance test, fibrinogen, von Willebrand factor and plasminogen activator inhibitor activity. Microalbuminuric patients had increased blood glucose concentrations during the oral glucose tolerance test and higher plasma fibrinogen levels compared with the normoalbuminuric patients. In a randomly selected subgroup (n = 36), insulin-mediated glucose disposal was lower in microalbuminuric than in normoalbuminuric patients, and an inverse relationship between insulin sensitivity and albuminuria (r = -0.37; P = 0.028) was found. This relationship was not significant after adjustment for body-mass index (P = 0.098). In the univariate analyses including all patients, albuminuria was associated with blood glucose, serum creatinine, body-mass index, systolic blood pressure, fibrinogen, von Willebrand factor and cholesterol (negatively). In a multiple regression analysis, only the body-mass index was independently related to urinary albumin excretion. Microalbuminuria was associated with insulin resistance but obesity was a confounding factor. Relationships between microalbuminuria and fibrinogen as well as von Willebrand factor were found, but only in univariate analysis.

Calorie sources and recovery from central nervous system ischemia

Glucose is the primary substrate for the energy requirements of the nervous system. Nevertheless, administration of glucose to critically ill patients with central nervous system trauma may have adverse effects on their neurologic recovery. The purpose of this study was to evaluate the effects of other sources of nonprotein calories on spinal cord lactate accumulation and on electrophysiologic recovery after a period of severe spinal cord ischemia. Two randomized, blinded studies were performed: one of glycolytic energy substrates (fructose, xylitol, sorbitol, glycerol) and one of ketogenic energy substrates (beta-hydroxybutyrate, acetate, butyrate). College teaching hospital laboratory. New Zealand albino rabbits (weight 3.5 to 4.5 kg). After infusion of the randomly assigned treatment, temporary ischemia was produced in the lumbosacral spinal cord by occluding the abdominal aorta with a balloon catheter. Blood concentrations of glucose, lactate, pyruvate, and ketone bodies and spinal cord dialysate concentration of lactate were measured before and after infusion of the assigned treatment, and during ischemia and during the first 2 hrs after reperfusion. Spinal somatosensory evoked potentials were recorded during ischemia to assure a similar severity of ischemia in all animals and during the first 2 hrs after reperfusion as a measure of electrophysiologic recovery. Infusion of the glycolytic nutrients xylitol and fructose increased blood glucose and lactate concentrations, and resulted in increased lactate accumulation in the spinal cord during ischemia and resulted in a significantly poorer recovery of the spinal somatosensory evoked potential than infusion of saline. Infusion of sorbitol and glycerol did not have these adverse effects in the doses administered. None of the ketogenic nutrients increased blood glucose concentration or increased lactate accumulation in the spinal cord during ischemia when compared with infusion of saline. Infusion of butyrate and acetate caused arterial hypotension and resulted in a poorer recovery of the spinal somatosensory evoked potential than saline. Infusion of beta-hydroxybutyrate did not have an adverse effect on blood pressure or on evoked potential recovery. Glycerol, sorbitol, and beta-hydroxybutyrate deserve further evaluation as potential nonprotein calorie sources in patients with neurologic injury. Xylitol and fructose are not suitable since these substrates resulted in hyperglycemia and increased lactate accumulation in the central nervous system, and had detrimental effects on electrophysiologic recovery after ischemia. The short-chain fatty acids (acetate and butyrate) also had adverse effects on electrophysiologic recovery after ischemia, probably because of their hypotensive effects when given intravenously, rather than from the effects of their metabolism.

Calorie sources and recovery from central nervous system ischemia

Objectives: Glucose is the primary substrate for the energy requirements of the nervous system. Nevertheless, administration of glucose to critically ill patients with central nervous system trauma may have adverse effects on their neurologic recovery. The purpose of this study was to evaluate the effects of other sources of nonprotein calories on spinal cord lactate accumulation and on electrophysiologic recovery after a period of severe spinal cord ischemia. Design: Two randomized, blinded studies were performed: one of glycolytic energy substrates (fructose, xylitol, sorbitol, glycerol) and one of ketogenic energy substrates (β-hydroxy-butyrate, acetate, butyrate). Setting: College teaching hospital laboratory. Subjects: New Zealand albino rabbits (weight 3.5 to 4.5 kg). Interventions: After infusion of the randomly assigned treatment, temporary ischemia was produced in the lumbosacral spinal cord by occluding the abdominal aorta with a balloon catheter. Measurements and Main Results: Blood concentrations of glucose, lactate, pyruvate, and ketone bodies and spinal cord dialysate concentration of lactate were measured before and after infusion of the assigned treatment, and during ischemia and during the first 2 hrs after reperfusion. Spinal somatosensory evoked potentials were recorded during ischemia to assure a similar severity of ischemia in all animals and during the first 2 hrs after reperfusion as a measure of electrophysiologic recovery. Infusion of the glycolytic nutrients xylitol and fructose increased blood glucose and lactate concentrations, and resulted in increased lactate accumulation in the spinal cord during ischemia and resulted in a significantly poorer recovery of the spinal somatosensory evoked potential than infusion of saline. Infusion of sorbitol and glycerol did not have these adverse effects in the doses administered. None of the ketogenic nutrients increased blood glucose concentration or increased lactate accumulation in the spinal cord during ischemia when compared with infusion of saline. Infusion of butyrate and acetate caused arterial hypotension and resulted in a poorer recovery of the spinal somatosensory evoked potential than saline. Infusion of β-hydroxybu-tyrate did not have an adverse effect on blood pressure or on evoked potential recovery. Conclusions: Glycerol, sorbitol, and β-hydroxybutyrate deserve further evaluation as potential nonprotein calorie sources in patients with neurologic injury. Xylitol and fructose are not suitable since these substrates resulted in hyperglycemia and increased lactate accumulation in the central nervous system, and had detrimental effects on electrophysiologic recovery after ischemia. The short-chain fatty acids (acetate and butyrate) also had adverse effects on electrophysiologic recovery after ischemia, probably because of their hypotensive effects when given intravenously, rather than from the effects of their metabolism. (Crit Care Med 1994; 22:1841–1850)

Administration of Propionate to Day-Old Turkeys

The effects of salts of propionic acid on newly hatched turkeys were examined. In Experiment 1, poults were injected with .25 mL of 1 M solutions of either sodium propionate or calcium propionate. After a 24-h holding period, the poults were killed and assayed for blood glucose, liver weight, and liver glycogen. Sodium propionate increased blood glucose concentration but did not alter liver weight or liver glycogen compared with controls. Calcium propionate had no effect on blood glucose but increased liver weight and liver glycogen compared with controls. There was no mortality in saline-injected controls or sodium propionate poults; 4 of 10 poults injected with calcium propionate died. In Experiment 2, poults were administered 0 or 4% sodium propionate in the feed or 0 or 2% sodium propionate in the drinking water in a 2 × 2 factorial arrangement. Propionate depressed feed intake and body weight by both routes of administration. Propionate in the feed, but not drinking water, depressed liver weight and liver glycogen. Plasma uric acid was increased by propionate in either the feed or the water but was not above control amounts when propionate was given in both the feed and water at the same time. Plasma propionic acid was increased by propionate in the water but not by propionate in the feed. We conclude that the use of propionate in injectibles, drinking water, or feed of newly hatched turkeys is contraindicated.

Four different fluid regimes during and after minor paediatric surgery—a study of blood glucose concentrations

SummaryIn order to evaluate the efficiency of glucose homeostatic mechanisms in otherwise healthy infants and children during and after anaesthesia and surgery four different fluid regimes were studied in 40 patients, 6–24 months old. The four regimes all resulted in a total fluid volume of 10 ml·kg−1·h−1 intraoperatively and 3 ml·kg−1 h−1 postoperatively. One group received a combination of glucose 300 mg·kg−1h−1 and Ringer acetate intraoperatively and glucose postoperatively, a second group was given the same intraoperative fluid followed by glucose free Ringer acetate postoperatively. A third group received Ringer acetate both intra‐ and postoperatively and a fourth group was given Ringer acetate intraoperatively and glucose postoperatively. Blood glucose concentrations were measured after induction (Preop.), immediately after surgery (Postop.) and after 30, 60 and 120 min. Increased blood glucose concentrations were found in all children immediately after surgery. The concentrations were highest among children given glucose. Postoperatively blood glucose remained elevated in children receiving glucose after surgery. In patients without postoperative glucose supply blood glucose concentrations declined. Hypoglycaemia was not seen on any occasion. The differences in blood glucose concentrations with different regimes were significant but small. We conclude that the studied group of healthy children appeared to be capable of regulating blood glucose levels within normal limits with or without intraoperative glucose and also if the intraoperative glucose supply was interrupted postoperatively.

Pancreatic Islet Blood Flow in the Rat After Administration of Islet Amyloid Polypeptide or Calcitonin Gene-Related Peptide

Anesthetized male Sprague-Dawley rats (350-400 g) were injected intravenously with either 0.1, 1, 15, or 25 nmol rat islet amyloid polypeptide (IAPP), 65 or 650 pmol rat calcitonin gene-related peptide (CGRP), or saline alone. IAPP at the two highest doses decreased the mean arterial blood pressure (BP), increased blood glucose concentrations, and decreased serum insulin concentrations. CGRP at both doses decreased the BP but did not affect the blood glucose concentrations. The blood flow to the whole pancreas, pancreatic islets, adrenal glands, colon, duodenum, liver, and kidney was measured with a microsphere technique 30 min after administration of IAPP and 3 min after injection of CGRP. The two higher doses of IAPP (15 and 25 nmol) markedly reduced the whole pancreatic blood flow, whereas the islet blood flow remained unaffected. This resulted in an increase in the fraction of whole pancreatic blood flow diverted through the islets from approximately 10 to 17%. No blood flow changes in the pancreas or the islets were observed when 0.1 or 1 nmol IAPP was injected. CGRP at both doses caused a decrease in both whole pancreatic and islet blood flow. No changes in fractional islet blood flow were observed, despite similar effects on mean arterial BP as observed after IAPP injections. Neither adrenal, duodenal, colonic, hepatic, skeletal muscle, nor renal blood flow were significantly affected by any of the concentrations of IAPP used, whereas 650 pmol CGRP decreased both duodenal and colonic blood flow. We conclude that IAPP and CGRP have different effects on pancreatic islet blood flow and that IAPP may be of importance for islet blood flow regulation.

Development of a glucose sensor for glucose monitoring in man: The disposable implant concept

This paper describes the issues related to glucose sensing in the framework of the concept of disposable implants. The possibility of providing a diabetic patient with a continuous access to his blood glucose concentration and of detecting nocturnal hypoglycaemia would be a major breakthrough in diabetes therapy. To this end, our laboratories have developed a miniaturized, subcutaneous glucose sensor for glucose monitoring. It is based on the enzymatic, amperometric detection of glucose. This glucose sensor has been extensively evaluated in rats, dogs and more recently in human volunteers. Under experimental conditions, a controlled increase in blood glucose concentration is followed by an increase in the current delivered by the sensor. It is then possible to transform this current into an estimation of the glucose concentration. Experiments in rats have shown that the glucose sensor functions for up to 10 days when implanted in the subcutaneous tissue. Experiments in conscious dogs have shown that it works in a subcutaneous tissue closer to the human one. More recently, the glucose sensor was investigated in non-diabetic volunteers. These studies have demonstrated that this subcutaneous glucose sensor is able to provide a reliable estimation of blood glucose concentration in man, making it suitable for blood glucose monitoring. Biocompatibility of the glucose sensor, and particularly long-term tolerance, remains to be demonstrated.

Metabolic control in insulin-dependent diabetes mellitus, as reflected in the in vitro effects of platelets on endothelial cell proliferation and prostacyclin production.

We tested the hypothesis that the degree of metabolic control in diabetes mellitus may be a determinant of the ability of platelets to stimulate proliferation of endothelial cells (ECs) and smooth muscle cells (SMCs). Platelets were obtained from 24 patients (two groups of 12 patients each) with insulin-dependent diabetes mellitus (IDDM) and increased blood glucose concentrations (HbA1c > 10% Hb), duration of disease 2-45 years, on no other medication than insulin at the time of blood sampling or during the preceding 6 months, and with no signs of coronary artery disease, nephropathy, hypertension or retinopathy. The patients served as their own controls, platelets being obtained from them again 2-4 months later when their mean glucose values were lower (HbA1c < 6.5% Hb). EC proliferation was significantly reduced after exposure to platelets obtained from the patients when their metabolic control had improved, whereas no significant differences were seen in either SMC proliferation or prostacyclin production. There was no correlation between changes in insulin dosage and either cell proliferation or prostacyclin production, or between changes in lipid values and cell proliferative capacity. It is concluded that, EC proliferation will be greater, owing to the platelet effects found in vitro, when metabolic control in diabetics is poor than when it is good, which may be of importance regarding the repair of endothelial lesions.

Oral glucose tolerance and its relationship to overweight and other cardiovascular risk factors in men aged 33-42. A study in the community of Habo, Sweden.

To study the prevalence of family history of diabetes, overweight, and glucose intolerance in a defined general population, and the associations between these variables and others involved in the so-called metabolic syndrome (blood pressure, obesity, serum lipids). An oral glucose tolerance test (OGTT) was done on all participants in a population study who reported a family history of diabetes or had a body mass index (BMI) > or = 27. A population study of men aged 33-42 was carried out at Habo in southwestern Sweden (participation rate 86.1%). An OGTT was done on 170 men who fulfilled the criteria stated above. Overweight was a risk factor for impaired glucose tolerance and was more strongly associated with this state than was a family history of diabetes. Glucose intolerance was also associated with increased blood glucose concentration during the OGTT and with other metabolic disturbances such as increased serum lipids, increased blood pressure, and physical inactivity. The combination of overweight and impaired glucose tolerance is already common at a rather young age in men and is often combined with impairment of arterial blood pressure and serum lipids. The results indicate that it is urgent to start preventive measures early in life.

Overfeeding-induced obesity in rats: Insulin sensitivity and autonomic regulation of metabolism

The metabolic consequences of the development of obesity and the underlying mechanisms were investigated. For this purpose, male rats were overfed for 5 weeks through long-term gastric catheters. Permanent cardiac cannulas implanted before the overfeeding period allowed frequent blood sampling and infusions without disturbing the rats. Hyperalimented rats became grossly obese, displayed elevated basal plasma norepinephrine (NE) concentrations, and developed hyperinsulinemia and insulin insensitivity, but remained normoglycemic and preserved normal intravenous (IV) glucose tolerance. During physical exercise (ie, 15 minutes of swimming), obese rats displayed exaggerated increases in blood glucose concentrations, whereas plasma free fatty acid (FFA) responses were blunted. These alterations were probably due to decreased NE release by the sympathetic nervous system during exercise and to altered tissue responsivity to adrenergic stimulation. The latter was demonstrated by infusions of catecholamines in the resting state. Responses to mild stress were increased in obese animals, as indicated by increased responses of plasma epinephrine (E) and corticosterone during handling and first contact with water. The results of the present study indicate that overfeeding induces changes in the sympathetic control of metabolism and insulin secretion. Whereas elevated NE levels in the basal state probably reflect increased energy expenditure, the pattern of nutrient mobilization during exercise is directed toward sparing of fats.

Glucagon and the paraventricular hypothalamus: modulation of energy balance

The effects of glucagon injections (25, 100 and 200 ng) into the paraventricular nucleus of the hypothalamus (PVN) were investigated in an open-circuit calorimeter. Wistar rats were tested, with no food available during the tests. High doses of glucagon (100 and 200 ng) produced small and short-lasting increases in energy expenditure. The independence of these changes from changes in locomotor activity suggests that the thermogenesis represents a primary modulation and is not secondary to increased locomotion. All three doses of glucagon produced long-lasting and dose-related increases in respiratory quotient which were unrelated to any changes in locomotor activity. As with the changes in energy expenditure, this dissociation indicates that the effects are not secondary to changes in locomotor activity. These data constitute the first evidence that glucagon in the PVN modulates the metabolic parameters central to energy balance. In separate experiments, the three doses of glucagon increased blood glucose concentration over a one hour period, but they did not affect food and water intake and body weight over 24 h. These findings suggest that glucagon normally acts on the PVN in conditions of increased body fat to initiate autonomic mechanisms which increase glycemic levels, thermogenesis and carbohydrate utilization. These data constitute the first direct evidence for the involvement of the PVN in the regulation of energy balance by glucagon. The main effect of glucagon in the PVN is anabolic in that it increases dependence on carbohydrates as an energy substrate which results in a sparing of fat reserves.

Somatostatin and the paraventricular hypothalamus: modulation of energy balance

The effects of somatostatin injections (0.1, 1 and 5 μg) into the paraventricular nucleus of the hypothalamus (PVN) were investigated in an open-circuit calorimeter. Wistar rats were tested, with no food available during the tests. The 0.1 and 1 μg doses produced large and long-lasting decreases in respiratory quotient, which indicates the preferential utilization of fats as an energy substrate. The 5 μg dose produced a brief decrease in energy expenditure. Locomotor activity was not affected by any treatment which indicates that the effects on respiratory quotient and energy expenditure are not secondary to changes in activity. These findings demonstrate that somatostatin in the PVN inhibits thermogenesis and induces the preferential utilization of fats while sparing carbohydrate reserves. However, it is significant that the effects on energy expenditure and energy substrate utilisation occured at different doses. These data constitute the first evidence that somatostatin in the PVN produces a primary modulation of the metabolic parameters central to energy balance. In separate experiments, all three doses of somatostatin increased blood glucose concentration over a one hour period, and the 5 μg dose decreased body weight over a 24 h period. Food and water intake were not affected by the somatostatin injections. Taken together, these findings are interpreted in a model in which somatostatin is a signal to the PVN of increased body fat. This mobilises sympathetic mechanisms which increase fat utilization and blood glucose levels.

Noninvasive measurement of blood glucose concentrations by analysing Fourier transform infra-red absorbance spectra through oral mucosa.

Whether Fourier transform infra-red spectroscopy with an attenuated total reflection prism could be applied for noninvasive glucose measurement through oral mucosa was evaluated. As a result, the same absorbance peak at 1033 cm-1 as in glucose aqueous solution was found in the absorbance spectra through mucous membrane. However, these glucose specific peaks were interfered with by the baseline drifts owing to prism attachment and the background spectra from body constituents other than glucose. Therefore, to eliminate these interferences, the calibration curve between the second derivatives of the absorbance peak at 1033 cm-1 and those at 2920 cm-1 was calculated (r = 0.910). By using this calibration curve, the spectral changes due to prism attachment were first eliminated. Secondly, by obtaining the second derivative of the difference between the postprandial absorbance peak and the fasting sample as a characteristic of an individual, high correlations between the corrected second derivatives of absorbance spectra through the mucous membrane of the lip at 1033 cm-1 and the increases in blood glucose concentrations above fasting levels were observed (r = 0.910). In conclusion, it was suggested that Fourier transform infra-red spectroscopy could be useful for noninvasive monitoring of glucose through oral mucosa.

Dexfenfluramine treatment influences plasma catecholamines and energy substrate metabolism in rats

The effect of chronic intragastric administration of dexfenfluramine (FFL, 1 mg/kg, twice a day), a drug that increases serotonergic transmission, on peripheral energy substrate metabolism was investigated. Rats were provided with permanent cannulas, allowing stress-free intragastric treatment and blood sampling. Fenfluramine-treated and control animals were submitted to strenuous swimming at days —2, 1, 4, and 7 relative to the onset of FFL treatment at day O. Blood samples were taken before, during, and after exercise. Thereafter, possible changes in catecholamine sensitivity were investigated during intravenous of norepinephrine (NE) and epinephrine. Finally, energy expenditure, including resting respiratory quotient (RQ), and carbohydrate and fat utilization were measured under baseline conditions. It was found that chronic administration of FFL led to a transient reduction in the exercise-induced increase of blood glucose concentrations. Plasma norepinephrine responses to exercise gradually increased in the FFL-treated animals. Baseline RQ was markedly increased in the FFL-treated animals, indicating an increase of carbohydrate utilization and a decrease of fat combustion. Total energy expenditure remained unchanged. The increased RQ was accompanied by increased sensitivity for NE and significantly decreased baseline concentrations of plasma free fatty acids.

Comparison of the hemodynamic effects of hydroxocobalamin and cobalt edetate at equipotent cyanide antidotal doses in conscious dogs

The hemodynamic effects of two cyanide antidotes, hydroxocobalamin and cobalt edetate were compared. This experimental study was performed in chronically instrumented conscious dogs and at equipotent cyanide antidotal doses (hydroxocobalamin 70 mg.kg-1; cobalt edetate 10.5 mg.kg-1). Peak plasma cobalt concentrations did not differ in the two groups (412 +/- 183 vs 400 +/- 160 mumol.l-1). Hydroxocobalamin induced a slight increase in mean arterial pressure (+17 +/- 9%, p < 0.05) and systemic resistance (+19 +/- 15%, p < 0.05). In contrast, cobalt edetate induced an increase in heart rate (+78 +/- 33%, p < 0.05), in cardiac output (+63 +/- 39%, p < 0.05), and in maximum rise of left ventricular pressure (+33 +/- 15%, p < 0.05), did not modify mean arterial pressure, and decreased systemic resistance (-36 +/- 15%, p < 0.05). These hemodynamic effects were associated with an increase in plasma catecholamine concentrations (epinephrine: 2524 +/- 3025 vs. 58 +/- 37 pg.ml-1, p < 0.05; norepinephrine: 1106 +/- 609 vs. 343 +/- 146 pg.ml-1, p < 0.05), which in contrast remained unchanged after hydroxocobalamin administration. Cobalt edetate also induced an increase in blood glucose concentrations (9.9 +/- 1.9 vs. 6.1 +/- 1.2 mmol.l-1, p < 0.05) and a moderate metabolic acidosis, whereas hydroxocobalamin did not. After adrenergic (alpha 1, beta) and cholinergic receptor blockade, cobalt edetate did not modify heart rate and various indices of cardiac function, suggesting that it has no direct cardiac effects. Considering its lack of hemodynamically relevant effects, these results indicate that hydroxocobalamin is potentially a safer cyanide antidote than cobalt edetate.

Glucose-Insulin Kinetics of the Extravascular Bioartificial Pancreas A Study Using Microencapsulated Rat Islets

The success of the extravascular bioartificial pancreas (BAP) is contingent on the rapid transfer of the glycemic signal across both an extravascular compartment and a semipermeable membrane and of insulin from the BAP to the recipient. To examine the possibility of microencapsulated islets such as the BAP to achieve satisfactory in vivo glucose-insulin kinetics, islets were isolated from Lewis rats, encapsulated in poly-L-lysine-alginate membranes, and isogenically transplanted into the peritoneal cavity of 14 streptozotocin induced diabetic rats. Fasting blood glucose (BG) was measured and intravenous glucose tolerance was tested at 8-10 weeks and compared with three control groups: 1) normal Lewis rats (n = 6); 2) untreated diabetic rats (n = 5); and 3) diabetic rats that received intraperitoneal implants of empty capsules (n = 4). Ten animals that received microencapsulated islets (5,271 +/- 431) promptly became normoglycemic, with a mean BG of 128 +/- 17 ng/dl 3 days after transplantation and maintained this level > 100 days. Intravenous glucose tolerance K-value for the group was 3.84 +/- 0.32 compared with 3.96 +/- 0.39 (p = 0.83) for the normal control group, and 0.60 +/- 0.12 (p < 0.01) and 0.40 +/- 0.15 (p < 0.01) for the diabetic control groups with and without empty capsules. The authors conclude from these results that, given sufficient beta-cell mass, a BAP without any vascular access can respond appropriately to an increase in blood glucose concentration, without overshoot hypoglycemia and within a lag lapse compatible with normal physiologic insulin delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of serum fructosamine concentration as an index of blood glucose control in cats with diabetes mellitus

SUMMARY Fructosamine, a glycated serum protein, was evaluated as an index of glycemic control in normal and diabetic cats. Fructosamine was determined manually by use of a modification of an automated method. The within-run precision was 2.4 to 3.2%, and the day-to-day precision was 2.7 to 3.1%. Fructosamine was found to be stable in serum samples stored for 1 week at 4 C and for 2 weeks at − 20 C. The reference range for serum fructosamine concentration in 31 clinically normal colony cats was 2.19 to 3.47 mmol/L (mean, 2.83 ± 0.32 mmol/L). In 27 samples from 16 cats with poorly controlled diabetes mellitus, the range for fructosamine concentration was 3.04 to 8.83 mmol/L (mean, 5.93 ± 1.35 mmol/L). Fructosamine concentration was directly and highly correlated to blood glucose concentration. Fructosamine concentration also remained high in consort with increased blood glucose concentration in cats with poorly controlled diabetes mellitus over extended periods. It is concluded that measurement of serum fructosamine concentration can be a valuable adjunct to blood glucose monitoring to evaluate glycemic control in diabetic cats. The question of whether fructosamine can replace glucose for monitoring control of diabetes mellitus requires further study.

The effect of administering or withholding dextrose in pre-bypass intravenous fluids on intraoperative blood glucose concentrations in infants undergoing hypothermic circulatory arrest

Thirty-six fasted infants under 1 year of age who were scheduled for elective cardiac surgery using hypothermic bypass with circulatory arrest were randomized to receive a lactated Ringer's (LR) solution (group I) or a LR with 5% dextrose solution (group II) in the pre-bypass period. Marked increases in blood glucose concentrations were found following institution of bypass and circulatory arrest in the children in both groups. There was no correlation between the amount of dextrose infused in the pre-bypass period and the presence of hyperglycemia following institution of bypass. A single patient in group I was hypoglycemic (blood glu cose <30 mg/dL) on the initial glucose determination and the blood glucose did not increase during the pre-bypass period. Elimination of dextrose from the parenteral fluids given before bypass will not eliminate hyperglycemia following institution of bypass: however, it may expose pediatric patients to the risks of hypoglycemia before bypass.

Effects of xylazine on the stress response to transport in male goats

A 20-min van journey increased plasma cortisol concentrations to 15–25 ng/ml in male goats, blood glucose concentrations were not affected, but respiratory rates and heart rates were increased, the latter by 40 beats per min. A 2-h van journey increased plasma cortisol to >25 ng/ml and blood glucose to >5 mmol/l. Respiratory rates were increased to >40 breaths per min and heart rates by >100 beats per min. Xylazine alone (0.01 mg/kg) suppressed resting plasma cortisol concentrations, increased blood glucose concentrations to 4.5 ± 0.8 mmol/l and suppressed respiratory rates by 5–10 breaths per min and heart rates by 20 beats per min. Cortisol concentrations were suppressed by xylazine treatment if given before a 20-min van journey, and for approximately 60 min if given 20 min after the start of a 2-h journey. When combined with transport, xylazine caused an additive effect on glucose concentrations, but suppressed respiratory and heart rates. However, for the latter criteria the timing of suppression was different depending on the time of onset and duration of the stressor. Injection of 50 μg ovine corticotrophin releasing factor (CRF) caused an immediate elevation of cortisol concentrations (but not glucose) which lasted for at least 6 h compared with the return to baseline within 60 min after either length of journey. Xylazine pretreatment did not alter the cortisol response to CRF, suggesting that xylazine must act centrally above pituitary level when blocking the cortisol response to transport. It is proposed that under resting conditions the hypothalamus is under alpha 2-adrenergic suppression. Stimulation of cortisol secretion in response to a stressor can be inhibited by an alpha 2-adrenergic agonist.

Aminoguanidine treatment reduces the increase in collagen stability of rats with experimental diabetes mellitus.

Alterations in the biophysical properties of connective tissues in diabetes mellitus have been attributed to the nonenzymatic glycation of the collagens and the subsequent formation of browning products, cross-linking the proteins. Aminoguanidine may bind to carbonyl groups of these nonenzymatic glycation products and thereby block the process. Rats with streptozotocin-induced diabetes were treated with aminoguanidine, 25 mg.kg-1.day-1, for 120 days. The aminoguanidine treatment did not counteract the increase in blood glucose concentrations, nor did it prevent the arrest in weight gain of diabetic rats. The increased stability in 7 mol/l urea and increased tensile strength of tail tendons from the diabetic rats, however, were prevented by the aminoguanidine treatment. Aminoguanidine did not reduce the formation of early nonenzymatic glycation products (aldimine and Amadori rearrangement products), whereas the amount of browning products (fluorescent compounds) was reduced in the tail tendon collagen of the diabetic rats. Aminoguanidine treatment of intact rats did not influence these parameters. These findings indicate that the biophysical alterations of collagens induced by experimental diabetes are caused by cross-links derived from the nonenzymatic glycation, and furthermore, that aminoguanidine treatment may prevent the concomitant changes in biophysical properties of connective tissues.