[Disorders of the water and electrolyte metabolism in intensive care patients].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to F W Kemmer.
Explore the source record for details and available documents.
The course of 13 pregnancies in 12 women (mean age 28 [19-34] years) after renal transplantation was analysed retrospectively. The average period from renal transplantation to the beginning of pregnancy was 45 [7-144] months. All patients received methylprednisolone for immunosuppression, while seven each additionally received azathioprine and/or cyclosporin. At the onset of pregnancy the transplant function was good or only slightly impaired in 11 women (serum creatinine 1.3 [0.8-1.8] mg/dl). But in one patient, a diabetic with nephrotic syndrome, serum creatinine concentration was raised to 2.4 mg/dl. In six patients the cyclosporin dosage had to be increased during the pregnancy. Severe complications were: acute rejection in the 16th week of pregnancy; acute renal failure during a recurrence of haemolytic-uraemic syndrome in the 36th week; and severe renal anaemia (haemoglobin 6.7 g/dl). An irreversible rise in creatinine concentration occurred in five women and hypertension got worse in eight. The mean duration of pregnancy was 35.5 (32-38) weeks. The average birth weight was low (1892 g [970-2560 g]): five children were dystrophic. The dystrophy rate was the same under cyclosporin as under the conventional immunosuppressants. The findings indicate that pregnancy after renal transplantation presents a high risk for mother and child. It demands intensive joint care by obstetrician, paediatrician and nephrologist.
Explore the source record for details and available documents.
Insulin-dependent (type I) diabetic subjects who exercise for whatever reason do this at the risk of hypoglycemia. To enjoy physical activities without major metabolic complications, diabetic patients can take measures to prevent exercise-induced hypoglycemia. These measures basically include preventing accelerated insulin absorption, mimicking physiological insulin secretion during exercise, supplying additional carbohydrates during exercise, and providing effective diabetes education. When adapting the insulin dose, duration and intensity of the work load, time of day, prevailing insulin levels, and the state of nutrition must be considered. Additional carbohydrates can prevent hypoglycemia when exercise is spontaneous and insulin dose reduction is impossible. Prevention of exercise-induced hypoglycemia may be best achieved if patients participate in intensive and comprehensive teaching programs for self-management of diabetes.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The study was performed to investigate the effects of mild to moderate exercise on blood glucose levels, metabolite concentrations and responses of counterregulatory hormones in tightly controlled Type 1 (insulin-dependent) diabetic patients treated by continuous subcutaneous insulin infusion, and to quantify the measures necessary to prevent acute and late exercise-induced hypoglycaemia. Seven male patients started a 60 min exercise period 90 min after an insulin bolus and a standard breakfast; they were monitored during a post-exercise resting period of 5 h 30 min. Different basal and premeal insulin infusion rates were applied. (Near)normoglycaemia prevailed throughout the study during the control protocol when the subjects did not exercise and received their usual insulin dose. When they exercised without changing the insulin dose, four patients were forced to stop due to hypoglycaemia. This effect of exercise could be attenuated but not completely avoided if the basal infusion rate of insulin was discontinued during the exercise period. The pronounced increase in catecholamine and growth hormone concentrations during exercise were not sufficient to prevent hypoglycaemic reactions. Hypoglycaemia during exercise could only be prevented when the premeal insulin bolus was reduced by 50% in addition to the discontinuation of the basal insulin infusion during exercise. In order to reduce late hypoglycaemic reactions after exercise the best measure proved to be a reduction of the basal insulin infusion rate by 25% during post-exercise hours. Administration of only 50% of the basal insulin infusion rate during this time was associated with blood glucose levels being raised up to 8 mmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)
Patients with end stage renal failure have elevated plasma levels of atrial natriuretic peptide (ANP) which seems to be a sensitive parameter of body fluid status. A prospective study comparing patients on hemodialysis (HD) and continuous ambulatory peritoneal dialysis (CAPD) was still missing. Six identical patients (59 +/- 10 yrs, residual diuresis 1.3 +/- 0.61, 1 data expressed as means +/- SEM) were studied in the predialysis phase and under steady state conditions on HD and on CAPD. Plasma levels of ANP, cyclic guanosine monophosphate (cGMP), adrenaline, noradrenaline and dopamine were determined. Blood and dialysate samples were repeatedly taken. Ultrafiltration-volume, dry weight and blood pressure were not different between HD and CAPD. ANP and cGMP reached the highest plasma levels in the predialysis phase with 421 +/- 180 pg/ml and 19.8 +/- 6.4 pmol/ml and decreased after the onset of dialysis treatment. On HD mean ANP levels of 279 +/- 175 pg/ml were not significantly different from those on CAPD (320 +/- 213 pg/ml). However, cGMP concentrations on CAPD (15.7 +/- 5.4 pmol/ml) surpassed the values measured on HD (10.5 +/- 3.4 pmol/ml, p less than 0.05). Plasma noradrenaline was markedly elevated in the predialysis phase (421 +/- 180 pg/ml) and decreased under dialysis treatment. Differences between HD and CAPD were not found. Adrenaline and dopamine concentrations fell within the normal range.
The effects of equipotent subcutaneously injected amounts of biosynthetic human proinsulin and biosynthetic human NPH insulin on blood glucose levels were compared in healthy male volunteers. Mean blood glucose levels decreased to approximately 50 mg/dl after injection of NPH insulin and to 46 mg/dl after injection of proinsulin. This difference reached statistical significance only between 200 and 310 min. after injection. Blood glucose levels rose only marginally thereafter, but increased promptly after ingestion of the standard meal. No differences were observed between the groups. The serum insulin levels reflected the known time insulin curves after NPH injection. The maximum of the proinsulin levels occurred about 4 hours after the injection. Subcutaneous injection of equipotent amounts of biosynthetic human proinsulin and biosynthetic human insulin have similar effects on blood glucose levels.
In order to determine the role of glucagon in futile or substrate cycling in diabetes, we measured tracer determined glucose kinetics during a combined infusion of 2-3H-glucose (total glucose production) and 6-3H-glucose (glucose production) in six alloxan-diabetic dogs. The animals received either a 420 min infusion of (1) somatostatin alone (0.3 microgram X kg-1 X min-1), (2) somatostatin with insulin replacement (100 microU X kg-1 X min-1) or (3) glucagon (6 ng X kg-1 X min-1) together with somatostatin and transient insulin replacement. When somatostatin was given alone, plasma glucagon (p less than 0.004) and insulin (p less than 0.0001) were suppressed. Glucose production and disappearance and plasma glucose concentrations fell (p less than 0.0001), but the metabolic clearance of glucose did not change significantly. In the basal state, futile cycling comprised 29 +/- 4%, 33 +/- 4% and 33 +/- 3% of total glucose production in the three groups of studies, which is high compared to normal dogs. The absolute rate of futile cycling fell slightly but significantly from 10.0 +/- 1.7 to 8.3 +/- 1.7 mumol X kg X -1 min-1 (p less than 0.0008). When insulin replacement was given during somatostatin infusion to correct for the small somatostatin-induced insulin suppression, there were similar changes in plasma glucagon, glucose concentrations and glucose kinetics as seen during the infusion of somatostatin alone. Futile cycling decreased to a slightly greater extent from 12.8 +/- 2.8 to 9.5 +/- 1.7 mumol X kg-1 X min.-1 (p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
Exercise-induced hypoglycemia in diabetic patients on sulfonylurea treatment is not uncommon. However, its pathophysiology has not been examined. We studied 9 postabsorptive nondiabetic subjects after oral administration of 1.75 mg glyburide (glibenclamide) (protocol A), during 60 min of leg exercise on a bicycle ergometer at a work load of 80 +/- 10 W (protocol B), and during a combination of these conditions (protocol C). Serum glibenclamide levels rose to similar levels (160 ng/ml) with protocols A and C. Heart rate, blood pressure, and blood lactate levels increased immediately after onset of exercise and were comparable under conditions of protocols B and C. Serum insulin levels fell during protocol B from 6.1 +/- 0.6 to 4.0 +/- 0.3 microU/ml (P less than .001) but increased from 6.5 +/- 0.6 to 12.3 +/- 2.8 microU/ml during protocol A and from 6.6 +/- 0.6 to 12.7 +/- 4.3 microU/ml during protocol C, P less than .001. Maximal levels were reached at 80 min under both conditions. Comparable responses were seen for serum C-peptide concentrations. Blood glucose concentrations did not change during exercise alone. Glycemia decreased markedly after administration of the drug reaching a nadir of 49 +/- 3 mg/dl with protocol A and a nadir of 46 +/- 3 mg/dl under protocol C. However, the nadir was reached 80 min after oral ingestion of the drug when exercise and glyburide were combined, compared to 110 min (P less than .01) after ingestion of the drug alone.(ABSTRACT TRUNCATED AT 250 WORDS)
Acute psychological stress is believed to cause disturbances of metabolic control in patients with Type I diabetes. To examine the validity of this assumption, we subjected nine healthy persons (mean [+/- SEM] blood glucose level, 74 +/- 2 mg per deciliter), nine patients with Type I diabetes who had normoglycemia (130 +/- 10 mg per deciliter), and nine diabetic patients with hyperglycemia (444 +/- 17 mg per deciliter) to two acute psychological stresses: mental arithmetic and public speaking. Subjects in the three groups were matched for age, weight, sex, and socioeconomic status. For all subjects, the mean increase in heart rate was 20 beats per minute while they were doing mental arithmetic and 25 beats per minute while they were speaking publicly (P less than 0.001). In all three groups, systolic and diastolic pressure rose markedly, the plasma epinephrine level increased by 50 to 150 pg per milliliter, and the norepinephrine level by 100 to 200 pg per milliliter under both stress conditions (P less than 0.001). The plasma cortisol level rose significantly after public speaking in all groups. Neither stress induced changes in circulating levels of glucose, ketones, free fatty acids, glucagon, or growth hormone. Thus, sudden, short-lived psychological stimuli causing marked cardiovascular responses and moderate elevations in plasma concentrations of catecholamines and cortisol are unlikely to disturb metabolic control in patients with Type I diabetes.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
To determine the effectiveness of glucagon suppression in improving glucose homeostasis in diabetes, tracer-determined glucose kinetics were measured during a 6-h somatostatin infusion in six alloxan-diabetic dogs (moderately severe diabetes) and five depancreatized dogs deprived of insulin treatment for 3 days (prolonged severe diabetes). Plasma immunoreactive glucagon (IRG) decreased 70 +/- 9% in the alloxan-diabetic and 80 +/- 4% in the depancreatized dogs. Portal vein levels of plasma immunoreactive insulin (IRI) fell (17.0 +/- 2.3 to 4 micro.5 +/- 0.4 microU/ml) as did peripheral vein IRI levels (6.7 +/- 0.9 to 4.7 +/- 0.5 microU/ml) in the alloxan-diabetic dogs. In the depancreatized dogs plasma IRI levels were undetectable. Plasma glucose concentrations fell (278 +/- 17 to 169 +/- 12 mg/dl) during IRG suppression in the alloxan-diabetic dogs due to a rapid and sustained decrease in glucose production (Ra) (6.0 + 0.9 to 3.6 + 0.3 mg X kg-1 X min-1). Glucose disappearance (Rd) decreased gradually (5.9 + 0.6 to 3.9 + 0.2 mg X kg-1 X min-1). In contrast, in the depancreatized dogs, IRG suppression did not alter glucose concentrations or kinetics. Thus, glucagon suppression decreased glycemia by decreasing Ra only in moderately severe diabetes. However, this was associated with decreased rather than improved glucose utilization. The ineffectiveness of glucagon suppression during prolonged severe diabetes could relate to the degree and duration of the metabolic derangement and/or indicate that the continuous presence of some insulin is necessary for glucagon suppression to improve glucose homeostasis.