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Biomedical subjects

C D Agardh

Publications and source records attributed to C D Agardh.

At least 127 records · Page 7Linked to original sources
PubMed1981

Hypoglycemic brain injury: metabolic and structural findings in rat cerebellar cortex during profound insulin-induced hypoglycemia and in the recovery period following glucose administration.

Previous results have shown that severe, prolonged hypoglycemia leads to neuronal cell damage in, among other structures, the cerebral cortex and the hippocampus but not the cerebellum. In order to study whether or not this sparing of cerebellar cells is due to preservation of cerebellar energy stores, hypoglycemia of sufficient severity to abolish spontaneous EEG activity was induced for 30 and 60 min. At the end of these periods of hypoglycemia, as well as after a 30 min recovery period, cerebellar tissue was sampled for biochemical analyses or for histopathological analyses or for histopathological analyses by means of light and electron microscopy. After 30 min of hypoglycemia. the cerebellar energy state, defined in terms of the phosphocreatine, ATP, ADP, and AMP concentrations, was better preserved than in the cerebral cortex. After 60 min, gross deterioration of cerebellar energy state was observed in the majority of animals, and analyses of carbohydrate metabolites and amino acids demonstrated extensive consumption of endogenous substrates. In spite of this metabolic disturbance, histopathologic alterations were surprisingly discrete. After 30 min, no clear structural changes were observed. After 60 min, only small neurons in the molecular layer (basket cells) were affected, while Purkinje cells and granule cells showed few signs of damage. The results support our previous conclusion that the pathogenesis of cell damage in hypoglycemia is different from that in hypoxia-ischemia and indicate that other mechanisms than energy failure must contribute to neuronal cell damage in the brain.

Adenosine Diphosphate↗
PubMed1981

Dietary fibre in type II diabetes.

Recent studies have indicated that diets rich in digestible carbohydrates and dietary fibre might be beneficial in the regulation of type II non insulin dependent diabetes (NIDD). Addition of the gel forming type of dietary fibre such as pectin and guar gum to meals or glucose solutions reduces post-prandial glucose and insulin response. Addition of cereal fibres in the form of bran seems to have long term beneficial effect improving glucose tolerance. Little is known, however, concerning effects of dietary fibre naturally occurring in food on postprandial glucose and hormone response. In the present study we prepared two breakfast meals which were similar regarding digestible carbohydrates but differed in their dietary fibre content. One of the meals, including whole grain bread and whole apples, contained 8.4 g of dietary fibre, and the other one, containing white bread and apple juice, 3.1 g. When given to eight NIDD, the fibre rich breakfast gave significantly lower blood glucose increment during the three hours following ingestion. The results indicate that foods rich in dietary fibre might be useful in the regulation of type II diabetes.

Blood Glucose↗
PubMed1981

Cerebrovascular response during and following severe insulin-induced hypoglycemia: CO2-sensitivity, autoregulation, and influence of prostaglandin synthesis inhibition.

The objective of the present experiments was to study mechanisms governing cerebrovascular responses during severe hypoglycemia, and in the posthypoglycemic recovery period. To that end, lightly anesthetized (70% N2O) and artificially ventilated rats were injected with insulin so as to abolish spontaneous EEG activity for 15 or 30 min ("coma"). In separate animals, recovery was induced by glucose administration. Previous experiments have shown that in normo- or moderately hypertensive animals hypoglycemic coma is accompanied by a relatively marked increase in cerebral blood flow (CBF), and that a delayed hypoperfusion develops in the recovery period. The present results demonstrate that oxygen supply is in excess of the demands during coma, and falls below control during recovery. During hypoglycemic coma, the CO2 response of the circulation was retained but autoregulation was lost. In the recovery period, both CO2 response and autoregulation were lost. Pretreatment with indomethacin was introduced in order to evaluate the possible influence of fatty acid cyclo-oxygenase products on the pattern of CBF changes. Measurements of local cerebral blood flow (1-CBF) showed that, in the majority of structures analysed, indomethacin failed to modulate the changes in CBF. It is concluded that alterations in cerebrovascular tone and loss of autoregulation induce flow changes that may influence substrate and oxygen availability during hypoglycemia. The pronounced decrease in CBF and the loss of autoregulation and CO2-response in the post-hypoglycemic period may influence functional, metabolic and morphological recovery. The 1-CBF findings indicate that neither the increase in CBF during hypoglycemia nor the reduction in flow in the posthypoglycemic period are mediated by mechanisms related to prostaglandin metabolism.

Animals↗
PubMed1980

Local cerebral blood flow in the rat during severe hypoglycemia, and in the recovery period following glucose injection.

In order to assess the influence of severe hypoglycemia on local cerebral blood flow (1-CBF) artificially ventilated rats, maintained on 70% N2O, were injected with insulin to provide either an EEG pattern of slow-wave polyspikes, or cessation of spontaneous EEG activity for 5, 15 or 30 min ("coma"). In other animals, glucose was injected at the end of a 30 min period of "coma" and 1-CBF was measured after recovery periods of 5, 30, 90, or 180 min. Local CBF was measured autoradiographically with 14C-iodoantipyrine as the diffusible tracer. In the slow-wave polyspike period 1-CBF was increased in most of the structures studied, and reached values that were 1.4 to 3.2 times greater than control. In many structures, cessation of EEG activity was accompanied by a further increase in 1-CBF, with some structures (thalamus, hypothalamus, pontine gray, and cerebellar cortex) showing flow rates of 400--500% of control. The increase in 1-CBF was unrelated to arterial hypertension, hypercapnia, or hypoxia. 5 min after glucose injection the hyperemia persisted in only some of the structures studied; in others, the 1-CBF were close to, or below, control values. During the subsequent recovery period 1-CBF was markedly reduced with some structures (cerebral cortical areas, hippocampus, and caudate-putamen) showing flow rates of only 20--35% of control. In others, notably pontine gray and cerebellar cortex, secondary hypoperfusion was never observed. The hypoperfusion was unrelated to arterial hypertension, hypocapnia, or increase in intracranial pressure. It is concluded that, like hypoxia and ischemia, substrate deficiency due to hypoglycemia is accompanied by vasodilatation in the brain. Furthermore, like long-lasting ischemia, severe hypoglycemia is followed by a delayed hypoperfusion syndrome that, by restricting oxygen supply, may well contribute to the final cell damage incurred.

Animals↗
PubMedDate not supplied

Urinary excretion of the carboxy terminal domain of type IV collagen is associated with kidney size and function in IDDM.

We evaluated whether urinary excretion of the carboxy terminal domain (NC1) of Type IV collagen is associated with glomerular filtration rate and kidney size in Type I (insulin-dependent) diabetes mellitus (IDDM). Urinary excretion rate of NC1, glomerular filtration rate (GFR), and kidney size were measured in 16 men with Type I diabetes. Their mean age was 33.3 +/- 6.1 years with a duration of diabetes of 14.9 +/- 3.7 years (mean +/- SD). The urinary excretion rate of NC1 was higher in the diabetic patients than in 18 healthy control subjects. Urinary excretion of NC1 was associated with both kidney size, parenchymal width, and GFR (r = 0.73, p = 0.001; r = 0.63, p = 0.009; r = 0.53, p = 0.04, respectively). The exact relationship between these factors and basement membrane turnover/synthesis remains to be elucidated.

Adult↗
PubMedDate not supplied

The influence of external precipitating factors and peripheral neuropathy on the development and outcome of diabetic foot ulcers.

The influence of external precipitating factors and the presence of peripheral neuropathy on the development and outcome of foot ulcers were evaluated in 314 consecutive diabetic patients. All patients were treated by the same foot care team. Each patient was represented by one ulcer, and primary healing was defined as intact skin for at least six months. External precipitating factors were identifiable in 264 of 314 patients. The most common factors were ill fitting shoes/socks, acute mechanical trauma, stress ulcer, and paronychia. The highest primary healing rates were seen in lesions caused by paronychia (84%) and stress ulcer (76%). Clinical signs of sensory and muscular disturbances were seen in the majority of patients (96%). Sensory neuropathy, evaluated with a biothesiometer, was more common among patients who had had amputations or, died subsequently compared to those who healed. This study suggests that a majority of diabetic foot ulcers might have been prevented, since a precipitating external factor was identified in four of five patients, stressing the importance of preventive foot care.

Amputation, Surgical↗
PubMedDate not supplied

Albuminuria and associated medical risk factors: a cross-sectional study in 476 type I (insulin-dependent) diabetic patients. Part 1.

Albumin concentration in a morning urine sample was analyzed in a cross-sectional study in 476 insulin-dependent diabetic patients. The following groups of patients were defined: A) normal urinary albumin (urine albumin less than 12.5 mg/L); B) high normal albuminuria (12.5-30 mg/L); C) microalbuminuria, ie, incipient nephropathy (31-299 mg/L); and D) clinical nephropathy (greater than or equal to 300 mg/L). The prevalences of incipient and clinical diabetic nephropathy were 24.8 and 14.4%, respectively. There were no differences in clinical parameters such as age, age at onset or duration of diabetes, blood pressure, serum creatinine, or HbA1c levels between groups A and B. The frequency of retinopathy in these groups was 55 and 50%, respectively. In group C, there were increases in age, duration of diabetes, blood pressure, serum creatinine, and HbA1c levels. The frequency of retinopathy was higher (80%), and more patients had severe forms (47%). In group D, there were further increases in all parameters and, in addition, younger age at onset of diabetes. The frequency of retinopathy was 97%, and severe forms of retinopathy were more common (86%). Seventeen percent of the patients were treated for hypertension. These patients were older, had longer duration of diabetes, and had higher levels of blood pressure, serum creatinine, and urinary albumin, as well as a younger age at onset of diabetes than patients not requiring antihypertensive treatment.

Adult↗