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Biomedical subjects

S Christensen

Publications and source records attributed to S Christensen.

At least 181 records · Page 10Linked to original sources
PubMed1984

Fractures of the proximal end of the humerus caused by convulsive seizures.

Fractures due to convulsions are known to occur. The purpose of this study was to find the frequency of convulsive seizures as the cause of fractures of the proximal end of the humerus, which are the most common of these fractures. Of 278 cases admitted to the department, 2 per cent occurred after a seizure without other contributory causes. The manner of injury is discussed, and it is demonstrated that the diagnosis is often delayed. The importance of early reduction in cases with dislocation or displacement of the fracture is emphasized.

Adult↗
PubMed1984

Lithium induced interstitial nephropathy associated with chronic renal failure. Reversibility and correlation between functional and structural changes.

We have previously shown that administration of lithium to rats in the first weeks after birth results in a severe interstitial nephropathy. The aim of the present work was to study the relationship between functional impairment and structural lesions and to evaluate whether the nephropathy regresses after withdrawal of lithium. Three groups of animals were studied: 16 weeks-old controls (group A), rats treated with lithium for 16 weeks (group B) and rats treated for 8 weeks followed by 8 weeks without lithium (group C). Plasma urea and renal concentrating ability were determined and one kidney fixed by vascular perfusion with glutaraldehyde for light microscope morphometry. The results show a significant reduction in renal function after lithium treatment. There was a highly significant reduction in proximal tubular length and a pronounced increase in interstitial volume due to severe fibrosis. The total mass of glomerular tufts was also reduced, but not when this parameter was divided by the body weight. Sclerotic glomeruli were not observed. The structural and functional lithium-induced lesions are independent of sex and irreversible, since they persist 8 weeks after withdrawal of lithium. It is proposed that lithium-induced interstitial fibrosis is followed by proximal tubular atrophy with a reduction in the amount of functioning proximal tubules. This leads to a decrease in proximal tubular reabsorption of sodium and a disturbance in the glomerulo-tubular balance resulting in a decrease in glomerular filtration rate.

Animals↗
PubMed1984

The consequences to the injured of occupational accidents. A follow-up study of an emergency department material.

The consequences of occupational accidents to the injured have been studied in a follow-up investigation of an emergency department material comprising almost 7 000 patients. The accident resulted in sick leave for 51% (on average 14.9 working days), in a reduced income for 31% (on average 2 125 Danish 1982 kroner), in a prolonged physical handicap for 6%, in hospitalization for 4.2% (on average 27 days), and in occupational consequences for 1.5%.

Absenteeism↗
PubMed1983

Effects of lithium on water intake and renal concentrating ability in rats with vasopressin-deficient diabetes insipidus (Brattleboro strain).

Male and female Long Evan rats and Brattleboro rats with ADH-deficient diabetes insipidus were treated with lithium administered in the diet for 12 weeks. The plasma lithium level was about 1 mmol/l in all groups. Lithium caused polydipsia and polyuria and lowering of renal concentrating ability in normal rats. In rats with ADH deficiency lithium tended to increase water intake, but did not influence spontaneous urine osmolality or maximal urine osmolality during water deprivation. The results indicate that the renal concentrating defect caused by lithium in rats can be explained by ADH-blockade as the only mechanism. However, there is circumstantial evidence that lithium in addition may stimulate thirst mechanisms by an ADH-independent action.

Animals↗
PubMed1983

Lithium-induced uremia in rats - a new model of chronic renal failure.

Three groups of new-born rats were studied: Group Li/Li treated with Li for 16 weeks, group Li/C treated for 8 weeks followed by 8 weeks without Li, and Group C/C 16 weeks old controls. Both Li-treated groups showed severe reduction of renal function, particularly group Li/Li, where the mean GFR was reduced by 80%. Plasma urea, creatinine, and osmolality were increased, blood hemoglobin and hematocrit were reduced, whereas plasma Na, K, and standard bicarbonate were unchanged. Na clearance was maintained and fractional Na excretion thus increased. Fractional Li excretion was also increased, indicating inhibition of proximal tubular salt and water reabsorption. Renal concentrating ability was markedly reduced. When Li was withdrawn, plasma urea levels remained unchanged or continued to rise, and the concentrating defect persisted. The results demonstrate that Li administration to new-born rats causes irreversible chronic renal failure which may progress even in the absence of Li. This model of chronic renal failure has several characteristics in common with chronic renal failure in humans.

Animals↗
PubMed1983

Some public expenses in connection with occupational accidents. A follow-up study of an emergency department material.

An attempt has been made to calculate some of the public expenses arising from occupational accidents, by means of a follow-up study of an ad hoc emergency department investigation of 6 941 consecutive cases. Each accident has given rise, on average, to two visits to a physician, and to hospitalization for 1.1 days. During a one-year period, the expenses of sick benefits, hospital admissions, and medical treatment alone for the whole of Denmark amount to a minimum of 1.2 milliard 1982 Danish kroner, and at least 8 900 man-working-years have been lost.

Accidents, Occupational↗
PubMed1983

Colistin inhibition of mannose-resistant haemagglutination by K88-positive and K99-positive escherichia coli strains. A preliminary report.

Two enteropathogenic E. coli strains isolated from a calf and a piglet succumbed to diarrhoea were studied. The bovine strain carried K99-antigen and the porcine strain was K88-positive. Both strains agglutinated pig erythrocytes in the presence of D-mannose. In the test a bacterial cell density of 3 x 10(9) per ml and doubling dilutions hereof were used. The haemagglutination titres were 16 and 128, respectively. When the bacteria were exposed to colistin before mixing with the red cells, haemagglutination was inhibited completely with 1.0 and 0.5 microgram/mg of colistin. At a colistin concentration of 0.25 microgram/ml (1/4-1/2 of the MIC's) the titres were lowered by a factor of 16-32.

Animals↗
PubMed1982

Effects of lithium on circadian cycles in food and water intake, urinary concentration and body weight in rats.

Circadian cycles in food and water intake, urinary concentration and body weight were studied in normal rats, lithium-polyuric rats, rats with hereditary diabetes insipidus and rats infused continuously with arginine vasopressin (ADH) 10 mU/hr IV. Normal rats showed characteristic cycles in body weight and urine flow and osmolality with diuresis in the dark (eating and drinking period) and antidiuresis in the light (resting) period. ADH-infusion eliminated the circadian cycle in urine osmolality, but not in urine flow, suggesting that factors besides. ADH mediate the antidiuresis during the resting period. Rats with ADH-deficient diabetes insipidus showed obliteration of all circadian cycles studied, indicating the importance of the renal concentrating mechanism for the amplitude of the circadian-cycles, observed in normal rats. In rats treated with lithium, circadian cycles in body weight and urine osmolality were absent. However, there was a significant circadian variation in urine flow and food and water consumption with peak values during the light period, when normal rats showed minimal values. It is concluded that in rats lithium causes marked changes in circadian cycles, which probably cannot be explained by its effect on the renal concentrating mechanisms alone.

Animals↗
PubMed1982

Severe functional and structural changes caused by lithium in the developing rat kidney.

Lithium (Li) was administered to rats during maternal pregnancy and/or 8 weeks post-natally, to study the effects on renal function and structure in the developing kidney. Plasma Li was 0.5-1.0 mmol/l 3 and 8 weeks post-natally. Functionally, post-natal Li leads to growth retardation, polyuria with lowering of renal concentration ability, and uremia associated with as much as 80% lowering of the normal glomerular filtration rate (GFR). Pre-natal Li alone did not affect the concentrating ability but caused a 20% increase in GFR when evaluated 8 weeks post-natally. Post-natal Li caused very severe structural changes, consisting of up to 3 mm cortical cysts (= dilated distal convoluted tubules), extensive interstitial fibrosis with cell infiltration, and atrophy of the cortical collecting ducts. Morphometric measurements showed a significant reduction in the volume of the proximal tubular cells. Pre-natal Li caused only slight structural changes, and animals treated both pre- and post-natally were less affected than animals treated post-natally only. The structural changes caused by post-natal Li were unrelated to changes in the concentrating ability but showed a significant correlation with the lowering of the GFR. It is concluded that the post-natally developing rat kidney is particularly sensitive to the nephrotoxic effects of Li, which in low concentrations causes impairment of renal function, leading to uremia. Pre-natal Li exposure by maternal lithium treatment had little effect on renal function and structure when evaluated post-natally.

Animals↗
PubMed1982

Functional and structural changes in the rat kidney by long-term lithium treatment.

The relation between functional and structural renal changes induced by lithium was studied in rats during long-term treatment and after withdrawal of lithium. Administration of LiCl in the diet for up to 21 weeks caused marked polyuria associated with a significant lowering of renal concentrating ability assessed by dehydration and vasopressin tests. Plasma creatinine and plasma urea were not significantly changed by the treatment. Upon withdrawal of lithium water intake and concentrating ability were normalized within 4--8 weeks. Lithium caused focal light microscopic changes in the distal convoluted tubule and the collecting duct, consisting of nuclear and cellular polymorphism and, after prolonged treatment, dilatation of tubular lumens with tubular cell atrophy. These changes appeared later than the concentrating defect and persisted when lithium was withdrawn after prolonged treatment. No significant correlation was found between the degree of tubular changes and water intake or concentrating ability. It is concluded that the reversible diabetes insipidus induced by lithium in rats cannot be explained directly by the light microscopical changes observed in the distal part of the nephron, although the structural changes may be secondary to the polyuric state induced by lithium.

Animals↗
PubMed1981

Effects of lithium and neuroleptics and combinations of the two on renal function and structure in rats.

The effects of 8 weeks of treatment with lithium and neuroleptics, alone and combined, on renal concentrating ability and morphology were studied in rats. LiCl was administered in the diet and neuroleptics were given as one daily dose: haloperidol 1 mg/kg, chlorpromazine 15 mg/kg, and perphenazine 4 mg/kg. Plasma lithium levels were about 1 mmol/l, and the area under the plasma concentration curve was not statistically different in the control and neuroleptic groups. Rats treated with lithium developed marked polyuria which was less in rats receiving neuroleptics concomitantly. After 8 weeks, rats treated with lithium alone showed marked impairment of renal concentrating ability and moderate degree of structural renal changes. Neuroleptics alone had no effect on concentrating ability or renal morphology, nor did they aggravate the changes caused by lithium. In fact, neuroleptics seemed to improve the concentrating ability in rats treated with lithium. It is concluded that in rats high doses of neuroleptics do not potentiate lithium-induced functional and structural renal changes.

Animals↗
PubMed1980

Failure of infusion of prostaglandin A2 to restore the response to antidiuretic hormone in rats with polyuria induced by lithium.

Male Wistar rats were fed a lithium diet for 2--3 months producing marked polyuria (greater than 75 ml/100 g in 24 h) and a plasma Li concentration of 0.7 mmol/l. In acute experiments animals were anaesthetized with 5-ethyl-5-(1-methylpropyl)-2-thiobarbituric acid and infused with hypotonic glucose-saline (15 ml/h). Addition of prostaglandin A2 (PGA2; 0.2 ng/min) for 180 min to the infusate did not restore the impaired antidiuretic response to arginine-vasopressin (AVP) whether this agent was infused continuously (150 micromicron./min) or given as bolus injections (2500 micromicron.). In long-term experiments animals were kept in metabolism cages and Alzet osmotic minipumps were implanted for intravenous infusion of drugs at 1 microliter/h. Again, PGA2 infusion at 0.2 ng/min failed to restore the impaired antidiuretic response to AVP (150 micromicron./min). It was therefore concluded that in rats with severe polyuria induced by long-term administration of lithium, infusion of PGA2 at 0.2 ng/min cannot restore the impaired response to antidiuretic hormone as has been reported by others.

Animals↗
PubMed1980

DDAVP (1-desamino-8-D-arginine-vasopressin) treatment of lithium-induced polyuria in the rat.

The antidiuretic responses of arginine vasopressin (AVP) and 1-desamino-8-D-arginine vasopressin (DDAVP) were studied in rats with marked lithium-polyuria (about 100 ml/100 g/24 h) induced by administration of lithium to the diet for 3-4 months. The hormones were infused i.v. and s.c. at a constant rate for 7 days using implantable osmotic minipumps. Body weight, food consumption and urine volume and osmolality were recorded daily. Whereas supramaximal doses of AVP only had little effect on spontaneous urine flow and osmolality, DDAVP (0.1 microgram/h i.v. or 1 microgram/H s.c.) restored urine volume and osmolality to near-normal values. Although the mechanism of the antidiuresis evoked by DDAVP was not investigated the ability of this compound to reverse AVP-resistant polyuria may be due to its specificity and high intrinsic activity in stimulating the vasopressin receptor. The reversibility of lithium-induced impairment of renal concentrating ability caused by excessive hormonal stimulation is not immediately compatible with the recent hypothesis that lithium-polyuria may reflect irreversible structural kidney damage.

Animals↗