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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a survey about all factors influencing the osmotic pressure. The actual osmotic pressure in the plasma of healthy individuals is regulated essentially by the natrium ions and the corresponding anions. The one exception is the dysfunctioning diabetes mellitus with distinctly advanced hyperglycaemia. Syndromes with an accompanying azotemia demonstrate a seeming hyperosmolality as long as the osmotic pressure is measured or calculated by the customary method. The real and present osmotic condition can only be calculated when the blood urea concentration is no longer considered. It is proposed that the term "corrected osmolality" be used for the values determined in this manner.
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PMID:[Osmolality problems]. 96 81

Patients in the coronary care unit with acute pulmonary edema, heart failure, and other organic heart disease were studied. Blood and urine samples were taken on admission prior to any treatment and later at prescribed intervals. All the patients with APE were found to have elevated plasma osmolalities and hyperglycemia on admission which decreased with treatment. This was in contrast to the other two groups excluding those factors such as ethyl alcohol and diabetes which can raise plasma osmolality or blood glucose. A discussion of this mild hyperosmolal state in APE follows including possible causes as well as cellular effects of hyperosmolality on humans.
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PMID:Acute pulmonary edema and hyperosmolality: a clinical study. 106 77

Ketoacidosis, severe hyperosmolality due to hyperglycemia, and severe hypoglycemia are all life-threatening emergencies that often occur in the absence of any history of diabetes mellitus. The key to management of diabetic ketoacidosis is understanding that treatment is aimed more at the breakdown and metabolism of triglycerides in adipose tissue than at hyperglycemia per se. The diabetic hyperosmolar state is most easily treated with aggressive fluid management, with the caveat that too-rapid administration of hypotonic fluids may increase the already significant mortality from this condition. Life-threatening hypoglycemia most commonly occurs with administration of oral hypoglycemic drugs or insulin, although other drugs and any malnourished state may also be precipitating factors. Acute administration of glucagon or dextrose alleviates life-threatening hypoglycemia. Success in managing these diabetic emergencies depends on rapidity of recognition and institution of direct treatment measures.
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PMID:'Diabetic' emergencies. They happen with or without diabetes. 211 37

We studied the effect of hyperosmolality on the tap-induced blink reflex (TBR) in patients with diabetes. The TBR, consisting of R1 and R2 components, was either absent or delayed in patients compared to controls. The abnormalities correlated better with the degree of hyperosmolality than with the level of blood glucose. TBR was usually absent in unconscious patients with greatly elevated serum osmolality. In some patients with similar elevations in serum osmolality the R2' component was absent at a time when consciousness was preserved. Hence, TBR may be useful in monitoring CNS dysfunction in diabetics with hyperosmolality.
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PMID:Tap-induced blink reflex and central nervous system dysfunction in diabetics with hyperosmolality. 235 8

In order to explore the pathogenetic mechanism underlying the changes in blood-brain barrier sodium transport in experimental diabetes, the effects of hyperglycemia and of hypoinsulinemia were studied in nondiabetic rats. In untreated diabetes, the neocortical blood-brain barrier permeability for sodium decreased by 20% (5.6 +/- 0.7 versus 7.0 +/- 0.8 X 10(5) ml/g/s) as compared to controls. Intravenous infusion of 50% glucose for 2 h was associated with a decrease in the blood-brain barrier permeability to sodium (5.4 +/- 1.2 X 10(5) ml/g/s), whereas rats treated with an inhibitor of insulin-secretion (SMS 201-995, a somatostatin-analogue) had normal sodium permeability (7.3 +/- 2.0 X 10(5) ml/g/s). Acute insulin treatment of diabetic rats normalized the sodium permeability within a few hours as compared to a separate control group (7.7 +/- 1.1 versus 6.9 +/- 1.4 X 10(5) ml/g/s). To elucidate whether the abnormal blood-brain barrier passage is caused by a metabolic effect of glucose or by the concomitant hyperosmolality, rats were made hyperosmolar by intravenous injection of 50% mannitol. Although not statistically significant, blood-brain barrier sodium permeability increased in hyperosmolar rats as compared to the control rats (8.3 +/- 1.0 and 7.0 +/- 1.9 X 10(5) ml/g/s, respectively). It is concluded that either hyperglycemia per se or a glucose metabolite is responsible for the blood-brain barrier abnormality which occurs in diabetes. Further, we suggest that the specific decrease of sodium permeability could be the result of glucose-mediated inhibition of the Na+K+-ATPase localized at the blood-brain barrier.
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PMID:Blood-brain barrier permeability to sodium. Modification by glucose or insulin? 264 96

Diabetic lipemia with and without acute pancreatitis in chronic alcoholism. A report of 4 cases. Diabetic lipemia was observed in 4 chronic alcoholic men after ingestion of high doses of alcohol and/or sugar-rich beverages, including one patient who was treated for insulin-dependent diabetes. None had a previous history of serum lipid disturbances. All had marked hyperglycemia, hyperosmolality and hypertriglyceridemia (mean: 60.8 mmol/l), 2 of undetermined type and 2 of type IV with eruptive xanthomas. Factitious hyponatremia was present in 3 cases, but true serum sodium was normal (138 mmol/l) or elevated (154, 156, 182 mmol/l) after correction. Three patients developed acute pancreatitis ascribed to high serum triglyceride levels and/or to alcohol ingestion. Serum and urine amylase activity was inhibited by hypertriglyceridemia. The diagnosis of pancreatitis was assessed twice by echography and computed tomographic scan, and once by tomographic scan and an elevation of the amylase on creatinine clearance ratio. It is likely that hypertriglyceridemia predisposed these patients to develop pancreatitis, alcoholism being a precipitating factor. We suggest that the diagnosis of acute pancreatitis should be systematically considered in any case of diabetic lipemia without true hyponatremia.
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PMID:[Diabetic hyperlipemia with or without acute pancreatitis in patients with chronic alcoholism. A study of 4 cases]. 274 Jun 61

The early local exudative cellular reaction in an inflammatory lesion was impaired in alloxan-induced diabetic rats due to reduced migration of neutrophils to the inflamed area. Neutrophils, however, were capable of moving from reserve compartments into blood in these animals. Furthermore, the functional integrity of their surface membranes, assessed by the capacity of the cells to adhere to nylon fiber, was not altered by alloxan diabetes. An intrinsic cellular defect also did not occur, because the cells were capable of responding to chemotactic stimuli in the Boyden chamber system, provided they were suspended in Eagle's medium or normal serum. Suspended in the corresponding diabetic serum, a blockade of the chemotactic response was observed. Increasing concentrations of diabetic serum, added to a suspension containing neutrophils collected from normal donors, progressively inhibited the response of the cells to a chemotactic stimulus. Hyperglycemia alone or hyperosmolality secondary to hyperglycemia, the presence of ketone bodies, or a direct effect of alloxan did not explain the results. In addition, the capacity to generate chemotactic factors remained intact in diabetic serum. Pretreatment of the diabetic animals with insulin resulted in a gradual recovery of the chemotactic response in vivo and in vitro. We conclude that alloxan-induced diabetic rat serum contains a substance that inhibits neutrophil chemotaxis and that insulin administration is essential for the clearance of this substance from plasma.
Diabetes 1987 Nov
PMID:Inhibition of leukocyte chemotaxis by factor in alloxan-induced diabetic rat plasma. 366 21

Four patients with severe hyperglycemia and hyperosmolality were studied to quantitate the major mechanisms responsible for the fall in blood glucose concentration. Insulin was not administered to any of these patients during the first 15 h of therapy. In each case, there was a fall in glucose concentration due to dilution; this was quantitated by chloride space analysis and accounted for 24-34% of the fall in concentration. The size of the glucose pool decreased for two reasons. Glucosuria accounted for the majority of the reduction in the size of the glucose pool in the patients with the smallest decrease in extracellular fluid (ECF) volume [and hence the best preserved glomerular filtration rate (GFR)]. In contrast, glucosuria was a less important factor in causing glucose loss in the patients with very low GFR values. The size of the glucose pool also decreased due to glucose metabolism that did not require exogenous insulin. Thus the fall in glucose concentration in the initial therapy in patients with the hyperglycemic hyperosmolar syndrome is multifactorial and is not absolutely dependent on exogenous insulin. Furthermore, the patients grouped in this diagnostic category represent a heterogeneous population with the common features of severe hyperglycemia, hyperosmolality, and a negative or weakly reactive test for serum ketones.
Diabetes Care
PMID:Quantitative analysis of glucose loss during acute therapy for hyperglycemic hyperosmolar syndrome. 376 16

The deterioration of glucose tolerance and insulin resistance observed in states of hypertonic dehydration are commonly ascribed to a concomitant increase in circulating insulin counterregulatory hormones. To examine the effect of hyperosmolality per se on carbohydrate metabolism, tissue sensitivity to insulin was assessed by means of the euglycemic insulin clamp technique and simultaneous 3H-3-glucose kinetic analysis. Eight healthy volunteers participated in three protocols: (1) In the hyperosmolal study, serum osmolality was raised from 280 +/- 1 to 302 +/- 1 mosm/kg by a primed continuous infusion of hypertonic mannitol. Following 2 h of hypertonicity, a euglycemic insulin clamp study was performed. The plasma insulin concentration was acutely raised and maintained at 147 +/- 20 microU/ml, while plasma glucose was maintained at basal levels; (2) In the control insulin clamp study, isotonic sodium chloride was infused instead of mannitol. No significant change in serum osmolality was observed during the control study; (3) To examine the effect of mannitol per se on insulin-mediated glucose metabolism, isotonic mannitol was infused in a third study to raise the plasma mannitol level to a similar extent as observed during the infusion of hypertonic mannitol. The serum tonicity did not change during the isotonic mannitol infusion. Insulin-mediated glucose utilization (M) was 6.69 +/- 0.51 mg/kg X min in the control study and decreased to 5.84 +/- 0.40 mg/kg X min following the exposure to hyperosmolality (P less than 0.05).2+ +/- 0.60 versus 4.30 +/- 0.43 mg/kg X min per microU/ml X 100).(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1983 Nov
PMID:Impairment of insulin-mediated glucose metabolism by hyperosmolality in man. 641 9

Fascicles of human sural nerve, fixed by immersion in isosmolar 2.5% glutaraldehyde solution and in isosmolar osmium tetroxide and embedded in epoxy, undergo a 10% shrinkage in area when compared with cryostal sections. By contrast, fascicles fixed in hyperosmolar solutions (whether 5.6% glutaraldehyde solution or 2.5% glutaraldehyde raised to the same level of hyperosmolality with sucrose) undergo a 43% shrinkage in area. Axis cylinders of myelinated fibers undergo a selective and severe shrinkage and assume noncircular shapes, the shapes allowing the transverse area to decrease when the perimeter remains unchanged. These studies raise the intriguing question of whether interstitial hyperosmolality in metabolic diseases, such as diabetes mellitus, or in uremia may cause osmotic axonal shrinkage, altered transverse fiber shape, and abnormality of function and structure of nerve.
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PMID:Effect of serum hyperosmolality on morphometry of healthy human sural nerve. 676 11


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