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Query: UMLS:C0011849 (diabetes)
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Abdominal aortic aneurysmectomy is being performed with progressively lower operative mortality and morbidity. Three hundred thirty seven patients have had elective aneurysm repair since 1954. Factors affecting mortality and morbidity in the last 108 cases are analyzed. Seventy-four per cent of patients had pre-existing disease, either cardiac, pulmonary, renal, cerebrovascular, diabetes mellitus, or hypertension. Six patients died following operation, a mortality rate of 5.5%. One died of pulmonary and 5 of cardiac causes. No patient died of renal failure or required dialysis. A signficant feature of management is the regimen of fluid therapy using dextrose in lactated Ringer's solution during and after operation to minimize hypotensive and renal complications. No patient developed a wound infection, graft infection, wound dehiscence, stroke, or intestinal ischemia. Serious postoperative complications were largely cardiac or pulmonary. Despite recent liberalization of indications for operation, comparative figures show continued reduction in operative mortality from 17% during 1954-1961, or 7.4% during 1962-1967, to 5.5% in the 1968-1974 era. This declining mortality is related to earlier diagnosis using non-invasive methods (sonogram), simplified operative techniques, improvement in fluid management, innovations in cardiopulmonary therapy, and recognition and proper handling of unusual manifestations of aortic aneurysms.
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PMID:Surgical management of abdominal aortic aneurysms: factors influencing mortality and morbidity--a 20-year experience. 12 60

We examined the effect of calcium administration on renal hyperfiltration in streptozotocin-treated diabetic rats. Rats were studied 7-10 days after streptozotocin injection. Intrarenal infusion of CaSO4 in Ringer's solution had no effect on the hyperfiltration of the diabetic kidney. Infusion of insulin in a dose that did not effect hyperglycemia also had no effect on the hyperfiltration. However, when insulin and calcium were infused together, a rapid decrease in glomerular filtration rate, single-nephron filtration rate, glomerular hydraulic pressure, and renal plasma flow occurred. The contralateral control kidney was unaffected. Verapamil infusion had no significant effect in untreated diabetic rats, but immediately reversed the vasoconstriction induced by insulin plus calcium. Similar intrarenal insulin and calcium infusions had no effect in euvolemic or chronically salt-loaded nondiabetic rats. The observations indicate that renal vascular cells (probably preglomerular) are hyperresponsive to calcium in early insulin-dependent diabetes mellitus and that this response requires insulin. We suggest that decreased renal vascular tone in early insulin-dependent diabetes mellitus may be due in part to defective transmembrane calcium flux across vascular smooth muscle cells. Insulin appears to be required for calcium entry or mobilization, to initiate renal vascular smooth muscle contraction in diabetes.
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PMID:Acute effect of calcium and insulin on hyperfiltration of early diabetes. 310 8

Perioperative control of blood glucose in patients with diabetes has been difficult due to frequent occurrence of hypoglycemia or hyperglycemia. We developed a two-step protocol for management of insulin-treated patients during general anesthesia. Regular insulin was given intravenously before anesthetic induction according to the step I formula (initial): initial blood glucose - 150/10 = U. Regular insulin was then given during surgery according to the step II formula (hourly): blood glucose 150-250 mg/dl = 2 U; blood glucose greater than 250 mg/dl = 4 U. Fluid replacement of 5% dextrose with lactated Ringer's solution, 3 ml/kg estimated ideal body weight, was given hourly and additional lactated Ringer's solution was given as indicated. Thirty patients received preoperative (long- or intermediate-acting) insulin and were managed by the two-step protocol. Ten patients received preoperative (long- or intermediate-acting) insulin and were managed by a standard method used in the same institution. Thirty patients did not receive preoperative insulin and were managed by the two-step protocol. All patients underwent retinal surgery under general anesthesia. In comparing the two groups pretreated with insulin, patients treated by the standard method had significantly higher (mean) blood glucose levels (360.2 +/- 100.4 mg/dl) than those treated with the two-step protocol (181.2 +/- 50.8 mg/dl) (P = 0.0001) at the end of surgery. Of the two-step protocol patients, those pretreated with one-half the usual morning dose of long- or intermediate-acting insulin had lower (mean) blood glucose levels (225 +/- 87 mg/dl) than patients not pretreated (310 +/- 130.8 mg/dl) (P = 0.0069) the morning after surgery.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes Care
PMID:Perioperative control of blood glucose in diabetic patients: a two-step protocol. 351 5

In vitro studies have suggested that ascorbate or dehydroascorbate share with glucose the same tissue-transport carrier. To determine if ascorbic acid or its oxidized form can inhibit tissue uptake of glucose, the brain uptake index (BUI) and muscle uptake index of glucose were determined by single arterial injection tissue-sampling technique. The injectate was either buffered Ringer's solution with varying concentrations of ascorbate, dehydroascorbate (pH 7.4), or 70% serum from individuals on vitamin C supplements. Ascorbic acid over a wide range of concentrations (0-10,000 mg/L) did not reduce the BUI. Ascorbic acid reduced BUI from the control value of 33 +/- 3.2 to 20.1 +/- 2.2% (P less than .01) only at 100,000 mg/L; this effect was probably secondary to osmotic disruption of blood-brain barrier. In contrast, dehydroascorbate inhibited the BUI of glucose from baseline value of 32.8 +/- 1.1 to 10.7 +/- 0.67%, with an estimated Ki of 13.0 mM. Masseter muscle glucose uptake was not significantly altered over a wide range of ascorbate or dehydroascorbate concentrations in the injectate. Dehydroascorbate (7500 mg/L) did not significantly reduce the BUI of [14C]phenylalanine (55.2 +/- 4.4 vs. 62.1 +/- 4.2% in controls). When serum from six individuals on calcium ascorbate (3-5 g/day) was compared with that of nine controls, the BUI was not different (19.3 +/- 1.7 vs. 19.3 +/- 1.1%). Similarly, supplementing the diet of eight healthy volunteers with 1 g calcium ascorbate for 8 days did not alter the BUI of glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
Diabetes 1987 Sep
PMID:Effect of ascorbate and dehydroascorbate on tissue uptake of glucose. 360 94

The effects of glucose in vitro at concentrations of 100, 200 and 400 mg/dl on responses of the guinea-pig ileum and mouse vas deferens to opiates were studied. Responses of the electrically stimulated ileum to normorphine were significantly reduced (IC50 values: 26.3 +/- 4.3, 40.5 +/- 3.7 and 71.8 +/- 16.6 nM) as the glucose concentration increased, whereas the potency of normorphine was not affected by equimolar substitutions of glucose with the nonmetabolizable sugar 3-O-methylglucose. The potency of naloxone to induce withdrawal contractions of ilea incubated in Ringer's solution for 3 or 4.5 hr with 1 microM morphine was also significantly decreased as the concentration of glucose in the incubations increased, indicating a reduction of acute dependence development by high glucose. The potency of normorphine was also reduced by increasing concentrations of glucose in electrically stimulated vasa deferentia from nondiabetic (db/m+, m+/m+) C57BL/KsJ mice (IC50 values: 0.53 +/- 0.01, 0.77 +/- 0.01 and 1.84 +/- 0.03 nM), but not in vasa deferentia from their diabetic (db/db) littermates. These results support our hypothesis that the decreased sensitivity to morphine and decreased development of physical dependence on morphine in in vivo models of diabetes reported previously by our laboratory is due primarily to the hyperglycemia associated with diabetes.
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PMID:Morphine dependence and diabetes. II. Alterations of normorphine potency in the guinea-pig ileum and mouse vas deferens and of ileal morphine dependence by changes in glucose concentration. 371 82

Microvessels in the cheek pouch of the hamster were investigated to determine their structural, reactivity, and permeability characteristics after the induction of diabetes. To induce diabetes, hamsters were injected with streptozotocin (50 mg/kg body wt./day, i.p., for 3 days). Vehicle-injected, age-matched hamsters were the controls. Diabetic hamsters were characterized by elevated serum glucose (greater than 300 mg/dl) and triglycerides and decreased serum insulin (50%). Microvascular studies were completed on cheek pouch microvessels suffused with Ringer's solution (37 degrees C, pH 7.4) bubbled with 95% N2-5% CO2. Vascular dimensions and reactivity of selected arterioles and venules to microapplications of norepinephrine were determined with a video micrometer using intravital microscopy. Restrictiveness of the microvascular membranes to fluorescein-labeled dextran fractions (mol wt: 150,000; 40,000; 20,000 daltons) was measured by determining the number of leaky sites. Stimulation of membrane permeability by histamine was investigated. There were no major alterations in arteriolar lumen and wall diameters, whereas venular lumen diameters were increased in hamsters diabetic for two months. Likewise, arteriolar responses to norepinephrine were not altered by diabetes; however, venular responses were decreased at two months. The restrictiveness of the vascular membrane to various dextran fractions was dramatically decreased in the diabetic animals at two months. Histamine did not alter microvascular leakage in the diabetic as it did in the normal hamsters. These studies indicate that microvascular alterations, venular dilation, and increased permeability to large molecules occur in the diabetic hamster within two months after the induction of diabetes.
Diabetes 1981 Feb
PMID:Microvascular alterations develop in Syrian hamsters after the induction of diabetes mellitus by streptozotocin. 616 95

We have previously shown that the rat with experimental diabetes (DM) of 4-6 months' duration exhibits complete functional and morphologic protection against gentamicin-induced acute renal failure. To assess the role of the duration of the diabetic state per se on the resistance to gentamicin, female Sprague-Dawley rats with diabetes of short (5 days, n = 7), intermediate (5 weeks, n = 5) and long duration (5 months, n = 7) were studied. Diabetes was induced by streptozotocin, 50-65 mg/kg b.w. i.v. Controls were identically treated sex- and age matched nondiabetic rats. The animals were kept in individual metabolic cages for 2 weeks and all received gentamicin 40 mg/kg/day for 9 days. Sham animals (DM and control) received Ringer's solution in place of gentamicin. Prior to gentamicin, plasma glucose levels and creatinine clearances (Ccr) were higher in the DM long duration group (619 +/- 25 (SE) mg/dl; 2.6 +/- 0.2 ml/min, respectively) than in the DM short (514 +/- 24; 2.0 +/- 0.1) and DM intermediate duration (442 +/- 30; 2.1 +/- 0.1) groups, while urine volume and glycosuria were similar. Following gentamicin the three control groups developed acute renal failure (maximal decrease in Ccr of 60 +/- 7, 72 +/- 9 and 71 +/- 7%, respectively; p less than 0.01 to less than 0.001), lysozymuria and acute tubular necrosis. There were no significant differences in the degree of renal impairment observed among the three control groups. In marked contrast, in the three DM groups these changes were absent and the renal cortical gentamicin content was lower than that of the control groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of duration of diabetes on the protection observed in the diabetic rat against gentamicin-induced acute renal failure. 672 8

The effect of three types of phosphodiesterase (PDE) inhibitors on in vivo antilipolysis was investigated in healthy subjects using a 2-h euglycemic, hyperinsulinemic (40 mU.m-2.min) clamp together with microdialysis of abdominal subcutaneous adipose tissue. During hyperinsulinemia (approximately 330 pmol/l), the circulating glycerol concentration was reduced to approximately 50% of the basal level of 53.2 +/- 3.6 mumol/l, indicating an antilipolytic effect. The decrease in adipose tissue dialysate glycerol, which mirrors the change in interstitial glycerol concentration, was about 40% during hyperinsulinemia when Ringer's solution alone was perfused. Local perfusion with a selective PDE IV inhibitor, rolipram (10(-4) mol/l), did not influence the insulin-induced decrease in dialysate glycerol (F = 0.8 vs. perfusion with Ringer's solution by two-factor analysis of variance [ANOVA]), although rolipram increased the dialysate glycerol level by 144 +/- 7% of the baseline value. However, local perfusion with a selective PDE III inhibitor, amrinone (10(-3) mol/l), or a nonselective PDE inhibitor, theophylline (10(-2) mol/l), abolished the ability of insulin to lower dialysate glycerol (F = 16.5, P < 0.01 and F = 8.5, P < 0.01, respectively, as compared with perfusion with Ringer's solution). The findings could not be explained by changes in the local blood flow (as measured by a microdialysis--ethanol escape technique), which was not affected by hyperinsulinemia in the presence or the absence of PDE inhibitors in the dialysis solvent. We conclude that PDEs play an important role in mediating the antilipolytic effect of insulin in vivo and that PDE III is the dominant isoenzyme modulating this effect.
Diabetes 1995 Oct
PMID:Role of phosphodiesterase III in the antilipolytic effect of insulin in vivo. 755 53

Rats with untreated diabetes mellitus are protected from gentamicin-induced nephrotoxicity. In order to evaluate the role of hyperglycemia, glycosuria, and polyuria in this phenomenon, miniosmotic pumps filled with insulin were implanted for 15 days in seven female Sprague-Dawley rats with streptozotocin-induced diabetes mellitus. Plasma glucose levels were successfully maintained under 126 mg/dl. To serve as the control group, eight age-matched diabetic (plasma glucose > 400 mg/dl) rats had miniosmotic pumps placed delivering only Ringer's solution. Six days after placement of the pumps, gentamicin (40 mg/Kg/day) was administered to all animals for 9 days. The insulin-treated diabetic rats exhibited clear signs of nephrotoxicity by Day 6 of gentamicin, whereas the diabetic control group remained free from any functional or morphological evidence of proximal tubular damage throughout the 9 days of the aminoglycoside administration. At the end of the experiment, the creatinine clearance in the insulin-treated diabetic group was 45% lower than in the untreated diabetic group (P < 0.005). In addition, there was a rise in plasma creatinine (P < 0.02), muramidase appeared in the urine, and mild patchy acute tubular necrosis of the renal cortex was observed by light microscopic examination. The insulin-treated group also accumulated more gentamicin in the renal cortex than the untreated animals (P < 0.005). It is concluded that protection against the nephrotoxic effects of gentamicin is a feature of untreated experimental diabetes mellitus in the rat and that correction of the hyperglycemic state with insulin reverses this resistance.
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PMID:Insulin reverses the protection given by diabetes against gentamicin nephrotoxicity in the rat. 807 55

To study the effects of chronic osmotic diuresis which were not associated with hyperglycaemia on the rat kidney, osmotic diuresis was induced by i.v. infusion of urea. A 5 mol/l urea solution was continuously infused at a rate of 100 ml.kg-1 x day-1 on the basis of body weight on day 0. Duration of infusion was 2, 6, 10 or 14 days. Control rats received continuously infused Ringer's solution. Urea-treated groups developed osmotic diuresis (urine flow = about 0.04 ml.min-1 x 100 g body weight-1) comparable to that in rats with experimental diabetes mellitus induced by i.v. streptozotocin (55 mg/kg), however urea-induced osmotic diuresis was not associated with blood glucose level increases. Compared with their controls, rats receiving urea for 2-14 days had markedly increased kidney weight. Rats receiving urea for 10 days showed greatest kidney weight increase, 0.565 +/- 0.044 g/100 g body weight (mean +/- SD), representing a 53% increase compared with the control (0.369 +/- 0.034 g/100 g body weight). Kidney weight was associated with increases in kidney protein content. In contrast, none of control kidney weight values differed significantly from day 0 values (= normal rats; 0.387 +/- 0.028 g/100 g body weight). Creatinine clearance values in urea-treated groups were also higher than those in controls. The maximum value, 0.65 +/- 0.17.ml-min-1 x 100 g body weight-1, was recorded in the 14-day group and was significantly higher than the corresponding control value (0.34 +/- 0.07 ml.min-1 x 100 g body weight-1) (p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of chronic, urea-induced osmotic diuresis on kidney weight and function in rats. 817 34


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