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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of acute moderate hyperglycemia on local cerebral pH (LCpH) and local cerebral blood flow (LCBF) were studied in rats infused with glucose before middle cerebral artery (MCA) occlusion, and compared with findings in MCA occlusion alone. The effects of nimodipine infusion on LCBF and LCpH in MCA-occluded hyperglycemic rats were also studied. LCpH and LCBF were determined simultaneously by a double-label autoradiographic technique. Hyperglycemia was induced by an intraperitoneal injection of 2 g/kg D-glucose before MCA occlusion. Nimodipine-treated rats received the drug as an intravenous infusion of 0.5 micrograms/kg/min starting 15 min after occlusion, and ending at decapitation 4 h postocclusion. Cortical LCpH of five structures in the MCA territory of hyperglycemic rats varied between 6.64 +/- 0.04 and 6.72 +/- 0.02 (mean +/- SEM). These values were significantly lower than LCpH in the same ischemic structures in the control rats, which varied between 6.76 +/- 0.04 and 6.82 +/- 0.03 (p less than 0.05 for four of five structures). Cortical LCpH of hyperglycemic nimodipine-treated rats ranged between 6.94 +/- 0.02 and 7.05 +/- 0.02, indicating significant elevations in LCpH (p less than 0.001) compared with the untreated ischemic hyperglycemic animals. LCBF in the ischemic structures was not modified by hyperglycemia or nimodipine treatment. This suggests that nimodipine, by mechanisms other than improvement in blood flow, can prevent the enhanced cerebral tissue acidosis produced by hyperglycemia before incomplete focal ischemia.
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PMID:Nimodipine prevents hyperglycemia-induced cerebral acidosis in middle cerebral artery occluded rats. 291 Aug 98

Two methods of administration of amphotericin B were compared for their ability to produce nephrotoxicity in 12 dogs. Six dogs received six alternate day doses of amphotericin B: 1 mg/kg administered as a rapid bolus in 25 mL 5% dextrose in water. Another six dogs received alternate day treatments of the same dose of amphotericin B in 1 L 5% dextrose in water over 5 h. Both treatment groups experienced significant reductions in glomerular filtration rate, as measured by inulin clearance, 24 h endogenous creatinine clearance, serum creatinine and serum urea. This reduction in glomerular filtration rate was most marked in the group receiving the drug as a rapid bolus. The inulin clearances decreased from 3.54 +/- 0.30 mL/min/kg (means +/- SEM) on day 0 to 1.15 +/- 0.25 mL/min/kg on day 12 in the slow infusion group and from 3.24 +/- 0.25 mL/min/kg on day 0 to 0.46 +/- 0.11 mL/min/kg on day 12 in the rapid bolus group. Renal lesions characteristic of amphotericin B administration were observed in all dogs tested. The dogs which received amphotericin B as a rapid bolus had a significantly greater number of tubular lesions than the slow infusion group. Systemic side effects, such as vomiting, diarrhea and weight loss, were observed in both treatment groups but were most severe in the rapid bolus group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nephrotoxicity of amphotericin B in dogs: a comparison of two methods of administration. 291 23

Twenty healthy female patients undergoing laparoscopy were allocated randomly to receive either cisapride 10 mg i.v. in 5% dextrose 20 ml or placebo 15 min before antagonism of residual neuromuscular blockade with atropine 1.2 mg and neostigmine 2.5 mg. Barrier pressure (BrP = lower oesophageal sphincter (LOS) pressure minus gastric pressure) increased significantly (by 25%) following cisapride, but not placebo, within 10 min of injection; following the combined administration of atropine and neostigmine, there was an abrupt decrease in mean BrP in the cisapride group from 37.0 (SEM 4.5) cm H2O to 24.1 (3.2) cm H2O (P less than 0.01) and in the control group from 26.6 (4.8) cm H2O to 19.9 (3.1) cm H2O (P less than 0.05) 2 min after injection. Subsequently, there was a small increase in BrP to values not significantly lower than control measurements. Thus the administration of cisapride before antagonism of neuromuscular blockade with atropine and neostigmine failed to block the adverse effect of atropine on the LOS.
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PMID:Effects on the lower oesophageal sphincter of cisapride given before the combined administration of atropine and neostigmine. 292 63

Few data are available on energy requirements of mechanically ventilated, critically ill children. We measured the resting energy expenditure in 18 mechanically ventilated patients between ages 2 and 18 years, using indirect calorimetry. All patients had fractional inspired oxygen concentration less than 0.6, no spontaneous respirations, hemodynamic stability, and no fever or active infection, and were receiving 5% dextrose. All subjects were hypermetabolic, since the measured resting energy expenditure divided by the predicted basal energy expenditure from the Harris-Benedict equations was 1.48 +/- 0.09 (mean +/- SEM). The energy requirements calculated using "injury factors" and "activity factors" adapted for adults is 1.62 times basal energy expenditure. The injury factor for the pediatric multiple trauma patients should be 1.25 compared with 1.35 in adults. In these pediatric intensive care patients 33% +/- 8% of the energy is derived from carbohydrates, 53% +/- 8% from fat, and 14% +/- 2% from protein oxidation. In individual critically ill pediatric patients, energy requirements should be estimated by measuring their resting energy expenditure whenever possible and adding 5% for their activity. In the absence of the actual measurement of resting energy expenditure, the recommended energy requirement is 1.5 times basal energy expenditure. In this acute phase of injury, the daily nitrogen requirement is 250 mg per kilogram of body weight.
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PMID:Measured energy expenditure in pediatric intensive care patients. 292 33

Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0 meq/liter). Hypoxic rats also showed evidence of tissue hypoxia; liver tryptophan oxygenase levels were increased to 21 +/- 2 nmole/min/mg protein. In the hypoxic animals there was decreased jejunal mucosal (Na+-K+)-ATPase activity and an inhibition of active intestinal transport of sodium, glucose, 3-O-methylglucose, galactose, tyrosine, phenylalanine, and glycine as determined by in vivo perfusion studies. Jejunal fructose transport, which has a large passive component, was unaffected by hypoxia. The electrolyte, carbohydrate, and amino acid transport alterations produced by hypoxia were seen in the absence of an effect on jejunal cell number, DNA synthesis, or cell turnover. There was also no evidence of histological or ultrastructural damage. Furthermore, studies with a luminal macromolecular tracer, horseradish peroxidase, indicated that the jejunal lumen-to-blood barrier to macromolecules was also unaltered in these hypoxic animals. In vitro local oxygenation of the jejunum, by bubbling of 95% O2:5% CO2, markedly improved sodium and glucose (but not 3-O-methylglucose) absorption in hypoxic rats and control rats. The (Na+-K+)-ATPase activity of the jejunal mucosa of hypoxic rats was significantly enhanced by the local bubbling of 95% O2:5% CO2. Overall, our data indicate that during relatively mild conditions of hypoxia there is an inhibition of jejunal (Na+-K+)-ATPase activity and related transport processes that is prevented by in situ oxygenation.
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PMID:Alterations in jejunal transport and (Na+-K+)-ATPase in an experimental model of hypoxia in rats. 300 54

The initial clearance of Candida albicans in situ by hepatic tissue was investigated using the isolated perfused mouse liver model in combination with various monosaccharides. When 10(6) yeasts were infused into untreated ICR mouse livers, approximately 61 +/- 2% (mean + SEM) were recovered from the liver and 13 +/- 2% in the effluent for a total recovery of 74 +/- 2%. This suggests that 26 +/- 2% of the infused yeasts were eliminated within the liver and that a total of 87 +/- 1% were trapped (% in the liver + % killed) by the liver. In contrast, when either D-mannose or alpha-methyl-D-mannoside, but not glucose, sucrose, lactose or mannitol, were added to perfusion media (1% w/v) the ability of hepatic tissue to trap C. albicans decreased, in a dose-dependent manner, with increasing concentrations of monosaccharide. Decreased trapping was due to the interaction of these monosaccharides with hepatic tissue and not directly with yeasts. The data suggest that one component of in situ hepatic clearance of C. albicans was the binding of mannose containing structures on the surface of yeasts, most probably by hepatic mannose receptors.
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PMID:The effect of monosaccharides on in situ hepatic trapping of Candida albicans. 306 44

Cultured IM-9 lymphocytes were preincubated with 1 microM insulin, a condition resulting in a 56% reduction in cell surface insulin receptors. Cellular proteins were then metabolically labeled, and the radioactivity incorporated into the insulin proreceptor and receptor mature subunits was measured over a 4-hr chase period. As early as 30 min of chase, incorporation into the proreceptor was 28 +/- 6% higher in down-regulated cells than in control cells (mean +/- SEM, P less than 0.05). By 1 hr of chase, the difference reached 41 +/- 14% for the proreceptor and 84 +/- 28% for the alpha subunit (P less than 0.01); values returned to normal by 2 hr. At 4 hr of chase, labeling of the alpha subunit of down-regulated cells was diminished 36 +/- 9% below control (P less than 0.05). The increased biosynthetic rate of the proreceptor was more prominent when the chase medium contained 25 microM monensin, an inhibitor of processing of the proreceptor into mature subunits. Similar effects occurred whether [3H]mannose or [3H]lysine was used as biosynthetic marker. The effect was specific for the insulin receptor. These data demonstrate that insulin receptor homologous down-regulation is associated with increased proreceptor biosynthesis and processing into mature subunits. This might represent a cellular mechanism compensating for insulin-induced receptor loss.
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PMID:Homologous down-regulation of the insulin receptor is associated with increased receptor biosynthesis in cultured human lymphocytes (IM-9 line). 309 91

Gastric emptying was measured in 12 patients with chronic duodenal ulceration and compared with the results from 10 healthy volunteers. The test meal of 300 ml 15% dextrose, labelled with 99mTc-DTPA, was ingested in increments over 6 min. Gamma camera imaging proceeded over 30 min, with a 1-min frame time. A direct correction was applied for the fraction emptying into the small bowel during the ingestion period. Gastric emptying at 6 min was significantly greater in the group with duodenal ulcer (14.4 +/- 2.7% vs. 4.2 +/- 0.9%: mean +/- SEM, p less than 0.01). From this time onwards there were no significant differences in the rates of gastric emptying. These results suggest that chronic duodenal ulcer is associated with an abnormal pattern of gastric emptying of liquid, characterised by an initial rapid phase.
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PMID:Abnormal pattern of gastric emptying of liquid in chronic duodenal ulcer. 323 30

To determine the safety, efficacy, and the ventilatory responses to carbon dioxide (CO2) of mini-dose intrathecal morphine, 33 healthy women who underwent cesarean section with spinal anesthesia using 0.75% bupivacaine in 8.25% dextrose were studied. Patients were randomly assigned to receive, in a double-blind fashion, either morphine 0.25 mg (group I, n = 11), morphine 0.1 mg (group II, n = 10), or saline (group III, placebo group, n = 12) in 0.5 ml volume mixed with the bupivacaine. In both groups I and II excellent postoperative analgesia with long duration was obtained (27.7 +/- 4.0 and 18.6 +/- 0.9 hours, respectively, X +/- SEM). All patients in group III required an analgesic (8 mg subcutaneous morphine) within 3 hours of spinal anesthesia. Seven patients in group I and four patients in group II developed mild pruritus that did not require treatment. Ventilatory responses to CO2 showed no evidence of depression attributable to either the 0.25 or 0.1 mg of morphine, but significant depression of the CO2 responses was observed in group III patients after administration of subcutaneous morphine. It is concluded that a dose as low as 0.1 mg of intrathecal morphine gives excellent analgesia with minimal to no side effects and that subcutaneous morphine is associated with marked depression of the ventilatory variables.
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PMID:Mini-dose intrathecal morphine for the relief of post-cesarean section pain: safety, efficacy, and ventilatory responses to carbon dioxide. 327 78

To demonstrate the dependence of fetal pituitary LH secretion endogenous GnRH, we studied the effects of bolus iv administration of a specific GnRH antagonist analog [GnRH-Ant; (N-acetyl-D-p-chloro-Phe1,2,D-Trp3,D-Arg6,D-Ala10)GnRH] on pulsatile LH release in 10 chronically cannulated ovine fetuses of 104-129 days gestation (term, 147 days). Vehicle alone was given to 13 control fetuses of 107-125 days gestation. Blood samples for LH determination by RIA (NIH LH S16 standard) were taken after injection of either GnRH-Ant (175-300 micrograms dissolved in 1 ml 5% dextrose in water) or vehicle alone for 1.75-5 h. The efficacy of GnRH receptor blockade was then assessed by a bolus iv challenge with 50 micrograms synthetic GnRH. The mean (+/- SEM) observation period per animal was similar for the two groups (3.8 +/- 0.2 h for GnRH-Ant; 3.6 +/- 0.2 h for controls). The frequency of spontaneous pulsatile LH secretion was significantly decreased in the fetuses given GhRH-Ant (2 pulses over 38 h total observation vs. 13 pulses over 47.3 h in control fetuses; P = 0.006). The average interpulse interval was 19.0 h in the GnRH-Ant group compared to 3.6 h in controls. Although the mean pulse amplitude was lower in the GnRH-Ant group (2.8 +/- 1.2 vs. 7.6 +/- 1.1 ng/ml for controls), this difference was not statistically significant (P = 0.065, by one-tailed t test). The mean peak serum LH concentration in response to the GnRH challenge was significantly blunted in the GnRH-Ant group (4.6 +/- 0.8 vs. 20.6 +/- 1.8 ng/ml for controls; P less than 0.001). These results indicate that GnRH-Ant administration causes a virtual cessation of pulsatile LH discharge. As this GnRH-Ant blocks GnRH action at the receptor level, these data demonstrate that pulsatile LH secretion in the ovine fetus is dependent on endogenous GnRH release as early as 104 days gestation.
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PMID:Control of gonadotropin secretion in the ovine fetus: the effects of a specific gonadotropin-releasing hormone antagonist on pulsatile luteinizing hormone secretion. 329 44


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