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

In this study the cryo-unit is introduced as a new and useful instrument to investigate water-containing specimens with the SEM. Often water-containing biological specimens are studied, but in our case we used water-swollen polymer membranes. The results show that application of a cryo-unit permits the study of this material at low temperatures up to magnifications of about 10 000 times, while other techniques failed to give reproducible results.
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PMID:A rapid preparation technique for studying highly water-swollen membranes with a scanning electron microscope (SEM) supplied with a cryo-unit. 73 87

A multilumen balloon tube constructed to separate duodenal and jejunal perfusion segments was placed in the proximal small bowel of 6 healthy volunteers. The effect of nutrient mixture in the duodenum on net jejunal water and electrolyte flux was then determined. The duodenum was perfused with a balanced electrolyte solution before and after the nutrient perfusion. Net water flux in the perfused jejunum changed from absorption 27.0 +/- 6.0 microliter/min/cm, (mean +/- SEM) to secretion 7.7 +/- 7.3 microliter/min/cm (P less than 0.025) during nutrient perfusion. There was also net chloride secretion and decreased net absorption of Na, K, and HCO3 (P less than 0.05). The jejunal absorption of water and electrolytes before and after the duodenal nutrient perfusion was the same. Results indicate that intestinal secretion may occur under physiologic conditions at sites remote to the application of food in humans.
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PMID:Jejunal secretion in response to a duodenal mixed nutrient perfusion. 75 54

Elevated intrathoracic pressure due to positive end-expiratory pressure (PEEP) has the potential for increasing intracranial pressure (ICP) and reducing arterial blood pressure (BP). Such changes could critically reduce cerebral perfusion pressure (CPP = BP - ICP), This possibility was investigated in 15 cats with artificially-produced expanding intracranial masses (intracranial balloon). The interrelationships among ICP and central venous and arterial pressures were observed during application and removal of graded levels of PEEP (5, 10, 15 cm H2O). The electroencephalogram and pupillary diameters were monitored. At various levels of ICP, nine of the cats were given oleic acid intravenously to embolize the lung and cause pulmonary dysfunction. In cats not given oleic acid, PEEP caused a maximal reduction in cerebral perfusion pressure of 45 +/- 4 torr(SEM), accompanied by variable changes in ICP. PEEP application in the absence of oleic acid embolization of the lungs caused electroencephalographic abnormalities in 77% of these cats, while pupillary diameters increased in 56%. Animals embolized wwith oleic acid had significantly less (P less than .001) severe CPP reductions (mean 21 +/- 4 torr) than did the non-embolized animals, and developed no EEG change due to PEEP. However, increases in pupillary diameter still occurred in 33% of cats given oleic acid when PEEP was applied. In 82% of the PEEP applications (n = 44) in both experimental groups only insignificant increases in intracranial tension occurred (average peak ICP gain less than 1.5 torr). Abrupt increases in ICP exceeding 11 torr (15 cm H2O) occurred in four animals in each group. This happened most frequently (63 per cent) when the intracranial tension before PEEP was above 15 torr. Sudden removal of or reduction in PEEP was accompanied by increases in arterial and intracranial pressures in both groups, although this response was attenuated in the cats given oleic acid. The results indicate a potential for PEEP to evoke neurolgic complications in patients who have intracranial disease and that the presence of pulmonary disease may attenuate these deleterious side effects. Monitoring of neurologic function as well as blood-gas and cardiovascular effects of PEEP in patients who have intracranial disease is suggested.
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PMID:Intracranial responses to PEEP. 78 78

The pharmacokinetics of orally administered aqueous 3H-beta-methyldigoxin solutions were studied at two dose levels, 0.3 and 0.6 mg, in healthy human subjects. The drug and its metabolites were specifically assayed in biological fluids and compared with results after intravenous doses to the same subjects. No significant dose dependency was observed. The apparent half-life of absorption was 16+/-6 min (SEM). Digoxin was the only metabolite observed in the plasma and comprised 28.6+/-3.7% of the dose in the urine. 3H-beta-Methyldigoxin, renally excreted unchanged, comprised 25.7+/-1.7% (SEM). Water-soluble metabolites in the urine comprised 9.0+/-1.8%. Fecal and urinary excretion accounted for 85% of the dose at 144 hr. The oral absorption of unchanged 3H-beta-methyldigoxin from solution was 59+/-6% by area under the curve methods and 60+/-4% by renal excretion. A total of 73% of the dose in the solution was absorbed as beta-methyldigoxin and digoxin. First-pass metabolism prior to absorption was largely prehepatic and assignable to GI degradation; 21.9+/-2.8% was degraded with 12.8+/-4.0% to digoxin and 9.1+/-4.0% to water-soluble metabolites. From 14 to 18% of the administered oral dose did not reach the systemic circulation. Analog computer fitting of plasma and urine levels of drug and digoxin was consistent with the first-pass premise with a delayed absorption of GI-generated digoxin and other metabolites. There were no significant differences between the oral absorption of a tablet formulation and the solution. Orally administered beta-methyldigoxin solution delivered 97% cardioactivity as itself and digoxin with respect to an equivalent amount of intravenously administered digoxin. This value contrasts to the 140% delivered by intravenously administered beta-methyldigoxin on the premise of pharmacodynamic equivalence of systemically appearing digoxin and beta-methyl-digoxin. Literature reports on the oral bioavailability of solutions and solid dosage forms of digoxin were critically reviewed, but no reliable comparison of the extent and reproducibility of oral absorption of cardioactive agents from administered digoxin or beta-methyldigoxin could be made from the widely variable digoxin studies with nonspecific assays.
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PMID:Pharmacokinetics of beta-methyldigoxin in healthy humans II: Oral studies and bioavailability. 84 95

Rat posterior pituitaries were extracted in acid and total rat neurophysins were isolated. Preparative disc gel electrophoresis separated the total neurophysins into three main peptides of differing electrophoretic mobility. Antisera raised in rabbits recognized a common antigenic site in the three peptides and identical radioimmunoassay standard curves were obtained with each of the isolated rat neurophysins. A homologous rat neurophysin radioimmunoassay was utilized to measure neurophysin in samples of unextracted rat plasma. Basal neurophysin levels, 3.7 +/- 0.2 ng/ml (mean +/- SEM), did not differ in samples collected by decapitation, carotid artery cannulation, or tail vein bleeding. Water-loading caused a significant reduction in neurophysin, 2.8 +/- 0.1 ng/ml, while hypertonic saline and dehydration caused a significant elevation, 10.4 +/- 2.1 and 8.0 +/- 1.4 ng/ml, respectively. A step-wise decrease in blood volume caused a step-wise increase in plasma neurophysin concentrations which returned to baseline with reinfusion of the withdrawn blood. A second hemorrhage caused an even greater release of neurophysin indicating large neurophysin reserve in the pituitary. In periodic tail vein samples over 23 days of pregnancy a rise in plasma neurophysin was found from day 14 continuing to parturition with a peak value of greater than 13 ng/ml by day 21. Two days postpartum the value was 4.6 +/- 0.3 ng/ml. With this homologous assay, the basal levels of plasma neurophysin are lower and the stimulated values higher than with previously reported heterologous assays. Therefore, the relative change with physiologic maneuvers is distinctly increased.
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PMID:Isolation, radioimmunoassay and physiologic secretion of rat neurophysins. 84 27

Six patients with vasopressin-responsive diabetes insipidus (DI) received clofibrate and chlorpropamide, singly and in combination. Decrease in urinary output averaged (mean +/- SEM): (1) clofibrate 2 g/day, 47% +/- 6%; (2) chlorpropamide 250 mg/day 59% +/- 5%; (3) clofibrate 2 g/day plus chlorpropamide 125 mg/day, 54% +/- 7%; (4) clofibrate 2 g/day plus chlorpropamide 250 mg/day 61% +/- 4%. Water deprivation tests before and during treatment showed significantly higher basal, final, and peak urinary osmolalities (Uosm) and lower free water clearance (CH20) on chlorpropamide, singly and in combination: clofibrate raised Uosm less but significantly decreased CH2O. Water load tests before and during treatment showed that chlorpropamide, singly and in combination, markedly decreased maximal urinary flow, maximal CH2O, percentage water load excreted, and increased minimal Uosm; clofibrate significantly decreased maximal urinary flow and CH2O only. One patient responded only to combination therapy. Chlorporpamide caused serious hypoglycemia in three of six patients. Clofibrate had no significant side effects.
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PMID:Comparison of clofibrate and chlorpropamide in vasopressin-responsive diabetes insipidus. 86 82

The purpose of this study was to determine the effects of chronic administration of nicotine on red blood cell (RBC) velocity in single capillaries of the mesentery. Ten male rats consumed an average of 2.38 mg nicotine/kg/day, an approximate '2 pack' equivalent, in their drinking water for a period of 15-20 weeks. At the end of this time RBC velocity was measured in single capillaries of the mesentery. The data were compared to RBC velocities measured in a group of matched control rats. Red cell velocities in the control and nicotine groups averaged 1.22+/-0.23 and 0.59+/-0.10 mm/sec SEM, respectively. These values were significantly different (p less than or equal to 0.01). It is concluded that chronic administration of nicotine to rats in levels equivalent to tobacco smoking reduces resting capillary blood flow in the mesenteric circulation as indicated by differences in erythrocyte velocity.
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PMID:Effects of chronic nicotine administration on RBC velocity in mesenteric capillaries of the rat. 87 34

The urinary exretion of chromium was studied for relationships to atherosclerotic diseases in two rural Finnish male populations, aged 55 to 74; one from eastern Finland, the other from the southwestern part of the country. A 10-year follow-up had shown a particularly high mortality from coronary heart disease in the eastern area where the concentrations of chromium in the drinking water were lower than in the western area. The 24-hr urinary excretions of chromium of the two populations were markedly low (east, mean +/- SEM, 3.60 +/- 0.15 microgram; west, 3.74 +/- 0.13 microgram), suggesting a suboptimal chromium intake in both populations. No consistent differences were found in urinary chromium excretions between groups with atherosclerotic diseases and reference groups. The role of low chromium intake in the pathogenesis of atherosclerosis deserves further study.
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PMID:Urinary chromium excretion and atherosclerotic manifestations in two Finnish male populations. 88 61

To test the hypothesis that fetal lung maturation can be accelerated by one of the xanthine derivatives, aminophyllin was given to 40 pregnant rabbits beginning on the 20th gestational day for a period of 7-10 days. The fetuses were delivered by cesarean section and fetal lung maturity was assessed by determining the biochemical, functional, and ultrastructural characteristics of aminophyllin-treated vs. control animals. The phospholipid content of the lung tissue homogenate from the aminophyllin-treated group was significantly higher than in the control subjects (saline injected) at 28 days of gestation (421 +/- 9 vs. 368 +/- 12 mug/mg wet wt, mean +/- SEM) and at 29 days of gestation (531 +/- 10 vs. 475 +/- 20). The alveolar wash phospholipid content of the aminophyllin-treated group was higher at 30 days (167 +/- 9 mug/mg dry wt, mean +/- SEM vs. 117 +/- 17). The lung compliance derived from pressure volume curves was also significantly higher in the aminophyllin-treated group when compared with controls at 27 days of gestation (0.023 +/- 0.0005 ml/cm H2O, mean +/- SEM vs 0.010 +/- 0.0002) and at 28 days of gestation (0.048 +/- 0.0003 vs 0.035 +/- 0.0006). There was no significant difference in the number of lamellar bodies in the type II cells between the aminophyllin-treated and the control groups. The data show that aminophyllin has accelerating effects on fetal lung maturation in rabbits when the drug is given to pregnant rabbits during the last 7-10 days of gestation.
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PMID:Acceleration of fetal lung maturation by aminophyllin in pregnant rabbits. 94 Jun 98

To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 mug/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0+/-0.5 to 27.0+/-5.5 (SEM) ml/h (P less than 0.05), lymph; plasma globulin concentration ratio to increase from 0.62+/-0.01 to 0.67+/-0.02 (P less than 0.05), left atrial pressure to fall from 1+/-1 to -3+/-1 cm H2O (P less than 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial PCO2, pH, and hematocrit, and decreases in cardiac output and arterial PO2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/kg per h) did not affect the histamine lymph response. We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions.
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PMID:Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability. 95 73


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