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

We assessed the effect of nedocromil sodium on bronchoconstriction and airway responsiveness induced by platelet-activating factor (PAF) in eight normal subjects, in a double-blind, placebo-controlled cross-over study. Subjects inhaled PAF by a dosimeter method in 5 doses of 18 micrograms each, separated by an interval of 15 min, (total dose of 90 micrograms). Airway calibre was measured by partial expiratory flow at 30% of vital capacity (Vp30) before and at 1, 3, 5, 10 and 15 min after each dose of PAF. The bronchoconstrictor response was assessed by measuring the area under the curve of the percentage fall in Vp30 over time. There was a significant reduction in PAF-induced bronchoconstriction after nedocromil sodium (1,225 +/- 392 arbitrary units; mean +/- SEM) compared to placebo (2,395 +/- 598; p < 0.01). There was no significant difference in the fall in peripheral neutrophil count measured at 5 min after PAF with nedocromil sodium (48.5 +/- 9.5%) compared to placebo (43.3 +/- 6.8%). In conclusion, nedocromil sodium significantly attenuates PAF-induced bronchoconstriction but not the peripheral neutropenia in normal subjects. Since PAF is not a direct constrictor of human airway smooth muscle, this effect of nedocromil sodium may indicate inhibition of release of bronchoconstrictor mediators.
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PMID:Attenuation of platelet-activating factor induced bronchoconstriction by nedocromil sodium. 133 35

Intracellular pH (pHi) of cultured bovine trabecular cells was measured using video-imaging techniques with a pH-sensitive intracellular fluorescent dye, BCECF. In bicarbonate-rich Ringer at pH 7.4, pHi was 7.29 +/- 0.03 (+/- SEM, n = 12 monolayers, 120 cells sampled). Exposure to 20 mM NH4Cl immediately alkalinized pHi: replacement with a Na(+)-rich solution acidified pHi before recovery to resting levels. When NH4Cl was replaced by a low Na+ solution, acidification was sustained but pHi recovery occurred after Na(+)-rich solution. A pHi of 7.11 +/- 0.02 (n = 2 monolayers, 20 cells) occurred in pH 6.8 and pHi was 7.72 +/- 0.03 (n = 2 monolayers, 20 cells) in pH 8.0. Amiloride (1 mM) acidified pHi but DIDS (1 mM) treatment, HCO3(-)-free condition, 1 mM ouabain, 50 mM K+, and 2 mM BaCl2 failed to change pHi. Hydrogen peroxide (1 mM) acidified pHi but no change occurred with 50 microM. Trabecular cells possess an Na+/H+ exchanger similar to that in other cell types.
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PMID:Intracellular pH regulation by a Na+/H+ exchanger in cultured bovine trabecular cells. 133 29

The potential of hydrogen peroxide to reduce the levels of salivary thiol precursors of oral malodor was investigated in-vitro and in-vivo. In both cases the concentration of thiol groups was determined colorimetrically by quantitative reaction with 4,4'-bis (dimethylamino) diphenyl carbinol. Addition of volumes of hydrogen peroxide solution (containing between 0.18 and 0.90 mmol) to premeasured aliquots of saliva in-vitro, resulted in reductions in salivary thiol levels of between 53% and 75% compared to controls. This positive indication prompted an in-vivo investigation. The efficacy of a fluoride-containing test toothpaste also containing 0.67% hydrogen peroxide and 5.48% sodium bicarbonate was evaluated in a crossover study using ten male and female subjects (non-smokers). All subjects used the test product and a control fluoride dentifrice, in a random order. For the duration of the study subjects used a standard silica based toothpaste containing 1500 ppm F (as sodium monofluorophosphate) exclusively for their normal oral hygiene. On each sampling morning they refrained from oral hygiene and eating and drinking on rising. At the test facility they generated a background saliva sample stimulated by chewing unflavored, unsweetened gum. Subjects brushed for 1 minute with 1.50 (+/- 0.05) g test or control paste and generated another saliva sample as before, 30 minutes after product application. Using the same analytical procedures the mean (+/- SEM) percent reduction in salivary thiol levels post treatment compared to baseline was found to be 59.0 (+/- 7.0)% for the test product compared with 12.5 (+/- 5.2)% for the fluoride control paste.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction in the levels of oral malodor precursors by hydrogen peroxide: in-vitro and in-vivo assessments. 133 26

E. histolytica trophozoites cultivated for > 7 h in the presence of glycosidases, produced by a subset of the colonic anaerobic bacteria of healthy humans, and pancreatic proteases show decreased adherence to Chinese hamster ovary epithelial cells. Since activities of the glycosidases are enhanced by bile salts we investigated whether bile salts would enhance the E. histolytica-CHO cell adherence decreasing effects of the luminal hydrolases (glycosidases plus proteases). CHO cell adherence of control trophozoites was 78.4 +/- 1.2% (mean +/- SEM). Incubations with the hydrolases alone for 4 h did not change adherence. Addition of 5.0 mM sodium taurocholate to the hydrolases for 4 h decreased trophozoite adherence to 30.5 +/- 3.2% of that of control trophozoites (p < 0.05). The effect of sodium taurocholate was dose dependent over 0.5-5.0 mM. Four hour incubation with the hydrolases and sodium taurodeoxycholate at 2.0 and 5.0 mM also decreased trophozoite adherence to 25.1 +/- 2.9% and 29.4 +/- 1.7%, respectively, of that of control trophozoites. These findings show that bile salts enhance the effects of luminal hydrolases on E. histolytica trophozoites, decreasing their ability to adhere to epithelial cells.
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PMID:Bile salts promote adherence-decreasing effect of colonic luminal hydrolases on Entamoeba histolytica. 134 Feb 99

To investigate the effect of substrates during oral rehydration therapy, we studied intestinal cation cotransport (ICC) with glutamine (Gln), alanine (Ala) and glucose (Glu). The specific aims were to determine the biological effects of these three different cotransport systems on intestinal function. Isolated rabbit ileal mucosa preparations mounted in Ussing chambers were studied. ICC was determined by measuring short-circuit current (Isc) and potential difference (PD) while monitoring tissue resistance (TR). The data are reported as the mean +/- SEM of 4-6 experiments for each amino acid concentration. Increasing concentrations of Gln (10(-5) to 10(-2) M), Ala (10(-5) to 10(-1) M) and Glu (10(-5) to 10(-2) M) caused a significant (P < 0.05) increase in ICC. Gln (30 mM) and Ala (0.1 M) had a maximal effect (Em(Gln) = 100% and Em(Ala) = 66%, P < 0.05) which was higher than that obtained with 30 mM Glu (Em(Glu) = 35%). When sodium was replaced with choline on the mucosal side, Ringer solution completely abolished the response with Gln, Ala and Glu. The presence of all three substrates (10(-2) M Gln, 10(-1) M Ala, and 10(-2) M Glu) in Ringer solution on the mucosal side caused a significant increase in ICC (delta increase of short circuit current = 111 +/- 43 microA, P < 0.05). These results demonstrate that Gln, Ala and Glu each increased sodium-dependent cation cotransport, and that sodium-dependent intestinal cation cotransport was higher with Gln than with Ala or Glu.
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PMID:Cotransport of sodium with glutamine, alanine and glucose in the isolated rabbit ileal mucosa. 134 39

The goal of this study was to compare the efficacy of esmolol and sodium nitroprusside (SNP) as primary drugs for producing controlled hypotension and limiting blood loss during orthognathic surgery. Thirty ASA physical status I and II patients (mean age 22 yr) undergoing LeFort I maxillary osteotomies were randomly assigned to receive either esmolol (n = 15) or SNP (n = 15) as the primary drug to induce hypotension. All patients received a balanced anesthetic technique including isoflurane, with controlled hypotension during the downfracture of the maxilla. Patients assigned to the esmolol treatment group received boluses of 500 micrograms/kg of esmolol, followed by a continuous infusion of 100-300 micrograms.kg-1.min-1, and the SNP treatment group received a continuous infusion of SNP at 0.25-4.00 micrograms.kg-1.min-1; both infusions were titrated to obtain a mean arterial blood pressure within the target range of 55-65 mm Hg. The mean arterial blood pressure during the hypotensive period was 58.7 +/- 0.7 (mean +/- SEM) and 61.8 +/- 0.4 mm Hg for esmolol and SNP, respectively (P less than 0.001). In addition, 40% +/- 4% of the observed values in the esmolol group and 53% +/- 3% in the SNP group were outside the target range for mean arterial blood pressure (difference significant at P less than 0.05), and a greater proportion of the deviations were above 65 mm Hg in the SNP group than in the esmolol group (0.64 vs 0.46, respectively, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Esmolol is more effective than sodium nitroprusside in reducing blood loss during orthognathic surgery. 845 90

Currently normotensive offspring of essential hypertensive parents often have disturbances in blood pressure (BP) regulation such as abnormalities in electrolyte homoeostasis, increased salt-sensitivity and/or impaired renal Na(+)-excretion. Whether an altered reactivity to mineralocorticoids may also play a role is presently unknown. Therefore, we investigated BP (recorded during 24 h), plasma atrial natriuretic factor (ANF), cyclic guanosine monophosphate (cGMP), aldosterone (PA) and renin activity (PRA), 24-h urine electrolyte and cGMP excretions measured on 4 consecutive days, as well as other variables, after 1 week on placebo and after 3 weeks of 9 alpha-fludrocortisone-acetate (9 alpha F) administration, 0.6 mg/d in 12 normotensive sons of essential hypertensive parents (SEH) and 12 body-mass-index- and age-matched (25 +/- 1[+/-SEM]yr) sons of normotensive parents (SN). On placebo, the 2 groups did not differ significantly in average 24 h BP (mean BP 95 +/- 2 vs 95 +/- 2 mmHg), plasma-ANF (40 +/- 7 vs 30 +5 pg/ml), cGMP (6 +/- 0.4 vs 6 +/- 0.5 nmol/l), PRA (1.3 +/- 0.1 vs 1.6 +/- 0.2 ng/ml/h), PA (9 +/- 0.5 vs 10 +/- 0.9 ng/dl), hematocrit (44 +/- 0.7 vs 44 +/- 0.4%) and 96-h urinary-Na+ (mean 205 +/- 13 vs 195 +/- 16 mmol/d), -K+ (69 +/- 6 vs 78 +/- 7 mmol/d) or -cGMP (461 +/- 35 vs 483 +/- 32 nmol/d). 9 alpha F significantly increased BP in SEH (p < 0.005) but not SN (107 +/- 2 vs 100 +/- 2 mmHg, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhanced blood pressure response to mineralocorticoid stimulation in normotensive members of hypertensive families. 136 64

Triggered arrhythmias in rat right ventricular trabeculae are induced by triggered propagated contractions (TPCs) that start in damaged regions of the muscle and propagate along the preparation. We analyzed the effects of the Na+/Ca2+ overload inhibiting agents R 56865 on both TPCs and triggered arrhythmias. This compound has been shown to prevent ultrastructural signs of intracellular calcium overload and arrhythmias caused by exposure to toxic concentrations of cardiac glycosides. TPCs were induced by trains of 15 stimuli (2 Hz, 15 s intervals) at 19-21 degrees C and a [Ca2+]o of 1.0-2.5 mM in the superfusate. Force was measured with a silicon strain gauge; length and shortening of sarcomeres were measured at two sites of the muscle using laser diffraction techniques. Exposure to 1.14 x 10(-7) M R 56865 for 30 min decreased the force of the last stimulated twitch (twitch force) to 89.7 +/- 4.7% (mean +/- SEM) of control, the force produced by TPCs to 39.4 +/- 9.8%, and the velocity of propagation of TPCs to 52.8 +/- 6.3%, while TPC latency increased not significantly to 104.7 +/- 2.8% of control. R 56865 suppressed TPC force, for the same small decrease in twitch force (10%), significantly more than 100 nM D-600 did (29.5 +/- 2.0 vs. 12.4 +/- 3.1%). Eventually, TPCs disappeared in 8 of 14 muscles, in 2 of them without any decrease in twitch force. At 5.7 x 10(-7) M, R 56865 abolished TPCs in five additional trabeculae. An increase in [Ca2+]o reintroduced TPCs. During stimulation of 0.5 Hz, 1.14 x 10(-7) M R 56865 increased the stimulus threshold by 21 +/- 4% in 6 of 14 muscles and decreased the twitch force by 26 +/- 3% in 7 of 14 trabeculae. Triggered arrhythmias were induced in six muscles with the use of 0.5 mM caffeine or 5 nM Bay K 8644; R 56865 rapidly terminated these arrhythmias in all muscles. Although the mechanism of the antiarrhythmic effects of R 56865 remains to be determined, we speculate that the drug raises the threshold for both generation of triggered action potentials and calcium-induced calcium release from the sarcoplasmic reticulum.
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PMID:Suppressive effects of R 56865 on triggered propagated contractions and triggered arrhythmias in rat cardiac trabeculae. 138 Oct 9

Hyperammonemia increases brain glutamine levels, causes astrocytic swelling, and depresses cerebral blood flow (CBF) responsivity to CO2. Methionine sulfoximine (MSO) inhibition of glutamine synthetase activity, known to be enriched in astrocytes, prevents ammonia-induced increases in brain glutamine and water content. We tested the hypothesis that inhibition of glutamine accumulation restores CBF responsivity to CO2 during acute hyperammonemia. Pentobarbital-anesthetized rats treated with either vehicle or MSO (150 mg/kg i.p.) received a 6-hour intravenous infusion of either sodium or ammonium acetate. With subsequent induction of hypercapnia, CBF increased from 113 +/- 14 (mean +/- SEM) to 194 +/- 9 ml/min per 100 g in control rats but was unchanged from 107 +/- 13 to 79 +/- 10 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats restored the CBF response to hypercapnia (from 73 +/- 8 to 141 +/- 14 ml/min per 100 g). With induction of hypocapnia, CBF decreased from 114 +/- 11 to 88 +/- 11 ml/min per 100 g in control rats but increased from 112 +/- 13 to 142 +/- 19 ml/min per 100 g in hyperammonemic rats. Treatment with MSO in hyperammonemic rats did not fully restore the response to hypocapnia but prevented the paradoxical increase in CBF (from 80 +/- 8 to 80 +/- 8 ml/min per 100 g). In control rats, MSO did not affect CO2 responsivity. Treatment with MSO prevented ammonia-induced increases in intracranial pressure. Hyposmotic-induced increases in brain water content and intracranial pressure attenuated the CBF response to hypercapnia but, unlike hyperammonemia, did not attenuate the response to hypocapnia. In contrast to hypercapnia, vasodilation in response to arterial hypotension was intact in hyperammonemic rats. We conclude that the grossly abnormal CBF responsivity to CO2 alterations during hyperammonemia is linked to glutamine accumulation rather than ammonia per se. Cerebral edema secondary to glutamine accumulation may contribute in part to abnormal CBF responses, although other aspects of astrocyte dysfunction are likely to be important.
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PMID:Restoration of cerebrovascular CO2 responsivity by glutamine synthesis inhibition in hyperammonemic rats. 139 82

The renal effects of pulsatile (pulse pressure 18.0 +/- 1.5 mm Hg [mean +/- SEM]) or nonpulsatile perfusion (mean pulse pressure 1.9 +/- 0.4 mm Hg) during either alpha-stat (mean PaCO2 41.2 +/- 0.9 mm Hg measured at 37 degrees C) or pH-stat (mean PaCO2 60.6 +/- 1.7 mm Hg measured at 37 degrees C) pH management of hypothermic cardiopulmonary bypass (CPB) were studied in 100 patients undergoing elective coronary artery bypass surgery. Mean urine output, fractional excretion of sodium and potassium, and renal failure index all increased during the study period; however, there was no difference among the four different CPB management groups. Mean postoperative creatinine and blood urea nitrogen values decreased compared with preoperative values, again without differences among treatment groups. Three patients developed acute renal insufficiency; of these, two had received nonpulsatile perfusion and pH-stat management, and the other had been managed with pulsatile perfusion and pH-stat management. These three patients all had undergone prolonged CPB and required at least two vasoactive drugs and the use of an intraaortic balloon pump to be weaned from CPB. In patients with normal preoperative renal function undergoing hypothermic CPB, neither the mode of perfusion, pulsatile or nonpulsatile, nor the method of pH management, pH-stat or alpha-stat, influences perioperative renal function.
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PMID:Differences in pH management and pulsatile/nonpulsatile perfusion during cardiopulmonary bypass do not influence renal function. 141 20


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