Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine whether intense exercise training affects exercise-induced vasodilatation, six subjects underwent 4 weeks of handgrip training at 70% of maximal voluntary contraction. Exercise forearm vascular conductance (FVC) responses to an endothelium-dependent vasodilator (acetylcholine, ACH; 15, 30, 60 micrograms min-1) and an endothelium-independent vasodilator (sodium nitroprusside, SNP; 1.6, 3.2, 6.4 micrograms min-1) and FVC after 10 min of forearm ischaemia were determined before and after training. Training elicited significant (P < 0.001) increases in grip strength (43.4 +/- 2.3 vs. 64.1 +/- 3.5 kg, before vs. after, mean +/- SEM), forearm circumference (26.7 +/- 0.4 vs. 27.9 +/- 0.4 cm) and maximal FVC (0.4630 +/- 0.0387 vs. 0.6258 +/- 0.0389 units, P < 0.05). Resting FVC did not change significantly with training (0.0723 +/- 0.0162 vs. 0.0985 +/- 0.0171 units, P > 0.4), but exercise FVC increased (0.1330 +/- 0.0190 vs. 0.2534 +/- 0.0387 units, P < 0.05). Before and after the training, ACH increased exercise FVC above the control (no drug) exercise FVC, whereas SNP did not. Training increased (P < 0.05) the exercise FVC responses to ACH (0.3344 +/- 0.1208 vs. 0.4303 +/- 0.0858 units, before vs. after training, 60 micrograms min-1) and SNP (0.2066 +/- 0.0849 vs. 0.3172 +/- 0.0628 units, 6.4 micrograms min-1). However, these increases were due to the increase in control (no drug) exercise FVC, as the drug-associated increase in exercise FVC above control did not differ between trials (P > 0.6). These results suggest that exercise FVC is increased by both exercise training and stimulating the release of endothelium-dependent vasodilators. However, training does not affect the vascular response to these vasodilators.
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PMID:Effects of intense exercise training on endothelium-dependent exercise-induced vasodilatation. 981 57

Cardiovascular mortality is excessive in hemodialyzed patients. Observations in atherosclerosis suggest that endothelial dysfunction and impaired nitric oxide (NO) may be involved. However, the relation of endothelial NO to its vascular effects has not been studied conclusively in uremia. Therefore, to study these questions an invasive technique was used in normotensive patients who were on hemodialysis (HD; n = 11) and in matched control subjects (n = 11). Pharmacologic agents were infused into the brachial artery to test the chain of events from NO generation to smooth muscle cell relaxation, measuring forearm blood flow by venous occlusion plethysmography. Glyceroltrinitrate (GTN 1:2.2 nmol/min; GTN 2:4.4; GTN 3:8.8), infused to establish the reaction of the vessel wall to defined doses of NO, caused a reduced response in HD patients (control subjects: 183 +/- 20 [SEM], 246 +/- 26, and 338 +/- 29%; HD patients: 161 +/- 7, 206 +/- 12, and 262 +/- 24%; baseline = 100% for each group, P: = 0.032 by ANOVA). All subsequent data were corrected for this decreased response to defined doses of NO in HD patients. L-arginine (10 mg/min), given to exclude substrate deficiency of NO synthase (NOS), caused no significant changes (control subjects: 108 +/- 4%; HD patients: 103 +/- 4%; P: = NS). Acetylcholine (ACH 1:55 nmol/min; ACH 2:110; ACH 3:220), infused to stimulate endothelial NOS, had a significantly reduced effect in HD patients (control subjects: 246 +/- 32, 340 +/- 40, and 465 +/- 52%; HD patients: 251 +/- 55, 244 +/- 36, and 318 +/- 50%; P: = 0.002). N:-monomethyl-L-arginine (LMA 1:1 micromol/min; LMA 2:2; LMA 3:4), given to block baseline NO generation, showed an enhanced response in HD patients (control subjects: 90 +/- 2, 83 +/- 2, and 74 +/- 4%; HD patients: 84 +/- 3, 73 +/- 3, and 64 +/- 4%; P: = 0.037). Vascular response to three doses of norepinephrine (60, 120, and 240 pmol/min) was comparable in both groups, which indicated similar endothelium-independent vasoconstriction. In summary, in normotensive HD patients, (1) vasodilation to defined doses of exogenous NO was reduced, (2) there was no evidence of substrate deficiency of NOS, and (3) stimulation of NOS was impaired; however, (4) baseline NO generation was increased. It is concluded that in HD patients, the NO system has a reduced capacity to regulate vascular tone and this impairment is most significant under conditions of NOS stimulation.
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PMID:Evidence in vivo showing increase of baseline nitric oxide generation and impairment of endothelium-dependent vasodilation in normotensive patients on chronic hemodialysis. 1096 98

This study highlights cellulose conversion for the production of 5-Hydroxymethyl Furfural using synergistic effect of modified activated carbon and ionic liquid under moderate reaction conditions. Modified Activated carbon after acid treatment (ACS, ACP, ACH) were used to examine their catalytic activity on hydrolysis of cellulose in [Bmim]Cl medium. Changes in physical-chemical properties were characterized using XRD, FE-SEM, EDX, FT-IR and BET surface area analyser techniques. Modified activated carbon is found competent in enhancing cellulose conversion to Total Reducing Sugars and 5-Hydroxymethyl Furfural. Further, the effect of six metal ions i.e Cr+3, Fe+3, Cu+2, Zn+2, K+ and Al+3 impregnated on sulfuric acid treated activated carbon (ACS) was explored. The catalytic performance improves with the impregnation of metals in the decreasing order: Cr+3> Fe+3> Cu+2> Zn+2> Al+3> K+. These modified catalysts with ionic liquid as solvent are found promising to generate eco-friendly system and cost effective cellulose conversion to value added products.
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PMID:Synergistic effect of modified activated carbon and ionic liquid in the conversion of microcrystalline cellulose to 5-Hydroxymethyl Furfural. 3002 78