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S L Nuttall

Publications and source records attributed to S L Nuttall.

31 records · Page 2Linked to original sources
PubMed2000

A pilot study of streptokinase-induced endothelial injury and platelet activation following acute myocardial infarction.

OBJECTIVE: To relate the changes in serum vitamin E, an essential antioxidant, to changes in fibrinogen, as well as indices of endothelial damage [as indicated by plasma markers, soluble thrombomodulin (sTM) and von Willebrand factor (vWf), and an index of platelet activation (soluble P selectin (sPsel)], in myocardial infarction treated with thrombolytic therapy. DESIGN AND SETTING: Prospective longitudinal pilot study in a teaching hospital Coronary Care Unit. SUBJECTS AND INTERVENTION: Seventeen patients (12 men: mean age (62 years +/- SD 11 years) admitted with acute myocardial infarction (AMI), who were given thrombolytic therapy, and 59 healthy controls. RESULTS: Baseline levels of fibrinogen (Mann-Whitney test, P = 0.0055) and vWf (P < 0.001) were significantly higher than controls, but sPsel, sTM or vitamin E levels were not significantly different. Following thrombolysis, as expected, median concentrations of plasma fibrinogen fell profoundly (Friedman ANOVA P < 0.001) so that after 45 min, levels were undetectable in 13 patients. At 24-h median fibrinogen concentration had recovered to approximately 30% of baseline (P < 0.01) and was still undetectable in three patients. Levels of vWf and sPsel increased steadily, reaching significance after three hours (both P < 0.05). However, levels of sTM rose immediately after thrombolysis, peaking between 1 and 3 h, and remained elevated at 24 h. These increases corresponded to a simultaneous early fall in serum vitamin E concentrations. CONCLUSION: The present pilot study demonstrates significant endothelial damage and platelet activation in association with increased oxidative stress following streptokinase therapy for AMI.

Aged↗
PubMed1999

Age-independent oxidative stress in elderly patients with non-insulin-dependent diabetes mellitus.

Impaired antioxidant defence is implicated in the development of cardiovascular complications in non-insulin-dependent diabetes (NIDDM). However, as many of these patients are elderly, observed changes in antioxidant status may be due to the patient's age rather than their disease. We sampled blood from 47 elderly NIDDM patients (21 male and 26 female; mean age +/- SD, 75.62 +/- 7.97 years), 66 young (30 male and 36 female; 24.52 +/- 4.72 years) and 58 healthy elderly volunteers (17 male and 41 female; 70.74 +/- 4.85 years), and measured the antioxidant glutathione, the marker for free-radical-damage lipid hydroperoxide products (LHP), vitamin E and total antioxidant capacity (TAC). There was a significant increase in LHP in the healthy elderly group compared with the young volunteers (3.14 +/- 1.5 vs. 2.14 +/- 1.38 mumol/l, p < 0.01). The values were much higher in NIDDM patients (7.02 +/- 2.29 mumol/l, p < 0.0001 vs. healthy elderly). There was a reduction in TAC in healthy elderly compared with the young (359.99 +/- 54.82 vs. 471.47 +/- 94.29 mumol/l trolox equivalents, p < 0.0001), but there was no further reduction in NIDDM patients. Similarly, glutathione was reduced to the same degree in healthy elderly and NIDDM patients (0.29 +/- 0.09, 0.30 +/- 0.11 vs. 0.54 +/- 0.19 mumol/l in young volunteers, p < 0.0001). Vitamin E concentrations were comparable in all groups (26.34 +/- 5.39 young volunteers, 31.50 +/- 8.23 healthy elderly and 30.98 +/- 9.03 mumol/l NIDDM patients), but after correction for serum cholesterol there was a significant reduction in the diabetic group compared with the young, but not with the elderly (5.54 +/- 1.55 vs. 6.67 +/- 1.86 vs. 6.31 +/- 1.85 (mumol/l)/(mmol/l), p < 0.01). We have demonstrated an age-dependent reduction in total antioxidant capacity and glutathione defence and an age-independent increase in LHP in elderly patients with NIDDM. Reduced concentrations of vitamin E were demonstrated in NIDDM patients compared with young, but not elderly, volunteers. Increased oxidative damage occurs independently of age in NIDDM patients despite comparable antioxidant defences in this age group.

Adult↗
PubMed1998

An evaluation of the antioxidant activity of a standardized grape seed extract, Leucoselect.

UNLABELLED: Coronary Artery Disease (CAD) remains the major cause of mortality and morbidity in the Western World. The oxidation of low-density lipoproteins (LDLs) by free radicals is associated with initiation of atherosclerosis and therefore, development of CAD. LDLs are protected from oxidation by antioxidants and in times of antioxidant deficiency are more likely to be oxidized. Hypercholesterolaemic patients are at a higher cardiovascular risk and may, therefore, require more antioxidant protection. Increased consumption of red wine containing antioxidants is thought to account for the lower incidence of CAD in Mediterranean countries. Red wine, although rich in antioxidants, is not suitable as routine therapy for prevention of CAD. OBJECTIVE: To evaluate the effects of a capsule formulation of an antioxidant polyphenolic extract of grapes on serum total antioxidant activity and vitamin C and E levels. METHOD: A single-blinded randomised, placebo-controlled cross-over study was undertaken in 20 young volunteers. Subjects were given two capsules containing 300 mg of grape procyanidin extracts (Leucoselect-phytosome) or placebo daily for 5 days. Blood samples were taken at the start of the study and end of the study and assayed for antioxidant activity and vitamins C and E levels. After a washout period of at least 2 weeks, the study was repeated with the second treatment. RESULTS: The extract had no effect on serum vitamins C and E levels but increased serum total antioxidant activity (TAC). On day 5, TAC increased from 408.1+/-22.9 to 453.3+/-453.3 micromol/l trolox equivalents 1 hour postdose. CONCLUSION: The capsules increased serum antioxidant activity but the longer-term clinical implications need to be assessed in further randomised clinical trials.

Adult↗