In 105 subjects (97 men and 8 women) aged <46 years (mean age 39.6 +/- 5.5 years), with recent acute myocardial infarction (T1), thiobarbituric acid reactive substances and total antioxidant status were determined; NO production was evaluated by measuring the nitrite and nitrate (NOx) concentration. The patients with acute myocardial infarction were subdivided according to the main risk factors, number of risk factors, and extent of coronary lesions. The evaluation was repeated after 12 months (T2). In these subjects, thiobarbituric acid reactive substances and NOx were significantly increased and total antioxidant status was significantly decreased at T1. In single risk factor, only NO metabolites were significantly lower in acute myocardial infarction subjects who smoke than in subjects who do not. Subdividing the subjects according to the number of risk factors and number of stenosed coronary vessels, there were no significant differences between the subgroups. At T2, thiobarbituric acid reactive substances and NOx were decreased and total antioxidant status was increased, but all parameters were still altered.

No abstract

We evaluated leukocyte rheology, expressed as leukocyte filtration, polymorphonuclear (PMN) membrane fluidity and cytosolic Ca²⁺ concentration in subjects with acute deep venous leg thrombosis (DVT). In 14 subjects with leg DVT we examined the leukocyte filtration [unfractionated, mononuclear cells (MN), PMNs], PMN membrane fluidity and PMN cytosolic Ca²⁺ concentration. Subsequently, we evaluated the same PMN variables after in vitro chemotactic activation with 4-phorbol-12-myristate-13-acetate. At baseline, we observed a significant difference in the filtration of unfractionated and MNs and in PMN cytosolic Ca²⁺ concentration. After PMN activation, a significant variation, greater in DVT subjects, was present in PMN filtration at 5 and 15 min. In normals, no variation was present in PMN membrane fluidity or cytosolic Ca²⁺ concentration after activation, while in subjects with DVT we found a significant variation in both PMN parameters. These results underline that there is a systemic leukocyte functional alteration in DVT.

there is a functional alteration of leukocytes in these patients whose mechanisms are not yet clear.

Dear Sir:Although cell membrane fluidity influences insulin activity (1,2), the clinical data regarding the relationships between this membrane property and insulin sensitivity are contrasting (3-6).Recently we enrolled 28 obese subjects (13 men and 15 women; mean age, 38.18 Ϯ 13.52 years; body mass index, 35.0 Ϯ 5.6 kg/m 2 ), which included 11 subjects with normal glucose tolerance (NGT) and 17 subjects with type 2 diabetes (DM). All subjects were insulin resistant. This was demonstrated by employing an euglycemic hyperinsulinemic clamp (7). In this group, the glucose disposal (M), calculated on the basis of the amount of glucose infused, was 1.45 Ϯ 1.01 mg/kg per minute (range, 0 to 3.27 mg/kg per minute), whereas the glucose metabolic clearance rate (MCR), calculated by dividing the amount of glucose metabolized by the plasma glucose concentration, was 1.67 Ϯ 1.15 mL/kg per minute (range, 0 to 3.80 mL/kg per minute). Leukocytes separated from fasting venous blood were subdivided into mononuclear (MN) and polymorphonuclear (PMN) cells using a Ficoll-Hypaque medium (Histopaque-1077; Sigma Diagnostics, St. Louis, MO). The PMN membrane fluidity was examined by labeling intact cells with the fluorescent probe 1-[4-(trimethylamino) phenyl]-6-phenyl 1,3,5-hexatriene (TMA-DPH), which explores the superficial regions of the membrane, and calculating the fluorescence polarization degree, inversely related to the membrane fluidity (8,9). The measurement was taken at 37°C, using a spectrophotofluorimeter (Mod. LS5; Perkin-Elmer, Beaconsfield, UK).In obese subjects, the PMN membrane fluidity was significantly reduced in comparison with normal subjects (normals, 0.338 Ϯ 0.008; obese NGT, 0.353 Ϯ 0.007; obese with type 2 DM, 0.350 Ϯ 0.012; p Ͻ 0.01). In normal patients, obese patients with NGT, and obese patients with type 2 DM, no significant correlation was found between PMN membrane fluidity and the following metabolic parameters: fasting blood glucose level, glycated hemoglobin, total cholesterol, and triglyceride level. In obese patients with NGT, no correlation was observed between PMN membrane fluidity and the parameters (M and MCR) reflecting insulin resistance, whereas in obese patients with type 2 DM, a significant negative relationship was present between PMN membrane fluidity and both of these clamp parameters, showing that the decrease of PMN membrane fluidity coincided with a reduction in the degree of insulin resistance.In a previous report (6), we observed a decrease of PMN membrane fluidity in a group of subjects with insulin resistance (12 obese subjects with normal or altered glucose tolerance and 7 type 2 diabetic subjects without obesity), but we did not observe any relationship between PMN membrane fluidity and the two clamp parameters, which reflected the degree of insulin resistance.Our present data confirm other studies that found, in obese subjects and in type 2 diabetic subjects, a decrease in membrane fluidity of erythrocytes (5,10) and platelets (11) and contrast with those obtained by Tong et a...