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Biomedical subjects

T J Hendra

Publications and source records attributed to T J Hendra.

26 records · Page 2Linked to original sources
PubMed1990

Effects of fish oil supplements in NIDDM subjects. Controlled study.

The aim of this study was to evaluate the effects of a fish oil preparation (MaxEPA) on hemostatic function and fasting lipid and glucose levels in non-insulin-dependent diabetic (NIDDM) subjects. Eighty NIDDM outpatients aged 55.9 yr (mean SD 11.5 yr) participated in a prospective double-blind placebo-controlled study of MaxEPA capsules (10 g/day) or olive oil (control) treatment over 6 wk. Patients received either MaxEPA or olive oil in addition to preexisting therapy. Metabolic and hemostatic variables were measured before treatment and after 3 and 6 wk. Platelet membrane eicosapentaenoic acid (EPA) content increased in the treatment group (P less than 0.001). MaxEPA supplementation was associated with a significant fall in total triglycerides (P less than 0.001) but did not affect total cholesterol (P = 0.7) compared with control treatment. Fasting plasma glucose increased after 3 wk (P = 0.01) but not after 6 wk (P = 0.17) treatment with MaxEPA. Spontaneous platelet aggregation in whole blood fell in the MaxEPA group (P less than 0.02) after 6 wk, but there were no changes in agonist-induced platelet aggregation, thromboxane generation in platelet-rich plasma, or plasma beta-thromboglobulin and platelet factor IV levels. An increase in clotting factor VII (P = 0.02), without changes in fibrinogen or factor X levels, occurred in the MaxEPA group. Similar reductions in blood pressure were observed in both groups. Dietary supplementation with MaxEPA capsules (10 g/day) in NIDDM subjects is associated with improvement in hypertriglyceridemia but with deleterious effects in factor VII and blood glucose levels. Most indices of platelet function are unaffected by this therapy.

Blood Glucose↗
PubMed1989

Anticardiolipin antibody levels in diabetic subjects with and without coronary artery disease.

Moderate (greater than 20 units) and high (greater than 80 units) IgG anticardiolipin antibody (aCL) titres are strongly predictive for recurrent thrombosis and early myocardial infarction in non-diabetic subjects. We have tested the hypothesis that the excess risk of myocardial infarction in diabetic subjects relates to the presence of aCL by measuring the frequency and titre of aCL in two groups of diabetic subjects and in 2500 healthy controls. One non-diabetic subject (0.04%) had low (5-20 units) IgG aCL titres. Seven out of 126 diabetics without cardiovascular disease (5.6%) and 9 out of 79 diabetics who were either myocardial infarction survivors or who had angiographically-proven coronary artery disease (11.4%) had low aCL titres (P less than 0.01 for comparison of either diabetic group with controls, and P less than 0.1 for comparison between diabetic groups). One subject in each diabetic group, but no non-diabetics, had moderate IgM aCL titres. No subjects had high aCL titres. Diabetics have an increased frequency of low aCL titres which may relate to macrovascular disease. Macrovascular disease in diabetics is not associated with moderate or high aCL titres.

Cardiolipins↗
PubMed1988

Exercise-induced changes in platelet aggregation; a comparison of whole blood and platelet rich plasma techniques.

Studies have been performed to assess the effect of exercise on spontaneous platelet aggregation in shaken whole blood, and on agonist-induced platelet aggregation in whole blood and platelet rich plasma (PRP). Spontaneous platelet aggregation in shaken whole blood was increased following exercise compared to pre-exercise values. The increase in spontaneous aggregation after exercise correlated inversely with the increase in white cell count in whole blood. Platelet sensitivity in whole blood to adrenaline, collagen and adenosine diphosphate (ADP) was increased following exercise. Changes in platelet sensitivity to adrenaline following exercise correlated with increases in plasma noradrenaline levels but not with changes in blood cell counts. In PRP, platelet sensitivity to ADP and to collagen was increased following exercise when the pre and post-exercise PRP platelet counts were not corrected to allow for the increase in platelet count which occurred with exercise. When the PRP platelet counts were corrected, no changes in platelet sensitivity to any agonist after exercise were observed.

Adenosine Diphosphate↗
PubMed1988

Increased mean platelet volume after acute myocardial infarction relates to diabetes and to cardiac failure.

Mean platelet volume, platelet count and an estimate of platelet volume distribution were studied following acute myocardial infarction in 59 diabetics and 88 non-diabetics and were compared with values in 100 non-diabetic and 50 diabetic non-infarct subjects. In the non-diabetics mean platelet volume and platelet distribution width were similar in the non-infarcted patients and in the infarcted patients without severe cardiac failure. All diabetics with myocardial infarction had larger mean platelet volumes and platelet distribution width than the diabetic non-infarct controls. All myocardial infarction patients with severe cardiac failure had larger platelet volumes than patients with mild or no failure. Increased mean platelet volume may reflect either increased platelet activation or increased numbers of large, hyperaggregable platelets. Abnormalities of platelet function may contribute to the relatively poor prognosis of myocardial infarction in patients with diabetes.

Aged↗
PubMed1988

Ex vivo platelet studies following oral nisoldipine in normotensive insulin-dependent diabetics and non-diabetic controls.

The effect of 24 hours and 7 days treatment with nisoldipine (10 mg, twice daily) on platelet function was studied in 12 normotensive volunteers of whom six were insulin-dependent diabetics without clinical evidence of vascular complications. Platelet aggregation was assessed by platelet rich plasma (PRP) and whole blood (WB) techniques. In addition, the effect of nisoldipine on platelet hyperaggregability following exercise was assessed. After taking nisoldipine for 24 hours, in vitro platelet hypersensitivity to adenosine diphosphate was observed in PRP (p less than 0.01) and WB (p less than 0.01), to adrenaline in WB (p less than 0.03), and to collagen in PRP (p less than 0.02). After seven days treatment, platelet sensitivities to all agonists at rest in both PRP and WB showed no differences from pre-treatment values. Exercise-induced platelet hypersensitivity in WB to all three agonists was unchanged after nisoldipine treatment. Plasma noradrenaline and adrenaline concentrations increased after 24 hours treatment, although changes in agonist EC50s at 24 hours were not related to changes in plasma catecholamine levels. No effects of nisoldipine were observed on platelet thromboxane B2 release in PRP, or on plasma beta-thromboglobulin levels. No differences in the effects of nisoldipine were observed between diabetic and non-diabetic subjects. Nisoldipine treatment for seven days is not associated with altered platelet function, but platelet hypersensitivity is observed after treatment for 24 hours in both insulin-dependent diabetics and controls.

Adenosine Diphosphate↗
PubMed1987

Deoxyribonucleic acid polymorphism of the apoprotein AI-CIII-AIV gene cluster and coronary heart disease in non-insulin-dependent diabetes.

The prevalence of an uncommon allelic variant (S2) of the apoprotein AI-CIII-AIV gene cluster was determined in non-insulin-dependent diabetics with or without evidence of coronary heart disease and in controls. Frequencies of the S2 allele were 14% for diabetics with coronary heart disease compared with 2% for non-diabetics with no clinical evidence of occlusive vascular disease. No subject with the S2 allele was detected among a further group of matched diabetics without clinical features of macrovascular disease. The results suggest that a genetic component contributes to the susceptibility to coronary heart disease in non-insulin-dependent diabetics. Whether the observed deoxyribonucleic acid variant is aetiological for atherosclerosis or in linkage disequilibrium with other atherogenic loci on chromosome 11 remains to be clarified.

Alleles↗
PubMedDate not supplied

Platelet function in uncomplicated insulin-dependent diabetic patients at rest and following exercise.

There are conflicting reports of platelet function abnormalities in diabetic patients without vascular complications. We have studied in vitro platelet aggregation, using platelet rich plasma and whole blood techniques, in 18 patients with uncomplicated insulin-dependent diabetes and a matched group of 24 non-diabetic subjects. In addition we measured plasma beta-thromboglobulin levels in these groups, as an index of in vivo platelet activation, and compared the indices of in vitro and in vivo platelet function before and after maximal bicycle exercise. Before exercise plasma beta-thromboglobulin levels and platelet sensitivities to ADP, collagen or adrenaline, as assessed by both methods of platelet aggregation, were the same in diabetic and control subjects. Both groups showed similar increases in beta-thromboglobulin levels and in platelet sensitivity to all agonists in whole blood following exercise. Using platelet rich plasma there were no changes in platelet sensitivity in either group after exercise. In non-diabetic subjects, increases in noradrenaline levels after exercise correlated with increases in platelet sensitivity to adrenaline in whole blood. This was not observed in the diabetic group. Abnormalities of platelet function, using the techniques described here, are not present in diabetic patients who do not have clinical evidence of vascular disease.

Adenosine Diphosphate↗