Thromboxane production and platelet aggregation in diabetic subjects with clinical complications

Butkus, Antanas; Skrinska, Victor; Schumacher, O. Peter

doi:10.1016/0049-3848(80)90420-x

Cited by 120 publications

(31 citation statements)

References 40 publications

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“…The arachidonic acid content in the phosphatidylcholine and phosphatidylinositol fraction is known to be an important modulating factor for TXA2 synthesis [3,11]. Therefore, increased arachidonic acid content in diabetic platelet phospholipids [3,4] was considered as one possible cause of increased TXA2 synthesis in diabetic platelets [12][13][14]. However, Jones et al [15] recently reported a significant decrease in arachidonic acid levels in diabetic platelet phospholipids, a result quite different from ours.…”

Section: Discussioncontrasting

confidence: 42%

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Increased arachidonic acid incorporation into platelet phospholipids in Type 2 (non-insulin-dependent) diabetes

et al. 1984

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Summary. Arachidonic acid uptake activity was measured in platelets obtained from 27 Type 2 diabetic patients and 18 agematched control subjects. In both groups after 1 h incubation almost all the incorporated 14C-arachidonic acid was located in the phospholipids of the platelets. Arachidonic acid was predominantly incorporated into phosphatidylcholine. The radioactivity incorporated into platelets increased linearly with incubation time, up to 90 min. The linear increase was observed at arachidonic acid concentrations of 0.1-1.0 ~tg/ml in both groups. The rate of incorporation of radioactivity in diabetic platelets was about 1.4 times higher than that in control platelets at all arachidonic acid concentrations studied. The arachidonic acid uptake activity of diabetic platelets (577 + 26 ng/60 min per 109platelets) was significantly higher than that in control platelets (410_ 26 ng/60 rain per 109plate -lets).No significant correlations were found between the arachidonic acid uptake activity and fasting plasma glucose, total cholesterol or triglyceride levels. The arachidonic acid uptake activity of platelets was significantly higher in diabetic patients with proliferative retinopathy than in those with little or no background retinopathy. In addition, there were no significant differences between control and diabetic subjects in the uptake activity of platelets for linoleic acid and oleic acid. These data may explain the elevated arachidonic acid content in diabetic platelet phospholipids and enhancement of thromboxane synthesis in diabetes.Key words: Arachidonic acid uptake, platelet phospholipids, Type 2 diabetes, retinopathy, platelet-rich plasma, non-esterifled fatty acid.Thromboxane A2 (TXA2), biosynthesized from arachidonic acid in platelet phospholipids, plays an important rrle in the process of platelet aggregation [1,2]. It is postulated that the balance between platelet TXA2 and vascular prostacyclin production might be a crucial step in the development of atherosclerosis and arterial thrombosis in diabetes mellitus. Recently, Kalofoutis and Lekakis [3] and we [4] have demonstrated that the arachidonic acid content of platelet phospholipids was increased in diabetes. It is generally accepted that the TXA2 synthesis rate is regulated at the step of liberation of arachidonic acid from membrane phospholipids [5]. Therefore, increased esterified arachidonic acid content in phospholipids might modulate TXA2 production in diabetes.In this study, we examined the t4C-arachidonic acid uptake activity of platelets obtained from Type 2 (noninsulin-dependent) diabetic patients and age-matched control subjects, to clarify the mechanisms of increased arachidonic acid levels in platelet phospholipids in diabetes. Subjects and methods SubjectsThe Type 2 diabetic subjects included in the study were t0 men and 17 women ranging in age between 48 and 86 years (mean 67 + 2 years). Eleven patients were treated with insulin and 16 were treated with sulphonylureas. The control subjects (five men and 13 women, age range 46-79...

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Section: Discussioncontrasting

confidence: 42%

“…3). Production of TXA2 by platelets after ADP, arachidonic acid or thrombin stimulation was higher in the diabetic patients with microangiopathy than in those without complications [12][13][14]20]. On the other hand, prostacyclin synthesis was decreased in the diabetic patients with microangiopathy [21].…”

Section: Discussionmentioning

confidence: 99%

Increased arachidonic acid incorporation into platelet phospholipids in Type 2 (non-insulin-dependent) diabetes

et al. 1984

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“…30 Extracts of platelets from diabetics also exert greater mitogenic effects on vascular smooth muscle than platelets prepared from normal subjects. 31 Hyperinsulinemia may further predispose the NIDDM patient to atherosclerosis. Eighty percent of NIDDM subjects are obese.…”

Section: Atherosclerosismentioning

confidence: 99%

Hypertension, the endothelial cell, and the vascular complications of diabetes mellitus.

1992

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Hypertension is a major factor that contributes to the development of the vascular complications of diabetes mellitus, which primarily include atherosclerosis, nephropathy, and retinopathy. The mechanism of the pathophyslologkal effects of hypertension lies at the cellular level in the blood vessel wall, which intimately involves the function and interaction of the endothelial and vascular smooth muscle cells. Both hypertension and diabetes mellitus alter endothelial cell structure and (unction. In large and medium size vessels and in the kidney, endothelial dysfunction leads to enhanced growth and vasoconstriction of vascular smooth muscle cells and mesangial cells, respectively. These changes in the cells of smooth muscle lineage play a key role in the development of both atherosclerosis and giomerulosclerosis. In diabetic retinopathy, damage and altered growth of retinal capillary endothelial cells is the major pathophysiological insult leading to proliferative lesions of the retina. Thus, the endothelium emerges as a key target organ of damage in diabetes mellitus; this damage is enhanced in the presence of hypertension. An overall approach to the understanding and treatment of diabetes mellitus and its complications will be to elucidate the mechanisms of vascular disease and endothelial cell dysfunction that occur in the setting of hypertension and diabetes. (Hypertension 1992^20:253-263) KEY WORDS • diabetes mellitus • endothelium, vascular • hypertension, essential V ascular damage underlies many of the major complications of diabetes mellitus such as atherosclerosis, nephropathy, and retinopathy. Altered blood vessel function may also influence insulinmediated glucose uptake in the peripheral tissue, which is a potential determinant of insulin sensitivity. Hypertension accelerates all the vascular complications of diabetes 1 and is itself, in the absence of obesity or diabetes, associated with insulin resistance.2 High blood pressure alters vascular structure, function, and autocrine-paracrine relations within the blood vessel wall; it is these vascular changes that are likely responsible for hypertension's profound impact on diabetic complications.Endothelial cells and vascular smooth muscle cells are the two major components of the vessel wall. Both hypertension and diabetes mellitus alter the function and interaction of these cells (Figure 1). In normal vessels, endothelial cells provide a mechanical barrier to underlying smooth muscle cells from circulating substances and blood cells and produce local factors that act in a paracrine fashion to alter vascular tone and growth. These factors are listed in Table 1. Endothelial cells are characterized by their production of angiotenDr. Hsueh was an invited speaker at

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“…Numerous studies have shown the relative risk of deep venous thrombosis and pulmonary embolism of oral contraceptive users ver sus non-users to vary from 2-11:1 [9], Aberrations of coagulation, fibrinolysis and haemodynamics have been described in oral contraceptive users as well as diabetics [11][12][13]. In the absence of other predisposing causes, it seems most plausible that our patient had a hypercoagu lable state secondary' to oral contraceptive use and possi bly diabetes mellitus which precipitated her acute right renal vein thrombosis.…”

Section: Discussionmentioning

confidence: 99%

Successful Treatment with Streptokinase of Renal Vein Thrombosis Associated with Oral Contraceptive Use

Barré¹,

Bishinsky

Roy

et al. 1986

Am J Nephrol

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The case of a 2 5-year-old diabetic female presenting with acute right main renal vein thrombosis associated with oral contraceptive usage is described. Rapid diagnosis with ultrasound and resolution of the thrombosis was accomplished with streptokinase. Ultrasound may be the diagnostic test of choice in selected patients with renal vein thrombosis. Streptokinase was an effective therapy in this case of acute renal vein thrombosis.

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Thromboxane production and platelet aggregation in diabetic subjects with clinical complications

Cited by 120 publications

References 40 publications

Increased arachidonic acid incorporation into platelet phospholipids in Type 2 (non-insulin-dependent) diabetes

Increased arachidonic acid incorporation into platelet phospholipids in Type 2 (non-insulin-dependent) diabetes

Hypertension, the endothelial cell, and the vascular complications of diabetes mellitus.

Successful Treatment with Streptokinase of Renal Vein Thrombosis Associated with Oral Contraceptive Use

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