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C D Stehouwer

Publications and source records attributed to C D Stehouwer.

At least 145 records · Page 8Linked to original sources
PubMed1997

The acute effect of hyperglycaemia on vessel wall properties.

Arterial distensibility is a marker of functional and structural vessel wall properties. A decreased distensibility is an important risk factor for cardiovascular disease. In insulin-dependent diabetes mellitus of short duration, arterial stiffness has been reported to be increased, decreased or the same as in healthy control subjects. The influence of acute hyperglycaemia on arterial stiffness is unclear and might be one of the factors responsible for the divergent results which have been observed. We investigated arterial distensibility locally in the carotid artery during hyper- and normoglycaemia using a glucose clamp technique. Eleven healthy normotensive men underwent both a hyperglycaemic and a euglycaemic clamp on separate days. Before and after 2 h of clamping, arterial diameter (D) and change in arterial diameter during the heart cycle (dD) were measured with a non-invasive vessel wall movement detector system. Blood pressure (BP), pulse pressure (dP) and heart rate (HR) were recorded with a semi-automated device. Distensibility coefficients (DC), reflecting the intrinsic vascular wall elasticity, and compliance coefficients (CC), reflecting the buffering capacity of the vessel, were calculated from D, dD and dP. (DC = 2*dD/ D*dP, CC = pi*dD*D/2*dP). There were no significant differences between the hyperglycaemic and the euglycaemic clamp for D, DC and CC. These results suggest that an acute systemic hyperglycaemia is not responsible for changes in diameter, distensibility and compliance of the carotid artery.

Carotid Arteries↗
PubMed1997

Endothelium-dependent vasodilatation and distensibility of large arteries in chronic haemodialysis patients.

BACKGROUND: Cardiovascular mortality is increased in chronic haemodialysis (HD) patients and is not completely explained by common cardiovascular risk factors. Hyperhomocysteinaemia and chronic HD per se may play a role, because these factors may adversely affect endothelial function and distensibility of conduit arteries, which are important determinants of the risk of atherosclerosis, thrombosis and cardiac hypertrophy. METHODS: A vessel wall movement detector system was used to investigate endothelium-dependent, flow-mediated and endothelium-independent, glyceryl trinitrate-induced vasodilatation in the brachial artery and compliance and distensibility coefficients (CC and DC) in the common carotid artery in 28 chronic HD patients and 28 control subjects. RESULTS: Endothelium-dependent, but not endothelium-independent, vasodilatation was markedly reduced in the HD group (3.7 +/- 1.1 vs. 9.7 +/- 1.2%; P = 0.001). The DC was reduced only in a subgroup of patients aged < 50 years: 16.9 +/- 1.5 vs. 22.4 +/- 2.0 10(-3)/kPa (P = 0.032) and was not related to endothelium-dependent vasodilatation. CC did not differ between the groups. Plasma total homocysteine was elevated in the HD patients, but was neither related to endothelium-dependent vasodilatation, nor to DC. CONCLUSION: Chronic renal failure and (or) chronic haemodialysis are associated with impaired endothelium-dependent vasodilatation, which may reflect an increased susceptibility for the development of atherosclerosis and thrombosis.

Adult↗
PubMed1997

Endothelial marker proteins in hyperhomocysteinemia.

Hyperhomocysteinemia is associated with severe, premature atherosclerosis and thromboembolism. The mechanisms involved in the atherogenic and thrombotic complications of hyperhomocysteinemia are not understood. It has been suggested that hyperhomocysteinemia predisposes to atherosclerosis by injuring the vascular endothelium. Whether hyperhomocysteinemia is independently associated with changed endothelial function, either in the absence or the presence of clinically manifest atherosclerotic disease, is, however, not known. Therefore we investigated, both in patients with peripheral arterial occlusive disease and in healthy individuals, whether plasma protein markers of endothelial function differed between subjects with, and subjects without hyperhomocysteinemia. We studied 80 individuals under the age of 56 years: healthy individuals with (n = 20) and without (n = 20) hyperhomocysteinemia and patients with peripheral arterial occlusive disease with (n = 20) and without (n = 20) hyperhomocysteinemia. The following endothelium-derived proteins were measured as markers of endothelial cell function: von Willebrand factor (vWf) and von Willebrand factor propeptide (vWf: AgII), tissue-type plasminogen activator (tPA), plasminogen activator inhibitor-1 (PAI-1), cellular fibronectin (cFN) and thrombomodulin (TM). In addition we assessed C-reactive protein (CRP). vWf, vWf: AgII, tPA and CRP were significantly higher in the patients with peripheral arterial occlusive disease than in the healthy individuals. No differences in marker protein plasma levels were found between individuals with, and those without hyperhomocysteinemia, apart from vWf, which was significantly raised in hyperhomocysteinemic as compared to normohomocysteinemic patients. We did not find any evidence for an independent association between hyperhomocysteinemia and protein markers of endothelial cell function in healthy subjects.

Adult↗
PubMed1996

Effects of insulin infusion on endothelium-derived vasoactive substances.

An association between insulin resistance and hypertension has been reported in several studies. In apparent contradiction, insulin infusion in healthy volunteers is associated with vasodilatation. Furthermore, there is evidence that some insulin effects may differ between the sexes. We performed three-step hyperinsulinaemic-euglycaemic clamp studies in six men and six women to test the hypotheses that: 1) insulin might affect the release of vasoactive substances by the endothelium, and 2): this putative effect on vasoactive substances might differ between men and women. Six other women and six men served as control subjects, receiving 154 mmol/l NaCl (saline) infusion. Plasma levels of insulin, immunoreactive endothelin, L-arginine (precursor of nitric oxide), L-citrulline (by-product of nitric oxide synthesis) and cyclic GMP (second messenger of nitric oxide) were measured during infusion of insulin or 154 mmol/l NaCl (saline), respectively. We also assessed urinary excretion of 6-keto PGF-1 alpha (a degradation product of prostacyclin reflecting prostacyclin production). Blood pressure was monitored in all subjects throughout the experiment. In women plasma levels of immunoreactive endothelin decreased from (mean +/- SD) 2.58 +/- 0.96 to 1.7 +/- 0.72 pmol/l during insulin infusion (p < 0.01), while remaining constant in female control subjects (p < 0.02). No changes in levels of endothelin were observed in men during infusion of insulin or saline. In women levels of cGMP rose and levels of L-arginine decreased significantly during insulin infusion, consistent with an increase in nitric oxide production. Excretion of 6-keto PGF-1 alpha also increased significantly in women during insulin infusion. No such effects were observed in men, or in women during infusion of saline. Blood pressure remained constant in all subjects during hyperinsulinaemia. We conclude that sex differences exist in the effects of insulin on the endothelium. Short-term hyperinsulinaemia in women is associated with a decline in levels of immunoreactive endothelin, and possibly with a rise in production of nitric oxide and prostacyclin. In contrast, levels of vasoactive substances remained constant in men during hyperinsulinaemia. Our findings may partly explain insulin's vasodilatory effects in healthy individuals. It remains to be investigated whether these effects are lost in insulin-resistant states. Our observation that there is a sex difference in insulin effects on the endothelium may help explain why the link between hyperinsulinaemia and cardiovascular disease appears to be clearer in men than in women.

6-Ketoprostaglandin F1 alpha↗
PubMed1996

Plasma homocysteine and severity of atherosclerosis in young patients with lower-limb atherosclerotic disease.

Elevated plasma homocysteine levels are recognized as an independent risk factor for atherosclerotic disease. It is not known (1) whether the severity of atherosclerotic disease is related to hyperhomocyst(e)inemia or (2) whether any such relation differs between fasting and post-methionine loading plasma homocysteine levels. Therefore, in 171 consecutive patients under 55 years of age with first symptoms of lower-limb disease, we examined the relation between severity of atherosclerosis and plasma homocysteine concentration. Severity of atherosclerotic disease was estimated from the prevalence of coronary artery disease and cerebrovascular disease and from the angiographic extent of lower-limb disease. Plasma homocysteine was measured after a period of fasting and in response to methionine loading (0.1 g/kg). In multivariate analysis, the prevalence of coronary artery disease plus cerebrovascular disease was related to both fasting and postmethionine homocysteine levels (odds ratio [OR] for the upper quartile versus the lower three quartiles, 2.8, 95% confidence interval [CI], 1.1 to 7.5; and OR 3.0, 95% CI, 1.1 to 7.8, respectively). The extent of lower-limb disease was weakly related to the fasting homocysteine level (partial correlation coefficient, .12; P = .17) and more strongly related to the postmethionine homocysteine level (partial correlation coefficient, .25; P = .003). These relations tended to be more pronounced in women than in men. They were independent of age, total serum cholesterol, blood pressure, and smoking habit. We concluded that the severity of atherosclerotic disease in young patients with lower-limb atherosclerotic disease is associated with high postmethionine and fasting homocysteine concentrations.

Adult↗
PubMed1996

Endothelium-dependent and -independent vasodilation of large arteries in normoalbuminuric insulin-dependent diabetes mellitus.

Vascular complications in diabetes mellitus are associated with endothelial dysfunction. Whether endothelium-dependent vasodilation is impaired in normoalbuminuric patients with insulin-dependent diabetes mellitus (IDDM) is controversial. Using a noninvasive echo-Doppler method, we investigated endothelium-dependent and endothelium-independent vasodilation in the brachial artery of IDDM patients. There were 52 normoalbuminuric and normotensive patients with IDDM (aged 31.9 +/- 9.8 years; diabetes duration, 14.9 +/- 7.9 years; glycated hemoglobin, 7.9 +/- 1.2%) and 52 healthy control group (C) subjects comparable for age and sex studied. Brachial artery diameter was measured at baseline, during postocclusion reactive hyperemia (flow-mediated, endothelium-dependent dilation [FMD]), and after 400 micrograms glyceryl trinitrate (GTN) sublingually (endothelium-independent vasodilation). Vasodilation was expressed as the percentage change relative to the baseline diameter. Baseline flow and blood pressure were similar for IDDM patients and C. Baseline vessel diameter was slightly larger in IDDM patients (3.10 +/- 0.52 mm) compared with C (2.89 +/- 0.55 mm, P = 5.0). FMD in IDDM patients was decreased (12.0 +/- 9.1% versus 15.7 +/- 9.5% in C, P = .046), as was GTN-induced vasodilation (14.9 +/- 8.2% versus 18.3 +/- 8.5% in C, P = .045). After correction for the difference in baseline diameter, FMD and GTN-induced dilation were not different between the groups. GTN-induced vasodilation decreased slightly with increasing diabetes duration. There was no relation between the vasodilatory responses and HbA1c. In normoalbuminuric IDDM patients, endothelium-dependent as well as endothelium-independent vasodilation are normal when the difference in baseline diameter is taken into account.

Adult↗