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At least 1,603 records · Page 89Linked to original sources
PubMed1993

Effects of a xanthine oxidase/hypoxanthine free radical and reactive oxygen species generating system on endothelial function in New Zealand white rabbit aortic rings.

We investigated the effects of the xanthine oxidase (XO)/hypoxanthine (HX) free radical (FR) generating system on the relaxant properties of aortic rings from New Zealand White rabbits. This system generates superoxide anions, hydroxyl radicals, and H2O2. We wished to identify which of these species is responsible for impairment of vascular function. After obtaining dose-response curves to phenylephrine (PE) and carbachol or sodium nitroprusside (SNP), we exposed rings to the FR generating system or H2O2 for 30 min, either with or without a range of potentially protective agents. Dose-response curves to carbachol or SNP were then repeated. Exposure to the XO/HX system impaired endothelium-dependent, carbachol-induced relaxation. The hydroxyl radical scavengers mannitol, N-(2-mercaptopropionyl)-glycine (MPG), and captopril offered no protection. Superoxide dismutase (SOD) increased the impairment of response, catalase provided partial protection, and a combination of SOD and catalase completely prevented impairment of the response. H2O2 mimicked the effects of XO/HX system. H2O2 appears to be the primary species involved in mediating the toxic effects of the XO/HX FR generating system, but the superoxide anion is probably responsible for some of the loss of relaxation and a role for intracellular generation of hydroxyl radicals cannot be excluded.

Animals↗
PubMed1995

Effect of long-term angiotensin-converting enzyme inhibition on endothelial function in patients with the insulin-resistance syndrome.

Cardiovascular risk factors such as hypertension, diabetes, and dyslipemia are associated with an impaired endothelium-dependent vasodilation. In patients with type 2 diabetes mellitus, these risk factors are frequently clustered. We investigated whether long-term treatment with the angiotensin-converting enzyme (ACE) inhibitor perindopril can improve endothelium-dependent vasodilation in this particular group of patients. We selected 10 patients with type 2 diabetes and hypertension (age 59.4 +/- 3.2 years, body mass-index 29.7 +/- 1.5 kg.m-2, blood pressure 169 +/- 6/92 +/- 1 mm Hg, total cholesterol 6.6 +/- 0.3 mM). Using venous occlusion plethysmography, we recorded the increases in forearm blood flow (FBF) in response to three vasodilator stimuli: (a) 5 min of forearm ischemia, (b) infusion of the endothelium-dependent vasodilator methacholine (Mch) into the brachial artery (0.03, 0.3, and 1.0 micrograms/min/100 ml), and (c) intraarterial infusion of the endothelium-independent vasodilator sodium nitroprusside (SNP 0.06, 0.2, 0.6 microgram/min/100 ml). This procedure was repeated after 6 months of treatment with perindopril 4-8 mg/day. Forearm vascular resistance (FVR) was calculated by the quotient of the mean arterial pressure (MAP) and the FBF. Perindopril reduced blood pressure (BP) by 19/10 mm Hg (p < 0.05) and increased baseline FVR, but improved neither the maximal percentage decrease in vascular resistance induced by Mch (from -80 +/- 2 to -82 +/- 2%) nor that induced by SNP (from -73 +/- 3 to -72 +/- 3%). Perindopril decreased the FVR reached after the ischemic stimulus from 6.5 +/- 1.2 to 4.8 +/- 0.6 U (p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2001

Endothelial function in patients with chronic heart failure.

Congestive heart failure is characteristically associated with systemic vasoconstriction and impaired vasodilatory capacity, leading to decreased peripheral perfusion. Factors identified as possible causes of reduced vasodilatory capacity include activation of the sympathetic nervous system and the renin-angiotensin system, vascular stiffness due to increased sodium and fluid retention, and structural vascular changes. More recently, the role of the endothelium as a mediator of vasoregulation and tissue perfusion has been recognized.

Endothelium, Vascular↗
PubMed1984

Growth hormone and endothelial function during exercise in diabetics with and without retinopathy.

Changes in plasma growth hormone (GH), factor VIII related antigen (VIIIR:Ag), and plasminogen activator activity (PAA) during exercise were evaluated in 50 insulin-dependent diabetics. In patients with a short to moderately long duration of diabetes (5-19 years, mean 11), GH increased only in those with retinopathy. VIIIR:Ag and PAA increased most pronouncedly in retinopathy patients as well. In diabetics with long duration of the disease (21-49 years, mean 35), GH, VIIIR:Ag and PAA increased almost equally in those with and without retinopathy.

Adult↗
PubMed2005

Growth hormone replacement reduces C-reactive protein and large-artery stiffness but does not alter endothelial function in patients with adult growth hormone deficiency.

Hypopituitary patients have an increased risk of vascular mortality that may relate to growth hormone deficiency (GHD). We investigated the effects of 6 months of GH therapy on large- and small-artery function and high-sensitivity C-reactive protein (hsCRP) in a cohort of GH-deficient patients. Sixteen hypopituitary patients were randomized to 6 months of GH therapy or no treatment, then vice versa. hsCRP, 24-h blood pressure (BP) and pulse wave velocity (PWV) were measured and resistance arteries were used to construct concentration-response curves to endothelium-dependent and -independent agents. GH therapy increased IGF-1 from 60 +/- 7.2 to 167 +/- 16.2 microg/l [confidence interval (CI) 94.9, 138.8, P < 0.001]. hsCRP declined after 6 months of GH from 3.8 +/- 0.88 to 2.0 +/- 0.49 mg/l (CI 0.73, 3.57, P = 0.006). Mean arterial BP fell from 91.7 +/- 1.5 to 89.3 +/- 1.2 mmHg (CI 0.81, 4.07, P = 0.005), as did PWV (8.1 +/- 0.4 to 6.7 +/- 0.5 m/s). The decline in PWV correlated with the decline in hsCRP (r = 0.68, P = 0.01). Resistance artery function was unchanged after GH therapy. GH replacement may lead to differentially altered production of vasorelaxant agents from the endothelium of large and small arteries. Reduction in vascular inflammation may be associated with reduced vascular risk.

Adult↗
PubMed2004

Arterial stiffness, endothelial function and novel pharmacological approaches.

1. Despite over half a century of intensive research, cardiovascular disease remains the leading cause of death world wide. Nevertheless, a number of risk factors for cardiovascular disease have been identified, such as hypertension and serum cholesterol, and therapies targeting such factors are effective in reducing cardiovascular and total mortality. Arterial stiffness is an additional independent risk factor for cardiovascular disease and strategies aimed at lowering arterial stiffness may be effective in reducing cardiovascular risk. However, in order to exploit fully the therapeutic potential of this approach, it is necessary first to understand the physiological and pathophysiological factors regulating the stiffness of the large arteries. 2. Until recently, stiffness was thought to depend largely upon structural components within the arterial wall, such as elastin and collagen and the distending pressure. However, we now recognize that arterial smooth muscle also regulates vessel stiffness and that a number of locally derived and circulating factors, including nitric oxide (NO), endothelin-1 and the natriuretic peptides, contribute to the short-term or functional regulation of large artery stiffness. Changes in the balance between these factors and, in particular, a reduction in NO production may well explain why conditions such as hypercholesterolaemia and diabetes are themselves associated with arterial stiffening before the development of manifest atherosclerosis. 3. The importance of smooth muscle in regulating arterial stiffness suggests that direct pharmacological manipulation of stiffness may be possible, thus providing novel therapeutic strategies to reduce cardiovascular risk. Furthermore, differences in the effect of existing drugs on larger artery stiffness may explain, in part, why some drugs produce better clinical outcomes than others.

Animals↗
PubMed1997

Reproducibility of brachial ultrasonography and flow-mediated dilatation (FMD) for assessing endothelial function.

BACKGROUND: High-resolution brachial artery ultrasonography is used to study vasodilator response induced by physiologic reactive hyperaemia. We examined the reproducibility of measuring flow-mediated dilatation (FMD) on two occasions. AIMS: To determine the degree of variability of this technique in our vascular laboratory for the design of clinical research studies. METHODS: Nineteen subjects were studied on two separate occasions using an Acuson 128 ultrasound device and a 7.0 MHz linear array transducer. Reactive hyperaemia was induced in the brachial artery by inflation and release of a blood pressure cuff. Nitrate-induced dilatation was assessed in 11 of the 19 subjects. Measurements were made by two observers blinded to subject details. RESULTS: The 11 subjects given sublingual GTN during the first ultrasound study had a mean nitrate-induced dilatation of 20.7% (sd 9.6). The mean vessel diameter of 3.78 mm (sd 0.7) at rest and 3.89 mm (sd 0.7) during reactive hyperaemia yielded a mean FMD of only 3.0% (sd 2.7). The mean difference in FMD within-observers was 0.13% (sd 2.07), between-observers 0.06% (sd 2.17) and between-studies was 0.57% (sd 6.83). CONCLUSIONS: The reproducibility of FMD measured by brachial artery ultrasound was poor and likely to render the measurements inaccurate for clinical research in our hands. Between-study variation contributed the largest proportion of total study variability. We suggest that investigators using this technique conduct their own careful reproducibility studies in order to avoid the misinterpretation of 'negative' studies.

Adult↗