Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fibromuscular dysplasia of renal arteries was the cause of hypertension in four consecutive children with renal artery stenosis. Two were asymptomatic, the third had had hypertension for seven years but had not been treated, and the fourth, a 9-month-old infant, presented with cardiac failure. Heart enlargement and left ventricular hypertrophy were present in all. Rapid sequence urograms demonstrated a smaller kidney and delayed appearance and disappearance of the contrast medium on the affected side in all. Angiograms showed left RAS in all. Peripheral plasma renin activity was elevated in only three of the four patients. Antihypertensive and diuretic drugs were not very effective therapeutically. Ischemia of the ipsilateral kidney probably prevented normal growth and led to shrinkage of the kidney in one patient. Following nephrectomy the BP has remained normal without any therapy for 24 to 64 months. With normalization of BP, accelerated growth ensued, the cardiomegaly regressed and the hypertensive retinopathy resolved. These patients demonstrate that: (1) FMD is an important cause of RAS. (2) the well-known radiologic feature of FMD, the beaded appearance, is usually not seen in children. (3) control of BP leads to normalization of linear growth, usually impaired in severe hypertension, and (4) target organ complications such as cardiomegaly, LVH, and hypertensive retinopathy are reversible in one to 10 months.
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PMID:Fibromuscular dysplasia of renal arteries: an important cause of renovascular hypertension in children. 15 54

Flow (shear stress)-mediated dilation (FMD) plays a key role in the local control of vascular diameter and blood flow supply. Although vasodilator treatments improve FMD in diverse models of hypertension, FMD may also change in situations where systemic blood pressure is not affected. In pathological situations such as ischemia, local blood flow and vascular density are increased by vasodilators not affecting systemic blood pressure. As the mechanisms involved remain obscure, we studied FMD in resistance arteries from mice treated chronically (1 month) with hydralazine (200 mg/L in drinking water). Blood flow in mesenteric arteries of mice treated with hydralazine was significantly increased (130 +/- 15 to 169 +/- 27 microl/min, n = 10/group), whereas mean arterial blood pressure was not affected (79 +/- 5 vs 82 +/- 3 mm Hg in controls). Mesenteric resistance arteries (90 microm internal diameter, 75 mm Hg) were isolated and mounted in vitro in an arteriograph. Pressure (myogenic tone)-, phenylephrine-, and KCl-induced contractions, as well as acetylcholine- and sodium nitroprusside-induced dilations, were unaffected by hydralazine. Flow-mediated dilation in arteries from hydralazine-treated mice was significantly increased, especially for low flow values (up to sevenfold). L-NAME-sensitive and indomethacin-sensitive FMD were both increased by hydralazine. Passive arterial diameter increased and arterial wall thickness decreased after chronic hydralazine. This is the first functional evidence that flow (shear stress)-mediated dilation in resistance arteries is improved by a chronic treatment with a nonselective vasodilator. This arteriolar adaptation to a chronic increase in blood flow might be of importance in the pathophysiology of ischemic diseases.
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PMID:Chronic hydralazine improves flow (shear stress)-induced endothelium-dependent dilation in mouse mesenteric resistance arteries in vitro. 1207 39

Impaired endothelium-dependent vasomotion is a diffuse disease process resulting in abnormal regulation of blood vessel tone and loss of several atheroprotective effects of the normal endothelium. The aim of the present study was to investigate the effects of aging and hypertension on endothelial function. Sixty-six geriatric subjects with ages over 60 (48 hypertensive and 18 healthy) and 40 middle-aged subjects (16 hypertensive and 24 healthy) were included in the study. Systemic vascular endothelial function was evaluated through measuring brachial arterial vasodilation, a physiologic answer to reactive hyperemia occured with increased blood flow in the vessel after transient ischemia (flow-mediated dilation, FMD%), and with carotid artery intima-media thickness (IMT) measurement, using high-resolution ultrasonography. Endothelial independent vasodilation was also measured after administration of sublingual isosorbide dinitrate (isosorbide dinitrate mediated dilation, IDNMD%). FMD% was significantly decreased in elderly and/or hypertensive (HT) patients (geriatric HT: 9.5 +/- 4.7%, geriatric non-HT: 12.7 +/- 5.5%, middle-aged HT: 12.9 +/- 4.3% and middle-aged non-HT: 18.9 +/- 8.1%) (geriatric HT versus geriatric non-HT (P = 0.02), geriatric HT versus middle-aged HT (P = 0.01), geriatric non-HT versus middle-aged non-HT (P = 0.008)). Both FMD% and IDNMD% were inversely correlated with age, baseline vessel diameter and carotid artery intima-media thickness. FMD% was also inversely correlated with diastolic blood pressure. No correlation was found between FMD% and systolic blood pressure, serum cholesterol and triglyceride levels. Endothelium dependent (EDD) and independent dilatation of large arteries decreased with aging even in the healthy elderly, and FMD further declined in HT elderly patients, indicating that age and hypertension independently impair endothelial function. Positive correlations with age and hypertension, and significant inverse correlation with FMD, makes carotid artery IMT a possible indicator of endothelial function.
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PMID:Non-invasive evaluation of endothelial function in hypertensive elderly patients. 1553 Oct 24

Fibromuscular dysplasia is a multifactorial arteriopathy most commonly affecting the renal and carotid arteries. In this report we present a case of visceral artery involvement, causing occlusion of the superior mesenteric artery and celiac trunk and resulting in visceral ischemia. Treatment consisted of superior mesenteric artery reimplantation. Visceral artery FMD can present as occlusive or aneurysmal disease and treatment depends on patient characteristics and symptoms.
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PMID:Fibromuscular dysplasia of the superior mesenteric artery--case report and review of the literature. 1631 39

Although several observations suggest that insulin resistance/compensatory hyperinsulinemia (IR/CH) has a direct effect on endothelial function, independently of the metabolic abnormalities associated with the defect in insulin action, this relation has not been evaluated in apparently healthy individuals. To address this issue, we measured endothelial-dependent vasodilation in response to forearm ischemia (flow-mediated dilation [FMD]) in 47 nonsmoking, healthy volunteers without known risk factors for atherosclerosis. Measurements were also made of multiple anthropometric, metabolic, and hemodynamic variables related to IR/CH. Decreases in FMD were significantly correlated (analysis of variance for linear trend) with (1) male gender (p = 0.003), (2) waist circumference (p = 0.038), (3) higher fasting plasma insulin (p = 0.015) and triglyceride concentrations (p = 0.023), and (4) lower concentrations of high-density lipoprotein cholesterol (p = 0.001). Multivariate linear regression analysis indicated that only plasma insulin (beta -0.424) was independently associated (p <0.001) with changes in FMD, and individual differences in insulin concentrations, along with gender and brachial artery diameter at baseline, accounted for approximately 39% of the variability in FMD. In conclusion, IR/CH is an independent predictor of decreases in endothelial-dependent vasodilation in apparently healthy individuals, in the absence of traditional risk factors for atherosclerosis.
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PMID:Relation of plasma insulin levels to forearm flow-mediated dilatation in healthy volunteers. 1661 36

Although microvascular dysfunction is of critical importance in the pathophysiology of myocardial ischemic syndromes, no study has investigated whether there are differences in the sensitivity to ischemia and reperfusion injury between microvessels and conduit arteries. Ten healthy young nonsmoking male volunteers (age range 24-45) were enrolled. Parameters measured included radial (conduit) artery (endothelium-dependent) flow-mediated dilation, microvascular cutaneous reactive hyperemia (using laser Doppler) and acetylcholine-induced microvascular vasodilation (laser Doppler iontophoresis). Data were acquired before and after ischemic injury (15 minutes of ischemia of the brachial artery followed by 15 minutes reperfusion) and analyzed in a randomized, blinded fashion. Conduit artery FMD was significantly blunted after ischemia (before: 7.5 +/- 1.1%; after: 2.9 +/- 1.0%, P < 0.05). Conversely, ischemia had no effect on microvascular reactive hyperemia (P = ns) and acetylcholine-induced vasodilation (P = ns). Using a human in vivo model, we demonstrate that microvessels are more resistant to ischemic injury as compared to conduit arteries.
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PMID:The effect of ischemia and reperfusion on microvascular function: a human in vivo comparative study with conduit arteries. 1689 23

Endothelial function is widely evaluated by vasodilatation of the brachial artery induced by ischemia (flow-mediated vasodilatation, FMD). The function of the endothelium, in this setting, is to sense wall shear stress (WSS) increase and to release vasodilators. Following current guidelines FMD is measured 50-60s after ischemia. It is not known whether this lapse of time is sufficient to observe maximal vasodilatation, especially in diseased subjects. Sixty-six subjects with type 2 diabetes and 30 controls underwent FMD-test. Brachial artery WSS was measured at rest and during the first 15s after ischemia as index of peripheral resistances vessels reactivity, and FMD at 50, 120, 180, and 300s after ischemia as index of conduit vessel function. All controls exhibited increased WSS and peak FMD at 50s. Among subjects with diabetes three groups were identified based on the time at which peak FMD occurred. Twenty subjects with diabetes exhibited peak at 50s (Early FMD), 28 at 2 min (Late FMD), and 18 showed no FMD (Absent FMD). Peak FMD in Late FMD subgroup was comparable to peak in control subjects and significantly higher than peak in other subjects with diabetes. The "Absent FMD" group showed also impaired WSS. The present findings demonstrate that brachial artery response to ischemia is heterogeneous in type 2 diabetes, suggesting different mechanisms responsible for FMD alteration in this condition.
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PMID:Endothelial dysfunction or dysfunctions? Identification of three different FMD responses in males with type 2 diabetes. 1826 89

This investigation set out to determine the effect of 56 days of head-down tilt bed rest (HDBR) and an exercise countermeasure on endothelial dependent and independent vascular function. 24women took part in this study. 8 subjects completed lower body resistance and aerobic exercise (EX, treadmill running 3-4 days per week for 40-min followed by 10-min of static LBNP, and resistive exercise on a flywheel device every 3rd day) and 16 subjects were considered as non-exercisers in a control group and a protein supplement group. FMD was induced by release of distal limb ischemia and NMD by sublingual administration of 0.3 mg of nitroglycerin before and after HDBR. Preliminary results of this study suggest that HDBR without EX results in a decreased resting diameter of the popliteal while EX increased the diameter. It is also suggested that FMD was elevated without exercise in both brachial and popliteal arteries, while pre-HDBR FMD was preserved by EX in the popliteal, but not the brachial artery. NMD appears to be elevated in the popliteal and femoral in the absence of exercise, but unchanged in the brachial artery or at any site for EX.
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PMID:WISE 2005: flow and nitroglycerin mediated dilation following 56 days of head down tilt bed rest with and without an exercise countermeasure. 1837 97

By the time the clinical findings of atherosclerotic disease appear, involvement is usually at an advanced stage and procedures after this stage are usually palliative or aimed at secondary protection. On the other hand, prevention can be achieved by the detection and treatment of endothelial dysfunction, which is one of the most important changes in the early subclinical stage of atherosclerotic disease. When the systemic involvement of endothelial dysfunction is taken into consideration, checking from the peripheral arteries with noninvasive methods gives one-to-one correct information. Currently, endothelial dysfunction can be detected using simple, inexpensive, and noninterventional methods. Particularly, easily accessible localization of the brachial artery is ideal for the evaluation of endothelial dysfunction. Flow-mediated dilation method (FMD; endothelial-dependent vasodilation), which can be carried out noninvasively with ultrasonography on the brachial artery, is a frequently used method for the assessment of endothelial dysfunction. A sphygmomanometer is placed on the forearm to create a flow stimulation in the brachial artery. The sphygmomanometer is inflated until the systolic pressure is above 50 mm Hg, thus stopping the antegrade blood flow and creating ischemia. Consequently, vasodilation occurs at the resistance arteries distal to where the flow is blocked. When the sphygmomanometer is deflated, a reactive hyperemia occurs in the brachial artery. The % difference between the diameter measured after reactive hyperemia and the basal diameter is taken as FMD. The effects of the treatments on endothelial dysfunction can be monitored with this method. Studies have shown that angiotensin-converting enzyme (ACE) inhibitors, angiotensin 1 (AT1) receptor blockers, latest-generation beta blockers such as nebivolol and carvediol, statins, estrogen treatment, diet, and exercise increase FMD. Before this method becomes a part of routine clinical evaluation of cardiovascular disease (CVD) risk, measurement technique and FMD values need to be standardized.
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PMID:Evaluation of endothelial dysfunction: flow-mediated dilation. 1866 19

Studies in animals show that fibroblast growth factor (FGF)-23 interferes with vascular reactivity induced by the nitric oxide (NO) system. To investigate the relationship between circulating FGF-23 levels and the response of forearm blood flow to ischemia (flow-mediated vasodilatation, FMD) and nitroglycerin, we tested 183 patients with stage 3-4 chronic kidney disease (CKD). None of them had cardiovascular complications or were taking drugs interfering with vascular function. Patients with FGF-23 levels above the median had significantly lower glomerular filtration rate, FMD, and fetuin-A levels (an anti-inflammatory molecule and potent inhibitor of calcification). They also had higher proteinuria and phosphate levels when compared to patients whose FGF-23 levels were below the median. The response to nitroglycerin was not different between the two groups. Multiple regression analysis showed that the relationship between FGF-23 and FMD was only modestly sensitive to adjustment for classical risk factors, biomarkers of bone mineral metabolism, high-sensitivity C-reactive protein, and homeostatic model assessment index. Adjustment for asymmetrical dimethyl arginine (ADMA) weakened the strength of this link; however, it remained highly significant. There was no independent association between FGF-23 and nitroglycerin. Thus, attenuation of FMD by ADMA suggests that this endogenous inhibitor of NO synthase may, in part, mediate the vascular effects of FGF-23 in patients with CKD.
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PMID:FGF-23 and vascular dysfunction in patients with stage 3 and 4 chronic kidney disease. 2061 14


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