SEARCH · PubMed Health

Results for “Endothelial function”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1988

Effects of oleic acid-, alpha-naphthylthiourea-, and phorbol myristate acetate-induced microvascular damage on indexes of pulmonary endothelial function in anesthetized dogs.

To study the value of indexes of endothelial cell function in experimentally induced pulmonary microvascular injury, lung damage was produced in anesthetized dogs by intravenous injection of oleic acid (OA; n = 6), alpha-naphthylthiourea (ANTU; n = 5), or phorbol myristate acetate (PMA; n = 6). Angiotensin-converting enzyme (ACE) activity in serum and simultaneous measurements of serotonin (SER) and propranolol (PROP) pulmonary extraction along with several physiologic parameters were determined and compared with those obtained in a control group (n = 5) before and then at 2-h intervals for 8 h after administration of the toxic agent. ACE activity in serum showed a sustained and significant increase in the PMA and OA groups throughout the whole study period, whereas it decreased significantly at 4 h in the ANTU group. SER pulmonary uptake decreased significantly, but slightly, only in the PMA group at 8 h (-5%). At 6 and 8 h respectively, PROP extraction dropped significantly in the PMA (-11 and -13%) and OA (-13 and -19%) groups. This decrease in PROP extraction was likely to result from physiologic changes due to the development of pulmonary edema as suggested by the correlation between the changes in amine uptake and those affecting pulmonary artery pressure and total static respiratory compliance. The lack of effects on SER uptake by the lungs under these experimental conditions indicate that dissociation exists between metabolic dysfunction of pulmonary endothelial cells and fluid leakage.

Anesthesia↗

PubMed1998

Losartan but not verapamil inhibits angiotensin II-induced tissue endothelin-1 increase: role of blood pressure and endothelial function.

Endothelin partially mediates angiotensin (Ang) II-induced vascular changes in vivo. This study investigated the effects of the angiotensin type 1 receptor antagonist losartan and the calcium channel blocker verapamil on vascular reactivity and tissue endothelin-1 levels in aortas of Wistar-Kyoto rats treated for 2 weeks with Ang II (200 ng x kg(-1) x min(-1)). Ang II increased systolic blood pressure (39+/-4 mm Hg, P<0.05). Concomitant treatment with losartan abolished the Ang II-induced pressure increase (P<0.05), whereas verapamil reduced it only partially (P<0.05). In the aortas of rats with Ang II-induced hypertension, tissue endothelin-1 content was increased threefold and contractions to endothelin-1 were impaired (P<0.05). Interestingly, these alterations were normalized by losartan (P<0.05) but not by verapamil. Hence, there was a strong, negative correlation between contractions to endothelin-1 and tissue endothelin-1 content (r=-0.733, P<0.0001). In contrast, both antihypertensive drugs normalized impaired endothelium-dependent relaxations to acetylcholine and reduced the sensitivity of vascular smooth muscle to sodium nitroprusside compared with Ang II-treated rats (P<0.05). Ang II-induced hypertension enhanced endothelium-dependent contractions to acetylcholine, and these were normalized by either drug. In conclusion, these findings suggest that long-term treatment with Ang II modulates endothelin-1 protein expression in the rat aorta. Although both antihypertensive agents lowered blood pressure and normalized endothelial function, only losartan prevented the increase in tissue endothelin-1 content, suggesting that angiotensin type 1 receptor antagonists but not calcium antagonists modulate tissue endothelin-1 in vivo.

Angiotensin II↗

PubMed1994

The protective effect of L-arginine on myocardial injury and endothelial function following ischaemia and reperfusion in the pig.

The protective effect of the nitric oxide (NO) substrate L-arginine on myocardial ischaemial/reperfusion injury was studied in pigs. Four groups were subjected to 45 min ischaemia and 4 h reperfusion. One control group received coronary venous retroinfusion of saline, the second retroinfusion of L-arginine (1 mg.kg-1.min-1), the third retroinfusion of L-arginine plus the NO synthase inhibitor N omega-nitro-L-arginine (L-NNA), and the fourth systemic i.v. infusion of L-arginine (1 mg.kg-1.min-1). The infarct size in the L-arginine retroinfusion group was 35 +/- 5% of the myocardial area at risk compared to 76 +/- 5% in saline treated controls (P < 0.001). In pigs receiving the combination of retroinfused L-arginine and L-NNA the infarct size was similar to that of controls (79 +/- 4%). Systemic i.v. infusion of L-arginine did not influence the infarct size. Administration of L-NNA+L-arginine slightly increased arterial blood pressure during ischaemia but the groups did not differ in blood pressure, heart rate, rate-pressure product, left ventricular dP/dt or coronary blood flow during the reperfusion period. Coronary vasodilatation by acetylcholine was significantly compromised in the saline retroinfusion group, but not in the L-arginine retroinfusion group as compared to pigs not subjected to myocardial ischaemia. The results show that coronary venous retroinfusion of L-arginine reduces myocardial infarct size and preserves endothelial function via a local action which seems to be related to maintained nitric oxide formation.

Acetylcholine↗

PubMed1987

[Endothelial function and arteriosclerosis].

Elevated levels of plasma LDL have been correlated with morphological endothelial damages, e.g. reduced antithrombogenity of endothelial cells. Numerical and functional defects of endothelial cells probably influence the necessary separation of blood fractions from subendothelial tissues in a negative sense. In order to describe an imaginable endothelial dysfunction with respect to LDL transport we examined human umbilical venous endothelial cells (HUVEC) in culture under physiological flow conditions. HUVEC in culture after incubation with a LDL concentration of 100 micrograms/ml medium were exposed to defined levels of physiological shear stress, fixed with formalin and stained with oil-red-O. After documentation of oil-red-O staining with a photomicroscope, the amount of stain has been characterized semiquantitatively with the help of an image-analysis system (IBAS II/Zeiss). HUVEC not exposed to shear stress only showed a marginal oil-red-O staining at the cell surface. If they were exposed to shear stress of 0.5 dyn/cm2 they showed in orthogonal view an average increase of 1.3%, in cross-sectional view an average increase of 0.3%. HUVEC exposed to shear stress of 2.5 dyn/cm2 showed in orthogonal view an average increase of 4.6%, in cross-sectional view an average increase of 8.7%.

Arteriosclerosis↗

PubMed1987

Acute hypertension selectively potentiates constrictor responses of large coronary arteries to serotonin by altering endothelial function in vivo.

We tested the hypothesis that acute coronary artery hypertension may damage vascular endothelium and alter vasomotor responses to humoral agents. We examined effects of intracoronary infusion of the endothelium-dependent agent serotonin and two endothelium-independent agents, angiotensin II and methoxamine, on large coronary artery diameter in the blood perfused dog heart. Responses were examined before and 30 minutes after brief periods of coronary hypertension (200 mm Hg for 10 seconds to 15 minutes). In open-chest anesthetized dogs, the left anterior descending coronary artery was perfused at constant pressure. Coronary diameter (D) was measured with piezoelectric crystals. At a control perfusion pressure of 80 mm Hg, serotonin produced dose-dependent constriction of the large coronary artery (mean +/- SEM; delta D = -22 +/- 10 microns at 5 micrograms/min; -108 +/- 50 microns at 50 micrograms/min). Increasing perfusion pressure to 200 mm Hg increased flow 515 +/- 79% and coronary diameter 509 +/- 9 microns. After 15 minutes of hypertension, when coronary diameter had returned to baseline values, the constriction of the large artery to serotonin was potentiated (delta D = -89 +/- 33 microns at 5 micrograms/min; -207 +/- 45 microns at 50 micrograms/min; p less than 0.05). Hypertension for 1-5 minutes potentiated constrictor responses of large coronary arteries for at least 2 1/2 hours. Removal of endothelium prevented effects of hypertension on constrictor responses of large arteries to serotonin. Hypertension did not alter constrictor responses to angiotension II (1 and 2.5 micrograms/min) or methoxamine (50 and 100 micrograms/min) or the dilator response to acetylcholine (40 micrograms/min). Acute hypertension altered endothelial morphology. There were small endothelial craters following 10 seconds of hypertension, and disruption of endothelial junctions with leukocyte adherence following 1-15 minutes of hypertension. We conclude that acute hypertension alters constrictor responses of large coronary arteries to serotonin by impairing endothelial function and not by directly affecting vascular smooth muscle. These effects of acute hypertension on vascular reactivity are selective in that they do not involve non-endothelium-dependent agents or the endothelium-dependent agent, acetylcholine. The effect of hypertension also persists long after pressure is restored to normotensive levels.

Acetylcholine↗

PubMed1996

Physical fitness and endothelial function (nitric oxide synthesis) are independent determinants of insulin-stimulated blood flow in normal subjects.

Insulin induces vasodilation via stimulation of nitric oxide (NO) synthesis. This action of insulin exhibits considerable interindividual variation. We determined whether the response of blood flow to endothelium-dependent vasoactive agents correlates with that to insulin or whether other factors, such as physical fitness, limb muscularity, or vasodilatory capacity, better explain variations in insulin-stimulated blood flow. Direct measurements of the forearm blood flow response to three 2-h sequential doses of insulin (1, 2, and 5 mU/ kg.min), endothelium-dependent (acetylcholine and NG-monomethyl-L-arginine) and endothelium-independent (sodium nitroprusside) vasoactive agents, and ischemia (reactive hyperemic forearm blood flow) were performed in 22 normal subjects (age, 24 +/- 1 yr; body mass index, 22.2 +/- 0.6 kg/m2; maximal aerobic power, 40 +/- 2 mL/kg.min). The highest insulin dose increased blood flow by 111 +/- 17%. The fraction of basal blood flow inhibited by NG-monomethyl-L-arginine (NO synthesis-dependent flow) varied from 6-47%. Maximal aerobic power (r = 0.52; P < 0.02), the percentage of forearm muscle (r = 0.50; P < 0.02), and the NO synthesis-dependent flow (r = 0.42; P < 0.05), but not reactive hyperemic, acetylcholine-stimulated, or sodium nitroprusside-stimulated flow, were significantly correlated with insulin-stimulated (5 mU/kg.min) blood flow. In multiple linear regression analysis, 52% of the variation (multiple R = 0.72; P < 0.001) in insulin-stimulated blood flow was explained by NO synthesis-dependent flow (P < 0.005) and the percentage of forearm muscle (P < 0.005). We conclude that endothelial function (NO synthesis-dependent basal blood flow) and forearm muscularity are independent determinants of insulin-stimulated blood flow.

Adult↗

PubMed1997

Dietary supplementation with marine fish oil improves in vitro small artery endothelial function in hypercholesterolemic patients: a double-blind placebo-controlled study.

BACKGROUND: Marine fish oils improve vascular function, but the mechanism of benefit is unclear. We conducted a study to examine the effects of fish oils given to hypercholesterolemic patients on small artery function in vitro. METHODS AND RESULTS: In a randomized, double-blind, placebo-controlled trial, subcutaneous gluteal fat biopsies were taken from 16 hypercholesterolemic patients (serum total cholesterol, 7.97+/-0.16 mmol/L [mean+/-SEM]) and 12 age- and sex-matched control subjects (mean cholesterol, 5.11+/-0.34 mmol/L). Small arteries were mounted on a wire myograph for isometric tension experiments. Patients and control subjects were randomized to receive fish oil (Maxepa 5 capsules BID) or placebo for 3 months. A second biopsy was taken and the studies were repeated. Relaxation to acetylcholine was significantly improved in the hypercholesterolemic group given Maxepa but not in the placebo group (mean maximum relaxation before and after, 48+/-6.2% and 68.83+/-2.19%, P=.0054). The dysfunction was not restored to control values (84.3+/-5.2%, P=.0002). There was also a smaller but significant impairment in endothelium-independent relaxation provoked by sodium nitroprusside (P<.01). A good correlation between the increase in eicosapentanoic acid (n=3) in red cell membrane and improvement in relaxation in the hypercholesterolemic group given fish oils was seen (r=.781, P<.02). CONCLUSIONS: Marine fish oil significantly improved endothelial function in peripheral small arteries in hypercholesterolemia patients. This may provide a mechanism for the beneficial effects of these fatty acids in coronary heart disease.

Adult↗

PubMed1998

Vascular remodeling and endothelial function in hypertensive patients: effects of antihypertensive therapy.

OBJECTIVE: To review studies of effects of antihypertensive agents on alterations in structure and function of small (resistance-size) arteries in hypertensive patients and in experimental hypertensive models, since these vessels may contribute to blood pressure elevation or to the complications of hypertension. MAIN OUTCOME MEASURES: The structure and endothelium-dependent relaxation of small arteries obtained in hypertensive humans from gluteal subcutaneous biopsies, and from different vascular beds in hypertensive rats, without and after antihypertensive treatment, and studied on a wire-myograph or as pressurized arteries, are described as reported in different studies. RESULTS: Treatment of spontaneously hypertensive rats (SHR) with angiotensin converting enzyme (ACE) inhibitors, calcium channel antagonists, angiotensin receptor antagonists and novel beta blockers such as carvedilol, has been shown to result in regression of the altered structure of small arteries in different vascular beds, in addition to improved endothelium-dependent relaxation. Several studies in hypertensive patients have now shown that treatment with some ACE inhibitors (cilazapril and perindopril) or extended release calcium channel antagonists (nifedipine GITS) induces similar effects in small arteries obtained from gluteal subcutaneous biopsies: both structure and endothelium-dependent relaxation improve under treatment. In contrast, hypertensive patients with equally well-controlled blood pressure but treated with the beta blocker atenolol did not in any of three studies exhibit any improvement in the structure of small arteries or in endothelial function. CONCLUSION: Although treatment for at least one year with some ACE inhibitors and extended release calcium channel antagonists corrects the structure and endothelium-dependent relaxation of gluteal subcutaneous small arteries, it still remains to be determined whether this apparently beneficial effect beyond blood pressure lowering of these and other agents with vascular protective properties will result in reduced morbidity and mortality in hypertensive patients.

Adrenergic beta-Antagonists↗

PubMed1992

Differential role of endothelial function on vasodilator responses in series-arranged arterioles.

Both in vitro and in vivo studies have revealed that removal of vascular endothelial cells abolishes the vasodilation to acetylcholine (Ach) but not sodium nitroprusside (SNP). Differential properties of endothelial cells in the series-arranged arterioles to vasodilator responses have not been studied. In this study, the cheek pouch microcirculation from the golden syrian hamster anesthetized with sodium pentobarbital (6 mg/100 g body wt, ip) was prepared for intravital microscopy. Measurements of lumen diameters of small series-arranged arterioles (2nd- and 4th-order) were made before, during, and after topical microapplication of different doses of either Ach or SNP. After control measurements, a light-dye (L-D) technique utilizing sodium fluorescein (FITC-dextran(150K), 50 mg/100 g body wt, iv) and illuminating a discrete area of the arteriole with 490-nm-wavelength light for 3 (4th) or 10 (2nd) min was used to impair endothelial cell function without damaging vascular smooth muscle cells. Responses to vasoactive substances for both 4th-order (10-20 microns) and second-order (30-50 microns) arterioles were retested. Vasodilatory responses to 10(-7) M Ach and SNP also were tested with and without the presence of NG-monomethyl L-arginine (L-NMMA), an inhibitor of EDRF/NO formation. In the control state, Ach and SNP produced a focal, dose-dependent increase in diameter in all arterioles tested. Endothelial impairment by L-D treatment significantly suppressed the vasodilator response to Ach in 4th- but not 2nd-order arterioles, whereas the SNP response was not significantly affected. Consistent with these observations, L-NMMA treatment significantly attenuated Ach-induced vasodilation in 4th-order arterioles, but it had no effect on 2nd-order arterioles. These studies document further the role of the endothelium in local modulation of arteriolar diameter in response to acetylcholine and demonstrate a differential effect for this response in series-arranged microvessels. Thus, there may be a heterogeneous distribution of endothelial cell functions for modulating vasodilator activity in microvessels.

Acetylcholine↗

PubMed1994

Effect of L-arginine on coronary endothelial function in cardiac transplant recipients. Relation to vessel wall morphology.

BACKGROUND: Coronary endothelial vasodilator dysfunction is a common finding in cardiac transplant recipients and may represent an early marker for the development of intimal thickening and graft atherosclerosis. The present study tested the hypothesis that endothelial dysfunction precedes intimal thickening and that administration of L-arginine, the precursor of endothelium-derived relaxing factor, improves endothelial vasodilator function of coronary conduit and resistance vessels if given at an early stage of graft atherosclerosis. METHODS AND RESULTS: Acetylcholine (10(-6), 10(-5), 10(-4) mol/L) was infused into the left anterior descending or circumflex artery and repeated after intravenous infusion of L-arginine (10 mg.kg-1.min-1 over 20 minutes) in 18 cardiac transplant recipients. Epicardial responses were evaluated by quantitative angiography, and the microcirculation was studied by determination of coronary blood flow with a Doppler flow velocity wire. Intimal thickening was assessed by intravascular ultrasound (n = 14). In epicardial coronary arteries, acetylcholine tended to elicit vasoconstriction. Epicardial coronary vasoconstriction elicited by acetylcholine was attenuated by infusion of L-arginine (10(-4) mol/L, -6.8% versus -2.8%; P < .01); this beneficial effect was observed predominantly in patients with normal intravascular ultrasound characteristics. In coronary resistance vessels, acetylcholine induced vasodilation, reflected by increases in coronary blood flow. The acetylcholine-induced increase in blood flow was significantly enhanced with L-arginine (at a dose of 10(-4) mol/L, + 121% versus 176%; before versus after L-arginine, P < .002). CONCLUSIONS: The coronary vasculature of cardiac transplant recipients exhibits a generalized endothelial dysfunction of conduit and resistance vessels. L-Arginine improves endothelial dysfunction of both coronary microvasculature and epicardial coronary arteries. The reversibility of epicardial endothelial dysfunction by L-arginine is more likely in vessels with normal wall morphology.

Acetylcholine↗

PubMed1994

Effect of chronic ANG I-converting enzyme inhibition on aging processes. III. Endothelial function of mesenteric arterial bed of rat.

Age-related changes in endothelial (E) function were studied in mesenteric arterial bed (MAB) preparations removed from male, normotensive, WAG/Rij rats. At the age of 6 mo, one-half of the animals was assigned to chronic treatment with a hypotensive dose of an angiotensin I (ANG I)-converting enzyme inhibitor (ACEI; perindopril, 1 mg.kg-1.day-1 po). Animals were killed at 6, 12, 24, or 30 mo of age; the MAB was perfused in vitro, perfusion pressure (PP) being taken as an index of arteriolar tone. Disruption of E function produced a fall in baseline PP in all groups except 30-mo-old rats, suggesting that 1) baseline tone is maintained by the release of E vasoconstrictor factor(s) and 2) this mechanism is impaired in 30-mo-old rats. The muscarinic agonist, carbachol, antagonized vasoconstriction produced by norepinephrine (NE) in the presence of E. This mechanism was impaired in 30-mo-old rats. NE vasoconstriction increased following disruption of E, suggesting that NE release of endothelium-derived relaxing factor attenuates vasoconstriction. This mechanism was impaired in 30-mo-old rats. Chronic ACEI postponed the age-related decrease in E function, possibly due to a direct effect, or an indirect effect via the prolonged hypotensive action of such treatment.

Aging↗

PubMed1992

Cytokine regulation of endothelial cell function.

Endothelial cells have long been viewed as a passive lining of blood vessels endowed essentially with negative properties such as that of being nonreactive to blood components. It is now evident that upon exposure to environmental signals, cytokines in particular, vascular cells undergo profound changes in gene expression and function that allow these cells to participate actively in inflammatory reactions, immunity, and thrombosis. Different mediators (e.g., interleukin-1 [IL-1] and interferon-gamma) activate relatively distinct sets of functions. These functional programs expressed in activated endothelial cells include the production by the same cells of cytokines (e.g., IL-1, IL-6, chemotactic cytokines, and colony-stimulating factors), which regulate hematopoiesis, the differentiation and proliferation of T and B lymphocytes, and the extravasation of leukocytes. The identification of cytokine circuits through which vascular cells participate to thrombotic, inflammatory, and immune reactions provides novel targets for therapeutic intervention.

Animals↗

PubMedDate not supplied

Endothelial function and coronary risk reduction: mechanisms and influences of nitric oxide.

The biological mechanisms related to progression and regression of CAD are indeed complex. While endothelial injury and lipid accumulation play an important role in the progression/regression of CAD, mechanisms of vascular function, particularly that of the endothelial modulation of vasodilation, cannot be ignored. Much is yet to be learned about the influences of endothelial function on the progression/regression and stabilization of CAD. Initial evidence suggesting that risk reduction interventions favorably influence vascular function argues for further investigation of this role. To date, much of the research on risk reduction has focused on lipid lowering and regression of artery plaque, a focus on artery structure. A focus on both function and structure is likely to expand our understanding of the effect of risk reduction interventions beyond lipid lowering. Given the multifactorial causes associated with development of CAD, such an approach is necessary.

Coronary Disease↗

PubMed1996

[Effect of vitamin E on the endothelial function of the regenerated aorta in rats following direct arterial injury].

Fibromuscular intimal injury is frequent after coronary or peripheral angioplasty. Peroxidation of circulating and membrane lipids have been implicated in intimal hyperplasia and endothelial dysfunction following direct arterial trauma. The aim of this study was to evaluate the effects of natural membrane antioxidant, vitamin E (VE), on the vascular reactivity of the regenerated endothelium. A first group of rats (n = 10) was pretreated with VE 100 IU/kg/day for a week before undergoing aortic (thoracic) endothelial denudation with a Fogarty catheter. Rats were then fed with the same VE supplemented diet for a 2-month period. A second group (n = 10), was similarly denudated and fed with soya oil (SO), VE vehicle, for the same period. A third group (n = 10) was denuded and used as control (CL). Endothelial-dependent and independent relaxations were assessed in organ chambers with acetylcholine (ACH), adenosine diphosphate (ADP), histamine (HIS), 5-hydroxytryptamine (5-HT) and sodium nitroprusside (SNP). Endothelial regeneration was evaluated with Evans blue staining. Vascular relaxation to SNP was not affected either by the regeneration process or the VE supplementation. However, endothelial-dependent relaxation to ACH and HIS were significantly impeded in the regenerated endothelium compared to control but was not influenced by the VE or the SO supplementation. Vascular contraction to 5-HT was significantly decreased in VE group compared to the other groups. Morphometric studies with Evans blue staining showed over 95% regeneration of the endothelial surface of the denuded aortas. Our results suggest that in spite of a complete anatomical regeneration, endothelial cells did not resume predenudation function. Endothelial-independent relaxation was preserved in all groups indicating that smooth muscle function was not altered by the regenerating process. The presence of dietary supplement of VE (up to 20 fold the daily requirement) did not prevent the endothelial dysfunction to ACH and HIS but attenuated the vaso-contraction to 5-HT and then could contribute to decreased vascular tone in endothelium-regenerated vessels.

Animals↗

PubMed1998

Insulin-induced vasodilatation and endothelial function in obesity/insulin resistance. Effects of troglitazone.

Insulin resistance is associated with a decreased vasodilator response to insulin. Because insulin's vasodilator effect is nitric oxide dependent, this impairment may reflect endothelial dysfunction. Troglitazone, an insulin-sensitiser, might thus improve insulin-dependent and/or endothelium-dependent vascular function in insulin resistant obese subjects. For 8 weeks, fifteen obese subjects were treated with either 400 mg troglitazone once daily or placebo, in a randomised, double-blind, cross-over design. At the end of each treatment period, we measured forearm vasodilator responses (plethysmography) to intra-arterial administered acetylcholine and sodium nitroprusside; insulin sensitivity and insulin-induced vascular and neurohumoral responses (clamp); vasoconstrictor responses to NC-monomethyl-L-arginine (L-NMMA) during hyperinsulinaemia; and ambulatory 24-h blood pressure (ABPM). Baseline data (placebo) of obese subjects were compared with those obtained in lean control subjects. Obese subjects were insulin resistant compared with leans (whole-body glucose uptake: 26.8+/-3.0 vs. 53.9+/-4.3 [tmol kgl min-, p < 0.001). Troglitazone improved whole-body glucose uptake (to 31.9+/-3.3 micromol x kg(-1) x min(-1) , p=0.028), and forearm glucose uptake (from 1.09+/-0.54 to 2.31+/-0.69 micromol dL(-1) x min(-1), p=0.006). Insulin-induced vasodilatation was blunted in obese subjects (percent increase in forearm blood flow (FBF) in lean 66.5+/-23.0%, vs. 10.1+/-11.3% in obese, p=0.04), but did not improve during troglitazone. Vascular responses to acetylcholine, sodium nitroprusside and L-NMMA did not differ between the obese and lean group, nor between both treatment periods in the obese individuals. In conclusion, in insulin resistant obese subjects, endothelial vascular function is normal despite impaired vasodilator responses to insulin. Troglitazone improved insulin sensitivity but it had no effects on endothelium-dependent and -independent vascular responses. These data do not support an association between insulin resistance and endothelial function.

Acetylcholine↗

PubMedDate not supplied

Zinc and endothelial function.

Zinc (Zn), an essential trace element, has antioxidant functions, stabilizes membranes, and plays a role in the activity of a host of Zn metalloenzymes. Zn deficiency has been shown to increase erythrocyte fragility, decrease the Zn content of the erythrocyte membrane, and alter erythrocyte membrane fluidity. Recent studies have shown that Zn deficiency induced by various mechanisms disrupts endothelial barrier cell function in vitro, and this was corrected with Zn supplementation. Moreover, physiological amounts of Zn attenuated the barrier dysfunction produced by the inflammatory cytokine tumor necrosis factor. These data have important implications for acute vascular processes, e.g., adult respiratory distress syndrome, and chronic vascular processes, e.g., atherosclerosis. The mechanisms by which Zn may affect endothelial cell function and attenuate cytokine-induced endothelial cell dysfunction are important areas of continuing investigation.

Arteriosclerosis↗

PubMed1994

Angiogenesis and endothelial cell function.

Endothelial cell growth is tightly regulated. During embryonic development endothelial cells rapidly proliferate thereby forming new blood vessels. Two different mechanisms contribute to the development of the vascular system: vasculogenesis, the development of blood vessels from in situ differentiating endothelial cells, and angiogenesis, the formation of capillaries from preexisting vessels. In the adult, endothelial cell turnover is very low but under a variety of pathological conditions such as tumor growth these cells quickly enter the cell cycle and divide. Vascular endothelial growth factor (VEGF) has been identified as a key regulatory paracrine growth factor for endothelial cells. Transient VEGF expression correlates with embryonic and tumor angiogenesis. On the other hand, constitutive expression of this factor in choroid plexus and kidney glomerular epithelium and its cognate receptors in adjacent fenestrated endothelium suggests a role for this ligand-receptor system in organotypic endothelial cell differentiation and capillary permeability of fenestrated endothelium.

Animals↗

PubMed1984

Corneal endothelial function and structure following cryo-injury in the rabbit.

Wide-field specular microscopy, fluorophotometry, pachymetry, and scanning electron microscopy are used to characterize a reproducible, in vivo model of corneal endothelial injury and recovery in the rabbit. Following an 8-mm central cryo-injury, the cornea remains thickened for as long as 3 weeks. Mean endothelial permeability to fluorescein is above normal for 10 days following injury, but by 14 days postinjury the endothelial permeability to fluorescein is not statistically significantly different from preinjury control values, thus indicating that endothelial permeability probably returns to normal by approximately 2 weeks postinjury. Cell morphology, as determined by scanning electron microscopy, is also essentially normal by 2 weeks postinjury. Endothelial permeability appears to recover before stromal thickness normalizes, suggesting a lag in recovery of endothelial pump function.

Animals↗