PubMed Health⌕ Search

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 55 records · Page 3Linked to original sources
PubMed1992

Alteration of endothelial function in arterioles of renal hypertensive rats at two levels of vascular tone.

DESIGN: Arterioles were studied in vivo to determine whether the altered response to endothelium-dependent and -independent vasodilators in one-kidney, one clip (1K1C) hypertensive rats was related to increased vascular tone or precontraction with norepinephrine. METHODS: Acetylcholine, bradykinin and nitroprusside were applied topically to arterioles in the spinotrapezius muscle of 4-week 1K1C hypertensive rats and normotensive control rats. The changes in internal diameter of arcade arterioles in response to four doses of each drug were measured with intravital microscopy before and during superfusion of indomethacin. Arteriolar responses were redetermined during enhancement of vascular tone by superfusion of norepinephrine. RESULTS: Vasodilation in response to acetylcholine, but not to nitroprusside, was reduced in 1K1C rats compared with normotensive rats. Indomethacin decreased the resting arteriolar diameter, but did not alter the response to acetylcholine or nitroprusside. The response to bradykinin, which was partly attenuated after cyclo-oxygenase inhibition, was also reduced in 1K1C rats. The attenuated endothelium-dependent responses in 1K1C rats may have been a result of changes in the synthesis or release of endothelium-derived relaxing factor because the response to the endothelium-independent vasodilator nitroprusside was unchanged. Indomethacin attenuated the vasodilation of bradykinin, which suggests that prostacyclin is involved in this action in vivo. CONCLUSIONS: Precontraction with norepinephrine did not change any of the responses, indicating that the reduced endothelial-dependent responses in hypertensive rats cannot be explained by differences in vascular tone.

Acetylcholine↗
PubMed1991

Endothelial function in human coronary arteries in vivo. Focus on hypercholesterolemia.

To examine whether and to what extent hypercholesterolemia may affect the vasoactive role of the endothelium before the onset of angiographically visible atherosclerosis in the coronary circulation, we studied normal subjects (group 1, n = 11), individuals with elevated low density lipoprotein plasma values but angiographically smooth coronary arteries (group 2, n = 8), and patients with hypercholesterolemia and minimal disease of the vessel under study (group 3, n = 8). Coronary vasomotor function was evaluated by three interventions: subselective intracoronary infusion of acetylcholine (0.036, 0.36, and 3.6 micrograms/min) with a 3F Doppler catheter in the left anterior descending artery, 0.3 mg intracoronary nitroglycerin ("endothelium-independent"), and increase in blood flow (assessment of flow-dependent, endothelium-mediated coronary dilation). In group 1, all interventions caused coronary dilation of the left anterior descending artery as assessed by automatic quantification of digitized cineframes. However, in group 2, acetylcholine elicited substantial coronary vasoconstriction, and the vasodilator response to nitroglycerin and to increases in flow (flow-dependent dilation) was preserved. In group 3, the acetylcholine-induced coronary vasoconstriction was even more pronounced, and the flow-dependent dilation was impaired (+5.1 +/- 1% versus +10.5 +/- 1.1% [group 1], p less than 0.05). The coronary flow reserve (derived from Doppler flow velocity measurements) in response to papaverine was not significantly different in normal and hypercholesterolemic individuals (groups 2 and 3). However, the increase in coronary flow exerted by acetylcholine was substantially depressed in patients with hypercholesterolemia (groups 2 and 3) as compared with normal individuals (+48 +/- 8.3% and +49 +/- 25% versus +220 +/- 28.5%, respectively, p less than 0.01). Thus, hypercholesterolemia elicits endothelial dysfunction in coronary conduit and resistance vessels in humans that precedes angiographically visible atherosclerotic lesions in large coronary arteries. Conceivably, these vascular alterations contribute to increased coronary vasomotor tone within the coronary circulation and may predispose these patients to myocardial ischemia.

Acetylcholine↗
PubMed1992

Nitrates in different vascular beds, nitrate tolerance, and interactions with endothelial function.

The favorable anti-ischemic effect of nitrates is based on the unique distribution pattern of vascular relaxation that they evoke in different vascular sections. Nitrovasodilators reduce cardiac preload and wall tension, and thus myocardial oxygen consumption. They increase precollateral coronary perfusion pressure, thereby augmenting oxygen delivery to ischemic sections, especially to the subendocardial layers. These vasodilator actions are caused by the nitric oxide (NO)-induced activation of soluble guanylyl cyclase, which augments vascular cyclic guanosine monophosphate (cGMP) levels to suppress intracellular Ca2+ concentrations. After some metabolic steps NO is finally cleaved from all nitrovasodilators and is probably identical with, or very closely related to, endothelium-derived relaxing factor (EDRF). A dinitrosyl-iron complex may serve under biologic conditions to stabilize the NO- radical, which has an extremely short half-life. NO derived from nitrovasodilators is used therapeutically to substitute for a deficient endothelium-mediated vascular control and autacoid production.

Animals↗
PubMed1992

Endothelial function in chronic congestive heart failure.

There is evidence that the endothelium plays an important role in the control of human vascular tone by releasing endothelium-derived nitric oxide. The hypothesis that an impairment of this mechanism is involved in the increased peripheral vasoconstriction of patients with chronic congestive heart failure (CHF) was tested. Acetylcholine and N-monomethyl-L-arginine (L-NMMA), a specific inhibitor of nitric oxide synthesis from L-arginine, were infused in the brachial artery of healthy volunteer subjects (controls) and patients with severe CHF. The radial artery diameter was determined by a high-precision A-mode ultrasound device, using a 10 MHz probe. Forearm blood flow was calculated from vessel diameter and blood flow velocity measured simultaneously by Doppler. The blood flow response to acetylcholine was blunted in patients with CHF compared with that in control subjects. In contrast, the decrease in blood flow induced by L-NMMA was exaggerated in CHF, and the blood flow response to nitroglycerin was preserved. The changes in radial artery diameter induced by acetylcholine and L-NMMA were not significant in control subjects and CHF patients, but dilation of the radial artery by nitroglycerin was significantly reduced in CHF. The results demonstrate an impaired endothelium-dependent dilation of forearm resistance vessels in CHF, suggesting a reduced release of nitric oxide on stimulation. In contrast, the basal release of nitric oxide from endothelium of forearm resistance vessels is preserved or may even be enhanced, and may play an important compensatory role in chronic CHF by antagonizing neurohumoral vasoconstrictor forces in CHF.

Acetylcholine↗
PubMed1989

Hepatic reticulo-endothelial function: a correlation of radioisotopic and immunohistochemical assessment.

Using an immunoperoxidase staining technique for muramidase (lysozyme)-containing cells in liver biopsies, the Kupffer cell population has been compared with the isotope liver scan abnormalities in 43 patients with various liver diseases. A significantly greater degree of scintigraphic abnormality was seen in cirrhotics compared with non-cirrhotics using both a visually assessed scan scoring technique (p less than 0.001) and computer-generated spleen-to-liver (S-L) relative activity ratios (p less than 0.01). The mean muramidase-positive cell count in cirrhotic biopsies was not significantly different from that in non-cirrhotics, neither was there any significant difference between alcoholic and non-alcoholic liver disease. The liver mass was shown to be significantly greater (p less than 0.02) in alcoholic compared with non-alcoholic disease, but even if corrections were made for this, no significant differences were found. A significant (p less than 0.02) negative correlation was found between liver scan score and muramidase-positive cell count in patients with cirrhosis but not in non-cirrhotic disorders. No significant correlations were observed if the computer-derived liver mass was taken into consideration. These results suggest that the scan defect seen in liver disease cannot be explained by loss of Kupffer cells alone, although they are consistent with the hypothesis that intrahepatic shunting plays a significant role. Chronic alcohol ingestion does not in itself appear to be a major independent influence.

Adult↗
PubMed1990

Effects of angiotensin converting enzyme inhibitors and of hydralazine on endothelial function in hypertensive rats.

The function of the endothelium is impaired in hypertension. In spontaneously hypertensive rats (SHR), acetylcholine-induced relaxation is decreased and serotonin-induced constriction is increased. The goal of our study was to evaluate the effect of a long-term treatment with cilazapril, a new angiotensin converting enzyme inhibitor, or hydralazine, a vasodilator, on the endothelium-dependent responses in aorta of SHR. Wistar-Kyoto rats were used as normotensive reference. Isolated aortic rings with or without endothelium were suspended in organ chambers. The rings with intact endothelium were contracted with norepinephrine. Acetylcholine-induced relaxation was markedly enhanced by cilazapril treatment. The tension achieved at maximal relaxation was 8 +/- 4% of norepinephrine contraction in the cilazapril-treated SHR versus 55 +/- 5% in the untreated SHR (p less than 0.001). Hydralazine had no significant effect. The effect of serotonin was also markedly modified by cilazapril. In untreated SHR, serotonin induced the release of a vasoconstrictor substance by the endothelium as assessed by the ratio of maximal tension induced by serotonin in rings with endothelium over maximal tension in rings without endothelium, which was greater than 1. This ratio was reversed in cilazapril-treated SHR but not in hydralazine-treated SHR. Captopril had effects similar to cilazapril. Finally, evaluation of carotid arteries showed that cilazapril also prevented morphological changes of the intima in SHR (i.e., infiltration by mononuclear cells). We conclude that angiotensin converting enzyme inhibitors prevent the functional and morphological alterations in endothelium that are found in hypertension and speculate that this action might participate in their antihypertensive effect.

Acetylcholine↗
PubMedDate not supplied

Alterations of the endothelial function of isolated aortae in rats with adjuvant arthritis.

Adjuvant arthritis was induced in 30 male Wistar rats by injection into the tail of heat-killed Mycobacterium butyricum. Three weeks later, 14 of these rats exhibited severe arthritic lesions. Their thoracic aortae were studied in parallel with those isolated from a control group. On rings precontracted with phenylephrine (0.1 microM), the endothelium-dependent relaxations produced by acetylcholine and histamine were significantly diminished in the arthritic group as compared to the control group. Moreover, the increase in tone induced by incubation with methylene blue (10 microM) (a nonspecific inhibitor of endothelium-derived relaxing factor) was significantly less pronounced in preparations isolated from the arthritic group. On the other hand, relaxations produced by the endothelium-independent vasodilators verapamil and nitroprusside were similar in both groups. It is concluded that adjuvant arthritis modifies the endothelium-derived relaxing factor-mediated responses of rat aorta.

Acetylcholine↗
PubMed1991

Modulation of membrane cholesterol levels: effects on endothelial cell function.

The endothelial cell lining of blood vessels is now recognized as an active interface between blood and the underlying tissue. Modulation of cholesterol levels in several cell types has resulted in altered cell function. We have removed cholesterol from the endothelial cell membrane and have observed corresponding alterations in endothelial cell function. Following depletion of cholesterol from the endothelial cells, polymorphonuclear leukocyte adhesion to the cells was decreased. Angiotensin-converting enzyme activity of the endothelial cells was increased following removal of cholesterol from the endothelial cell membranes. The results of fluorescence polarization measurements suggest that these changes may be partially explained by altered membrane order.

Animals↗
PubMed1992

Detrimental effects of temperature on the efficacy of the University of Wisconsin solution when used for cardioplegia at moderate hypothermia. Comparison with the St. Thomas Hospital solution at 4 degrees C and 20 degrees C.

BACKGROUND: We have previously reported the superior protective properties of the University of Wisconsin (UW) solution compared with the St. Thomas solution (ST) in the rat heart subjected to the deep hypothermia (4 degrees C), thus demonstrating its possible use in cardiac transplantation. We thought it was important to evaluate the potential of the UW solution as a cardioplegic solution under the moderately hypothermic (20 degrees C) conditions of routine intraoperative myocardial protection. METHODS AND RESULTS: Isolated rat hearts were subjected to 60 minutes of ischemia at 4 degrees C or 30 (or 60) minutes of ischemia at 20 degrees C with UW, ST, and ST plus 100 mM K (ST + 100) solutions. Coronary flow, mechanical function, endothelial function, and ultrastructure were observed. Mean time (seconds) to infuse 10 ml of cardioplegic solution under constant pressure, a measure of coronary vascular resistance at 4 degrees C and 20 degrees C, respectively, for each solution were ST, 69.2 +/- 6.9 and 64.7 +/- 3.8; UW, 142.2 +/- 8.8 and 187.2 +/- 10.0 (p < 0.01); and ST + 100, 78.2 +/- 8.0 and 176 +/- 8.1 (p < 0.001). Mean recovery values of cardiac output (expressed as percentage of its preischemic value) after 60 minutes of ischemia at 4 degrees C were ST, 95.5 +/- 2.1%; UW, 93.0 +/- 2.4%; and ST + 100, 96.5 +/- 1.5%. After 30 minutes of ischemia at 20 degrees C, values were ST, 88.0 +/- 1.3%; UW, 72.2 +/- 3.6% (p < 0.005 versus ST); and ST + 100, 53.3 +/- 1.8% (p < 0.001 versus ST). CONCLUSIONS: The efficacies of UW and severely hyperkalemic cardioplegic solutions are affected by the degree of hypothermia under which they are used. Under moderate hypothermia (20 degrees C), severe hyperkalemia induces a marked increase in coronary vascular resistance that is associated with impaired myocardial protection. These studies discourage the use of UW for routine intraoperative cardioplegic arrest where the degree of hypothermia cannot be readily controlled. The ST solution does not share this constraint.

Adenosine↗
PubMed1979

Photodynamically induced alteration of cornea endothelial cell function.

Corneal endothelial cells were perfused in the specular microscope with varying concentrations of rose bengal. Corneas perfused with rose bengal in concentrations of 10(-6)M to 10(-5)M and exposed to light for periods of 0.5 to 5 min swelled at rates which were more rapid with both increasing concentration of rose bengal and increasing duration of light exposure. Corneas perfused with similar concentrations of rose bengal but not exposed to light did not swell. Combining rose bengal with 100 micrograms/ml superoxide dismutase did not reduce the corneal swelling following exposure to light, indicating that the photodynamically induced endothelial bengal perfusing solution eliminated corneal swelling following exposure of corneas to light. This indicates that the photodynamic effect of endothelium is secondary to cell functional alterations from the hydrogen peroxide produced during the dismutation reaction of superoxide free radical which is catalyzed by superoxide dismutase.

Animals↗
PubMed1989

Endothelial barrier function.

The endothelial barrier in all organ beds allows the free exchange of water, but is restrictive to varying degrees to the transport of solutes such as albumin. For example, in the brain microvessels, the endothelial barrier restricts the transport of protein, whereas in fenestrated and continuous endothelial cells of the renal and lung endothelial cells, the endothelial barrier is semipermeable. The endothelial monolayer demonstrates selectivity, i.e., the permeation of molecules is inversely related to the molecular weight. Although the "pore" theory has been used to describe the transport across the endothelial barrier, the transport of solutes is also dependent on the charge of solutes and the endothelial cell, and the ability of the solute to bind to or be taken up by endothelial cells. Receptor-mediated trancytosis of albumin may contribute to albumin transport in addition to transport by paracellular pathways (i.e., through a so-called pore). Water permeability across the endothelium is determined by the interaction of albumin with glycocalyx and interstitial components of the endothelium (the "fiber matrix"). Ambient concentration of albumin serves to lower endothelial hydraulic conductivity. Increased endothelial permeability to solutes and water in inflammatory states is dependent on the shape and configuration of endothelial cells as determined by alterations in cytoskeletal elements, such as f-actin, and as regulated by intracellular second messengers such as free cytosolic calcium.

Animals↗
PubMed1992

The vascular endothelium in diabetes and hypertension.

PURPOSE: To review recent research into the function of endothelial cells in relation to diabetes and hypertension, and the implications for cardiovascular control. ENDOTHELIAL FUNCTIONS: Endothelial cells extract and inactive circulating hormones, convert inactive precursors into vasoactive products, and synthesize and secrete vasodilator and vasoconstrictor mediators, which also modify platelet function and cell growth. DIABETES: Abnormalities in endothelial cell morphology and function are recognized features of diabetes. Diminished endothelium-dependent relaxation and enhanced endothelium-dependent contraction have been described. HYPERTENSION: Similar defects in endothelial cell function have been demonstrated in animal and human hypertension. These might lead to increased vascular tone, vasospasm, platelet activation and atheroma. THERAPY: Certain drugs modify or mimic endothelium-derived mediators. Endothelial dysfunction may contribute to cardiovascular pathology, but the precise clinical and therapeutic significance of modifying endothelial function remains to be determined.

Blood Platelets↗