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At least 73 records · Page 4Linked to original sources
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↗
PubMedDate not supplied

Preliminary report on endothelial functional injury in brain arterioles of diabetic rats: in vivo observation of macromolecular transit across the vascular wall.

The coloring of longitudinal nuclei, resembling a convoy, was observed in vivo in the terminal arterioles of diabetic rat brain by means of a microcirculatory experimental model and Evans blue/albumin tracer. This emergency transit could confirm other well known passages across the vessel wall, or be considered as 'functional injury' of the diabetic endothelium, especially in case of the so-called brain-blood barrier.

Animals↗
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↗