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MeSH Review


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Disease relevance of Dilatation


High impact information on Dilatation


Chemical compound and disease context of Dilatation


Biological context of Dilatation


Anatomical context of Dilatation


Associations of Dilatation with chemical compounds

  • Maximum dilatations to both acetylcholine (p < 0.01) and sodium nitroprusside (p < 0.001) were greatly reduced by approximately 50% after 28 days and were normalized by the addition of the nitric oxide synthase inhibitor L-NNA and the antioxidant N-acetyl-L-cysteine, respectively [21].
  • The order of potency and maximum dilatations found for the receptor agonists were: H2 (43%) greater than histamine (28%) greater than H1 (17%) [22].
  • Dilatations were unchanged with XAC (3.0 +/- 0.5, 3.9 +/- 0.7 and 6.1 +/- 1.0 microm), but were significantly reduced with LNNA (to 1.8 +/- 0.6, 3.5 +/- 0.7 and 4.9 +/- 0.7 microm) or glibenclamide (to 0.4 +/- 0.3, 0.8 +/- 0.7 and 1.9 +/- 0.6 microm) [23].
  • Blockade of ganglionic nicotinic receptors (0.1-1 mM hexamethonium) delayed the onset and sometimes reduced the peak amplitude of dilatations, but slow dilatations persisted in 16 of 18 preparations [16].
  • 3. Dilatations to IAA-94 and DIDS were unaffected by potassium channel blockers, but were prevented by elevated potassium [24].

Gene context of Dilatation

  • Exogenous SOD or catalase normalized ACh dilatations and NO availability in vessels from aged APP+ mice but had no effect in those of TGF+ mice [25].
  • They were spindle-shaped dilatations, with a maximum diameter of about 200 microns, and appeared within vascular segments bearing severe amyloid deposition [26].
  • Some of these nerve processes showed local dilatations in contact with medullary cells and bone cells that were immunolabeled for synaptophysin, a nerve terminal marker [27].
  • The intermittent dilatations and growth cones also express strongly positive immunostaining for GFAP [28].
  • Treatment with omeprazole not only decreased the need for further dilatations, but also prolonged the mean time between any further dilatations to 26.3 months compared to 9.3 months for those on an H2-receptor antagonist (P<0.0001) [29].

Analytical, diagnostic and therapeutic context of Dilatation

  • Because optimal stent deployment is a prerequisite for optimal short- and long-term outcome, we performed an intravascular ultrasound study to the mode of stent deployment after delivery with the SDS and after high-pressure dilatations with low-compliant, oversized balloon catheters [30].
  • BACKGROUND: Traditionally, the presence of intrapulmonary vascular dilatations can be detected by using one of the three diagnostic modalities: contrast-enhanced echocardiography, technetium 99 m-labeled macroaggregated albumin scan, and pulmonary angiography [31].
  • All 16 were treated with antacids, H2-receptor blockers (Cimetidine), prokinetic agents, and intense nutritional resuscitation, together with preoperative stricture dilatations (average, 3.6 times) [32].
  • In 1967, care of esophageal burns from caustic substances was altered to include immediate esophagoscopy, high doses of steroid, and follow-up dilatations plus cine-esophagograms as needed [33].
  • RESULTS: The ACh-induced NO and prostaglandin-mediated dilatations decreased significantly during organ culture (NO: 84% in control and 36% in cultured; prostaglandins: 48% in control and 16% in cultured) [34].


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