International Journal of Gynecology & ObstetricsVolume 70, Issue S1 p. A134-A134 Quality assurance Evaluation of quality of care for treatment of primary breast cancer: Consistency with guidelines and recommendations U.-S. Albert, U.-S. AlbertSearch for more papers by this authorC. Heitmann, C. HeitmannSearch for more papers by this authorM. Koller, M. KollerSearch for more papers by this authorU. Bastian, U. BastianSearch for more papers by this authorS. Thommes, S. ThommesSearch for more papers by this author U.-S. Albert, U.-S. AlbertSearch for more papers by this authorC. Heitmann, C. HeitmannSearch for more papers by this authorM. Koller, M. KollerSearch for more papers by this authorU. Bastian, U. BastianSearch for more papers by this authorS. Thommes, S. ThommesSearch for more papers by this author First published: 10 December 2003 https://doi.org/10.1016/S0020-7292(00)83449-9AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinkedInRedditWechat No abstract is available for this article. Volume70, IssueS12000Pages A134-A134 RelatedInformation

In case of abnormal nipple discharge of the female breast galactography is a recognized radiological procedure to identify and to localize intraductal growths or other ductal abnormalities. However, it harbours several methodological problems. In ductal orientated sonography the availablity of high frequency linear transducers enables us now to visualize the mammary ducts in detail. The aim of this study was to compare both methods with respect to the detection of the cause of pathological nipple discharge. Thirthy-five patients were first examined by ductal orientated sonography with a 13 MHz linear transducer. The results of sonography were recorded in detail before galactography was performed. Ductal abnormalities were found by sonography in 26 patients and by galactography in 19 patients. In 24 cases both methods revealed concurring results. Among those, 17 cases showed pathological findings and seven cases had normal ducts. In nine patients sonography revealed pathological results whereas galactography was completely normal. In only two cases sonography failed to show ductal abnormalities which were detected by galactography. Our study underlines that ductal orientated sonography is a promising method of diagnosis in abnormal nipple discharge, which may be recommended to be performed routinely before galactography.

1. The controversial problem concerning the unusual haemodynamics of the deranged circulation during increased hydrostatic tissue pressure (PT) was elucidated by detailed studies of arterial, capillary and venous functions in cat skeletal muscle exposed to graded experimental changes of PT over a wide range. 2. The results indicated that the impaired circulatory state in skeletal muscle during raised tissue pressure is characterized by the following train of events: (a) a primary partial passive compression of the most distal part of the venous system due to negative vascular transmural pressure selectively at this site, in turn leading to the prompt development of a distinct ‘venous outflow orifice resistance’ graded in relation to the PT rise; (b) a consequent reduction of blood flow graded in relation to this resistance increase; (c) a rise in intramuscular venous pressure proximal of the ‘venous outflow orifice’ by the same extent as the PT increase; (d) transmission of the raised venous pressure to more proximal vessels in relation to the prevailing segmental resistance ratios; (e) a consequent maintenance of clearly positive transmural pressures in all vascular sections proximal to the ‘venous outflow orifice’, preventing collapse of these vessels; (f) maintenance of a largely normal capillary filtration coefficient and functional capillary surface area; and (g) an increase in capillary pressure by approximately 85% of the PT rise which reduces the rate of net transcapillary fluid absorption to about one‐seventh of that expected from the PT rise per se. 3. Previous concepts of a ‘vascular waterfall phenomenon’, a capillary collapse, or an arteriolar ‘critical closure phenomenon’ did not seem to be valid for the skeletal muscle circulation during increased PT. 4. The rate of net transcapillary fluid flux per unit PT change was much smaller during positive than negative PT, since capillary pressure rose considerably when PT was increased above control, but was largely unchanged when PT was decreased below control. 5. Possible ways to improve the circulatory state in conditions with an oedema‐induced tissue pressure rise are discussed.

Results from in vitro studies have indicated that endothelin-1 is a main candidate for endothelium-derived contracting factors. The aim of this in vivo study was to describe in quantitative terms the effects of endothelin-1 (ET-1), and of ETA receptor blockade, on vascular tone (resistance) in large-bore arterial resistance vessels (> 25 microns), small arterioles (< 25 microns) and the veins, as well as on capillary pressure and fluid exchange in cat gastrocnemius muscle. Endothelin-1 (100-1600 ng kg-1 min-1, i.a.) elicited, after an initial transient dilation, a strong dose-dependent constrictor response in all three consecutive vascular sections, yet with a preferential action on the small arterioles and the veins. The vasoconstriction developed very slowly over about 1 h and was also long-lasting after cessation of the infusion. Our main quantitative analysis refers to effects elicited by 20 min long i.a. infusions of ET-1 at a dose of 400 ng kg-1 min-1. At the end of this period, the peptide caused, on average, a three-fold increase in total regional vascular resistance, in turn explained by a 70% increase in large-bore arterial resistance, a 280% increase in arteriolar resistance and a 220% increase in venous resistance. The latter effect was also manifested as a pronounced capacitance response, and as a decrease in the pre- to post-capillary resistance ratio leading regularly to a rise in capillary pressure, net transcapillary fluid filtration and oedema formation which is unusual for a vasoconstrictor. The new specific competitive ETA receptor antagonist FR 139317 was found to be fully effective in vivo, insofar as it abolished the constrictor response to endothelin-1. ETA receptor blockade, or administration of phosphoramidon, an inhibitor of ET-1 production, did not influence the level of basal vascular tone, indicating no significant endogenous release of ET-1 under resting conditions. This contrasts to the established pronounced endogenous release of endothelium-derived nitric oxide. Finally, vascular myogenic regulation was found not to be mediated by ET-1. The results, taken together, suggest a possible role of ET-1 in long-term, rather than short-term, regulation of vascular tone in vivo, perhaps especially during pathophysiological conditions.

The hypothesis, based on in vitro experiments on large conduit arteries, that endothelium-derived nitric oxide is a mediator of vascular myogenic reactivity was tested in cat gastrocnemius muscle in vivo. This was done by comparing, in the absence and presence of effective endothelium-derived nitric oxide blockade by the specific inhibitors NG-monomethyl-L-arginine or NG-nitro-L-arginine methyl ester, myogenic responses in defined consecutive vascular sections to dynamic vascular transmural pressure stimuli, to arterial occlusion (reactive hyperaemia), and to arterial pressure changes (autoregulation of blood flow and capillary pressure). The results demonstrated that the myogenic vascular reactivity to quick ramp transmural pressure stimuli was not attenuated by endothelium-derived nitric oxide blockade, but rather reinforced. The amplitude of the reactive hyperaemia response was unaffected by endothelium-derived nitric oxide blockade, but its duration was shortened because of faster myogenic constriction, especially of large-bore arterial resistance vessels greater than 25 microns, in the recovery phase. Both the improved myogenic responsiveness to transmural pressure stimuli and the shortening of the reactive hyperaemia by endothelium-derived nitric oxide blockade suggested that endothelium-derived nitric oxide released in vivo acts as a 'metabolic' factor which certainly does not improve, but rather depresses myogenic vascular reactivity. Autoregulation of blood flow and capillary pressure were well preserved in the presence of endothelium-derived nitric oxide blockade. It was concluded from the results of these multifaceted tests that myogenic vascular regulation in skeletal muscle in vivo seems independent of endothelium-derived nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)

The reactive hyperaemia response cat skeletal muscle to 2-120 s arterial occlusions was analysed with regard to amplitude, duration, 'excess blood flow' and site of dilator action along the vascular bed. The last-mentioned was assessed with a new whole-organ technique permitting continuous segmental resistance recordings in arterial vessels greater than 25 microns, arterioles less than 25 microns and veins. Peak amplitude, duration and excess flow all increased with increasing occlusion length, of which excess flow was linearly related to occlusion length. The site of active dilatation was preferentially confined to arterioles less than 25 microns in which complete relaxation was observed after only 20 s occlusion, although the duration of the response continued to increase with more prolonged occlusions. A graded, but less pronounced, dilatation occurred in the arterial vessels greater than 25 microns and in the veins, the former exhibiting a 63% inhibition of tone as a maximum response at 120 s occlusion. The recovery phase was characterized by a vivid active constrictor component apparently protecting the capillaries from excessive pressure load upon arterial occlusion release, but this constriction became attenuated at long occlusions, thereby prolonging the hyperaemia response. The role of myogenic regulatory mechanisms in the responses was assessed from observed segmental resistance reactions to selectively applied transmural pressure stimuli similar to those elicited by arterial occlusion/release. It was concluded that myogenic mechanisms alone could explain the amplitude of the reactive hyperaemia response at short (up to 30 s) occlusions. Metabolic mechanisms seemed to be responsible for further relaxation of the proximal arterial vessels at longer occlusions, and also for the increased duration of the hyperaemia response at occlusions exceeding 10 s. Blockade of nitric oxide formation (endothelium-derived relaxing factor) did not seem to affect the reactive hyperaemia response.

Research Articles| July 21 2009 Histaminase Liberating and Anticoagulant Activity of Heparin Released in Anaphylactic Shock in the Guinea Pig Subject Area: Immunology and Allergy H. Giertz; H. Giertz Pharmacological Institute of the University (Director: Prof. F. Hahn) Freiburg im Br. Search for other works by this author on: This Site PubMed Google Scholar F. Hahn; F. Hahn Pharmacological Institute of the University (Director: Prof. F. Hahn) Freiburg im Br. Search for other works by this author on: This Site PubMed Google Scholar P. Krull; P. Krull Pharmacological Institute of the University (Director: Prof. F. Hahn) Freiburg im Br. Search for other works by this author on: This Site PubMed Google Scholar U. Albert U. Albert Pharmacological Institute of the University (Director: Prof. F. Hahn) Freiburg im Br. Search for other works by this author on: This Site PubMed Google Scholar International Archives of Allergy and Applied Immunology (1968) 33 (3): 306–312. https://doi.org/10.1159/000230048 Article history Published Online: July 21 2009 Content Tools Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn Email Tools Icon Tools Get Permissions Cite Icon Cite Search Site Citation H. Giertz, F. Hahn, P. Krull, U. Albert; Histaminase Liberating and Anticoagulant Activity of Heparin Released in Anaphylactic Shock in the Guinea Pig. International Archives of Allergy and Applied Immunology 1 March 1968; 33 (3): 306–312. https://doi.org/10.1159/000230048 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsInternational Archives of Allergy and Applied Immunology Search Advanced Search Article PDF first page preview Close Modal 1968Copyright / Drug Dosage / DisclaimerCopyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug.Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements. You do not currently have access to this content.