Linked Life Data

1362376

Source:http://linkedlifedata.com/resource/pubmed/id/1362376

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1993-2-16
pubmed:abstractText
Although the mechanism initiating and maintaining variceal hemorrhage is not completely understood, there has been general agreement in recent years on the concept that variceal rupture occurs when the tension on the wall of the varices reaches a critical value (the rupture point) that leads to the leakage of the elastic components of the wall. If this hypothesis is true, the aim of pharmacological treatment should be to reduce variceal wall tension or to prevent any abrupt increase in this parameter. Some vasoconstrictor drugs are currently used in order to achieve these goals and in the attempt to stop the acute bleeding episode. All these agents decrease either portal pressure and azygos blood flow. Vasopressin although effective, has significant cardiac and gastrointestinal adverse effects that discourage its use. Combination with nitroglycerin reduces its adverse effects while maintaining or even enhancing the reduction in portal pressure. Glypressin, which acts as a slow-release preparation of vasopressin, has a longer duration of action and can be administered as single intravenous injections instead of continuous infusion. However, the similarity of effects of these drugs on systemic circulation leads to an overlapping spectrum of untoward effects. Somatostatin and the synthetic octapeptide octreotide display similar pharmacological effects on splanchnic hemodynamics but have a better tolerability profile. Thanks to its longer duration of action and ease of administration, octreotide could become the drug of choice for the early, pre-hospital management of bleeding varices. A different approach to the pharmacological treatment of variceal bleeding may be the use of compounds, like metoclopramide and domperidone, that increase the lower esophageal sphincter pressure (LESP), thereby reducing the inflow of blood flow into the submucous venous plexus of the esophagus and hence into the esophageal varices. However, more studies are needed before these compounds be considered a real alternative to the above established drugs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0257-2753
pubmed:author
pubmed:issnType
Print
pubmed:volume
10 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
16-29
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Clinical pharmacology of active variceal bleeding.
pubmed:affiliation
Institute of Pharmacology, School of Medicine and Dentistry, University of Parma, Italy.
pubmed:publicationType
Journal Article, Review