Document Detail


The fundamental hemodynamic mechanism underlying gastric "stress ulceration" in cardiogenic shock.
MedLine Citation:
PMID:  3592803     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute hemorrhagic ulceration of the gastric mucosa is seen frequently in patients with hypovolemic or cardiogenic shock. Although such lesions clearly are related to regional gastric ischemia, little attention has been directed at the underlying mechanism(s) mediating the ischemia itself. To this end, anesthetized pigs were subjected to sustained cardiogenic shock (mild hemorrhage and pericardial tamponade) such that cardiac output was reduced to 38 +/- 1% of the baseline level for 4 hours, followed by release of the tamponade, reinfusion of the shed blood, and resuscitation for 2 hours. During the period of shock, there was profound regional gastric ischemia, resulting from severe and disproportionate gastric vasoconstriction. "Blinded" gross and microscopic evaluation of the stomachs removed after the experiment revealed severe mucosal ischemic necrosis, hemorrhage, and ulceration, whereas sham-operated pigs showed no lesions. The characteristics of this model therefore mimic the essential features of the gastric "stress ulceration" syndrome. Prior confirmed total alpha-adrenergic blockade with phenoxybenzamine failed to alter these features significantly. In contrast, prior ablation of the renin-angiotensin axis, whether by angiotensin-converting enzyme inhibition with teprotide or by bilateral nephrectomy, significantly and substantially ameliorated the ischemia, vasospasm, and mucosal injury. In this model of cardiogenic shock, acute gastric mucosal "stress ulceration" is caused by a disproportionately severe regional gastric ischemia resulting from selective splanchnic vasospasm that is unaffected by sympathetic blockade but abolished by prior ablation of the renin-angiotensin axis. Like nonocclusive small bowel ischemia, ischemic colitis, and the "shock liver" syndrome, gastric "stress ulceration" is yet another component of the multiple splanchnic organ failure syndrome that appears to be mediated primarily by the remarkable sensitivity of the splanchnic vascular bed to the renin-angiotensin axis.
Authors:
R W Bailey; G B Bulkley; S R Hamilton; J B Morris; U H Haglund; J E Meilahn
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Annals of surgery     Volume:  205     ISSN:  0003-4932     ISO Abbreviation:  Ann. Surg.     Publication Date:  1987 Jun 
Date Detail:
Created Date:  1987-06-29     Completed Date:  1987-06-29     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  0372354     Medline TA:  Ann Surg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  597-612     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Hemodynamics*
Shock, Cardiogenic / complications*,  physiopathology
Stomach Ulcer / etiology*,  physiopathology
Stress, Physiological / complications*,  physiopathology
Swine
Grant Support
ID/Acronym/Agency:
DK 31764/DK/NIDDK NIH HHS
Comments/Corrections

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