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Intestinal blood flow and intramucosal pH in experimental peritonitis.
1999 (Engelska)Ingår i: Shock, ISSN 1073-2322, E-ISSN 1540-0514, Vol. 11, nr 1, s. 44-50Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

BACKGROUND AND AIMS: Experimental peritonitis causes gut intramucosal acidosis indicating intramucosal ischemia. However, tissue acidosis may reflect other conditions than ischemia. An increased mucosal-arterial Pco2 difference ( Pco2-gap) is suggested to be a more adequate measure of tissue ischemia than intramucosal pH (pHi). This study was performed to elucidate whether keeping cardiac index (CI) and splanchnic blood flow normal or supranormal by administration of colloids and an inotropic drug could prevent the acidosis as well as reduce the Pco2-gap. A secondary aim was to study to what degree the low pHi in peritonitis really reflects ischemia.

SUBJECTS: 24 anesthetized pigs (18-27 kg) divided into four groups.

MODELS: A Swan-Ganz catheter, transonic flow meters and catheters for blood sampling were applied. pHi was calculated using tonometry. Standardized fecal peritonitis was induced, except in controls. One peritonitis group was given dextran (Group P(DEX)) and another in addition dobutamine (Group PDOB) to keep CI normal or supranormal, respectively.

RESULTS: After 4 h, a significant drop in pHi was found in all peritonitis groups, most pronounced in untreated peritonitis (to 7.09+/-.02). Corresponding values in Group P(DEX) and Group P(DOB) were 7.22+/-.03 and 7.22+/-.01, respectively, and in controls 7.30+/-.02. The Pco2-gap and the mucosal-arterial [H+] difference ([H+]-gap) increased significantly in untreated peritonitis but did not increase in groups given dextran and dextran + dobutamine.

CONCLUSION: Maintaining CI in peritonitis attenuated the reduction in pHi and prevented the increased Pco2- and [H+]-gap. It seems justified from these data to conclude that the somewhat reduced pHi in treated peritonitis groups did not reflect tissue ischemia.

Ort, förlag, år, upplaga, sidor
1999. Vol. 11, nr 1, s. 44-50
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URN: urn:nbn:se:uu:diva-395097DOI: 10.1097/00024382-199901000-00007PubMedID: 9921716OAI: oai:DiVA.org:uu-395097DiVA, id: diva2:1360386
Tillgänglig från: 2019-10-12 Skapad: 2019-10-12 Senast uppdaterad: 2019-10-12

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