Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-6-5
pubmed:abstractText
Port site metastases could be due to mechanical reasons or impairment of host defenses. As it is known that carbon dioxide is toxic for lymphocytes in vitro we decided to investigate lymphocyte stress during laparoscopy. Blood samples and peritoneal fluids were obtained before and after pneumoperitoneum from 16 patients undergoing laparoscopic cholecystectomy. Lymphocyte subsets were determined by flow cytometry. Propidium iodide was used as a lymphocyte vitality test. Cytokines were measured by an ELISA system. Significant falls in the absolute lymphocyte count and T3 and T4 lymphocytes occurred on postoperative day 1 with a quick return to the preoperative value on day 2. T8, natural killer cells, T4/T8, and T4+/T8+ counts were stable. Interleukins 1 beta and 6 and tumor necrosis factor-alpha were depressed during the two postoperative days. Peritoneal lymphocytes were not destroyed by pneumoperitoneum as demonstrated by the propidium test, nor were they locally impaired by carbon dioxide. The circulating lymphocyte subpopulation decrease favors moderate, brief immunodepression. The origin of port site metastases is not immunologic depression but, rather, facilitated implantation of malignant cells by hyperpressure into raw tissues.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0364-2313
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
353-6; discussion 357
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Influence of CO2 pneumoperitoneum on systemic and peritoneal cell-mediated immunity.
pubmed:affiliation
Department of Surgery A, Hôpital Civil, Strasbourg, France.
pubmed:publicationType
Journal Article