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11. |
Endotoxin-lnduced Release of Interleukin 6 and Interleukin 1β in Human Blood Is Independent of Tumor Necrosis Factor Alpha |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 55-62
C. Vasilescu,
D. Berger,
K. Buttenschön,
M. Seidelmann,
H.G. Beger,
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摘要:
It has been suggested that tumor necrosis factor alpha (TNFα) acts not only by direct toxicity, but also as a proximal mediator which is able to induce the production of other cytokines, especially interleukin 6 (IL-6) and interleukin 1β (IL-1β). In order to test the dependence of the release of these two cytokines from leukocytes upon induction by TNFα, we stimulated whole blood in vitro with TNFα and compared the cytokine levels with those induced by endotoxin. The cytokine release was also determined after stimulation by endotoxin with added TNFα and by endotoxin with monoclonal antibodies against TNFα (anti-TNFα) added in order to reduce TNFα. Unstimulated blood samples were used as controls. The plasma levels of both IL-6 and IL-1β were significantly higher after stimulation with endotoxin than after stimulation with TNFα. TNFα did not induce cytokine levels significantly higher than controls. The cytokine levels were the same whether or not anti-TNFα was included together with the endotoxm. Plasma from samples with added anti-TNFα had no detectable TNFα. Our results indicate that the leukocyte-derived production of IL-6 and IL-1β in whole blood is stimulated directly by endotoxin and is not m
ISSN:0014-312X
DOI:10.1159/000129440
出版商:S. Karger AG
年代:1996
数据来源: Karger
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12. |
Abstracts (Part 6 of 8) |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 61-72
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ISSN:0014-312X
DOI:10.1159/000318651
出版商:S. Karger AG
年代:1996
数据来源: Karger
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13. |
Changes of Bile Duct Mucosa after Choledochoduodenostomy in Rats |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 63-69
K. Kuo,
C.-G. Ker,
P.C. Sheen,
H.-J. Wang,
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摘要:
This study investigated the changes of bile duct mucosa in rats after choledochoduodenostomy. Wistar rats were divided into three groups: group I (n = 6) was treated with sham operation as control; group II (n = 10) was treated with common bile duct ligation without choledochoduodenostomy, and group III (n = 12) had both common bile duct ligation and choledochoduodenostomy creation 4 days after common bile duct ligation. From our observations, retrograde induced cholangitis due to enteric reflux into the common bile duct is the possible cause of chronic inflammation after choledochoduodenostomy. At the end of the study, Choledocholithiasis developed in 5 of 12 rats. Severe dysplasia was present in the bile duct mucosa in 6 of 12 rats in group III, but not in group I or II. A technique for silver staining of nucleolar organizing regions (AgNOR) was applied. This technique demonstrated differences in AgNOR counts between normal mucosa and dysplasia. Under AgNOR stain, the number of AgNOR was significantly greater than in the normal or benign counterparts and gradually increased from the normal bile duct mucosa group to the severe dysplasia group (group 12.1 ± 0.8, group II 3.2 ± 1.0, group III 5.3 ± 1.1). All of these observations suggest that ‘sump syndrome’ and bile stasis could occur after choledochoduodenostomy in rats and can result in chronic inflammation of the bile duct. It has been well established that calcium bilirubinate is the major type of choledocholithiasis in Orientals. β-Glucuronidase from bacteria, such as Escherichia coli present in the biliary tree, hydrolyzes bilirubin diglucuronide to bilirubin. Bilirubin combines with calcium in the bile flow to form calcium bilirubinate. Bacterial infection plays a key role in calcium bilirubinate stone formation. Since choledochoduodenostomy did increase reflux cholangitis, and bacterial infection would increase mucin overproduction, bile deconjugation and eventually new calcium bilirubinate stones would be formed. The dysplastic changes in the bile duct mucosa could possibly be related to the prolonged exposure to the biochemically altered infected bile. Thus choledochoduodenostomy might not be the perfect choice in treating calcium bilirubinate choledocholithiasis in Or
ISSN:0014-312X
DOI:10.1159/000129441
出版商:S. Karger AG
年代:1996
数据来源: Karger
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14. |
Origin of Intravascular Fluid Recruited by Vasodilatation during Epidural Anaesthesia |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 70-74
R.G. Hahn,
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摘要:
Arterial hypotension during induction of epidural anaesthesia is caused by peripheral vasodilatation and promotes intravascular fluid distribution. The excess fluid in the blood may result from either diffusion across the capillaries or enrichment of the fluid that is routinely infused intravenously to prevent severe hypotension. These alternatives were assessed in 40 urology patients who received 10 ml kg–1 25%) promoted mild dilutional hypoglycaemia when the infusion was glucose-free (-6% in hypotensive vs. +2% in normotensive) and hyperglycaemia when glucose was given (+15% in hypotensive vs. +7% in normotensive). The consistent deviation of the blood glucose level towards the concentration of the infused fluid suggests that the excess intravascular fluid associated with epidural-induced hypotension is derived directly from the ongoing infusion rather than by transcapillary transpor
ISSN:0014-312X
DOI:10.1159/000129442
出版商:S. Karger AG
年代:1996
数据来源: Karger
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15. |
Abstracts (Part 7 of 8) |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 73-84
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PDF (2016KB)
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ISSN:0014-312X
DOI:10.1159/000318652
出版商:S. Karger AG
年代:1996
数据来源: Karger
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16. |
Abstracts (Part 8 of 8) |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 85-93
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PDF (1442KB)
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ISSN:0014-312X
DOI:10.1159/000318653
出版商:S. Karger AG
年代:1996
数据来源: Karger
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17. |
Author Index Vol. 28 (suppl 1), 1996 |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page 95-99
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PDF (519KB)
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ISSN:0014-312X
DOI:10.1159/000129497
出版商:S. Karger AG
年代:1996
数据来源: Karger
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18. |
Title Page / Table of Contents |
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European Surgical Research,
Volume 28,
Issue 1,
1996,
Page -
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PDF (1436KB)
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ISSN:0014-312X
DOI:10.1159/000129496
出版商:S. Karger AG
年代:1996
数据来源: Karger
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