IL-8 is an essential mediator of the increased delayed-phase vascular permeability in LPS-induced rabbit pleurisy.

We investigated the involvement of IL-8 in the delayed vascular permeability (VP) in rabbit lipopolysaccharide (LPS)-pleurisy. Maximal level of interleukin-8 (IL-8) was detected in pleural fluid at 2 h after LPS injection and anti-IL-8 inhibited the delayed VP by 90%. Injection of homologous IL-8 induced VP, the time-course of which preceded that of LPS-induced delayed VP. Production of IL-8 in LPS-pleurisy was inhibited with anti-tumor necrosis factor alpha (TNF-alpha), whereas the production of TNF-alpha was not affected with anti-IL-8. Injection of IL-8 did not induce TNF-alpha production and anti-TNF-alpha had no effect on IL-8-induced VP. Injection of homologous TNF-alpha induced IL-8 production and VP, and TNF-alpha-induced delayed VP was blocked with anti-IL-8. These results indicate important roles of IL-8 in LPS-induced delayed VP and that TNF-alpha causes the delayed VP through the production of IL-8.

Role of TNF alpha, IL-1, and IL-1ra in the mediation of leukocyte infiltration and increased vascular permeability in rabbits with LPS-induced pleurisy.

We examined the generation of tumor necrosis factor-alpha (TNF alpha), interleukin-1 (IL-1), and IL-1 receptor antagonist (IL-1ra), and their role in the mediation of leukocyte infiltration and increased vascular permeability in rabbits with LPS-induced pleurisy. The leukocyte infiltration was largely mediated by both TNF alpha and IL-1 and could be divided into at least two phases: the early (within 3 hr) phase which was partly inhibited by anti-TNF alpha, but not by IL-1ra, and the late phase (4-12 hr) mediated by both TNF alpha and IL-1, and largely inhibited synergistically with anti-TNF alpha and IL-1ra. Endogenous IL-1ra may be responsible for the downregulation of the late phase of leukocyte infiltration in this type of inflammation. The increased vascular permeability was composed of two phases: immediate (15 min) and delayed (2 hr). The immediate permeability was inhibited by H1-antihistamine but was not affected by anti-TNF alpha, by IL-1ra, or by depletion of neutrophils. The delayed permeability was completely inhibited by either depletion of neutrophils or by anti-TNF alpha and was not affected by IL-1ra or antihistamine. Production of TNF alpha was maintained in the leukopenic rabbits. It would thus appear that the delayed permeability is mediated by a relatively early fraction of leukocyte infiltration initiated by TNF alpha; however, TNF alpha is not the direct mediator of this delayed permeability.

Lipoma arborescens with hemarthrosis of the knee. A case report.

Lipoma arborescens is a rare intraarticular lesion, typically with a clear yellow aspirate. We report a case of lipoma arborescens with hemarthrosis of the knee.

[Clinical evaluation of SPECT in cerebrovascular disease].

In 131 patients with cerebrovascular disease, regional cerebral blood flow was determined by 123I-IMP (N-isopropyl (123I)-iodoamphetamine) or 99mTc-HM-PAO (99mTc (d, l)-hexamethyl propyleneamine oxime) SPECT and findings were compared with those of X-CT or MRI. The perfusion deficit detected by SPECT was larger than the deficit by X-CT or MRI in every cases. The perfusion deficit area was more clearly demonstrated by SPECT than by X-CT or MRI in patients with acute cerebral infarction. The hypoperfusion area determined by 123I-IMP SPECT was wider than that by 99mTc-HM-PAO SPECT. The crossed cerebellar diaschisis was observed in 56 out of 131 cases (43%). The results of operation were quantitatively evaluated by 123I-IMP SPECT in 25 patients.

[Effect of various contrast media on platelet aggregation--an in vivo study].

Recently, some radiologists using non-ionic contrast media for angiography have noted the increased tendency of thrombus formation in the injection syringe or angiographic catheter contaminated with blood. In vitro studies by some authors have shown that non-ionic contrast media had only a slight anticoagulative effect as compared with ionic contrast media. But the in vivo studies comparing the anticoagulative effect of both ionic and non-ionic contrast media have not been performed previously. We investigated the effect of non-ionic and ionic contrast media on platelet aggregation in 40 patients undergoing angiography. The in vivo study revealed a negligible influence of both non-ionic and ionic contrast media on systemic platelet aggregation. The dose of contrast media also showed no significant correlation with platelet aggregation. Our study suggests that the data from in vitro experiments cannot be extended to in vivo study as for the relationship between contrast media and their anticoagulant effect.