International Journal of Clinical Oncology - This study aimed to compare the incidence of postoperative complications occurring within 30 days of surgery between octogenarians and younger... 相似文献
Background: The effects of inhalational anesthetics on the microcirculation, including leukocyte dynamics, remain to be clarified. The authors investigated halothane and sevoflurane anesthesia to determine if these agents evoked leukocyte adhesion through endothelial cell-dependent mechanisms involving such adhesion molecules.
Methods: Rats were anesthetized with halothane or sevoflurane in 100% oxygen and the lungs were mechanically ventilated. Leukocyte behavior in mesenteric venules was recorded through intravital video microscopy under monitoring microvascular hemodynamics. To examine the mechanisms for leukocyte rolling and adhesion, these studies were repeated after animals were pretreated with a monoclonal antibody against P-selectin (MAb PB1.3) or against intracellular adhesion molecule-1 (ICAM-1; MAb 1A29): P-selectin required for rolling of circulating leukocytes and ICAM-1 for firm adhesive interactions with leukocyte integrins.
Results: Under baseline anesthetic conditions (1 minimum alveolar concentration [MAC]), venular wall shear rates, an index of the disperse force on marginating leukocytes, in the sevoflurane-treated rats were about two times higher than those with halothane. At 2 MAC, halothane caused a marked arteriolar constriction and decreasing shear rates concurrent with an increasing density of venular leukocyte adhesion. Sevoflurane at 2 MAC induced leukocyte rolling and adhesion, which were attenuated by PB1.3 and 1A29, without alterations in the wall shear rates. Halothane-induced leukocyte adhesion was not prevented by PB1.3 but it was by 1A29. 相似文献
PURPOSE: To evaluate the interaction between nitrous oxide and propofol for the suppression of hypertension following electrical stimulation of the mental nerve in the rabbit. METHODS: Male Japan White rabbits were tracheostomized, cannulated and mechanically ventilated under isoflurane anesthesia. Square wave pulses (5 V, 0.5 msec, 50 Hz for 5 sec) were delivered to the left mental nerve. Animals received nitrous oxide 20, 40, 60 and 80% (Group 1); propofol 200, 400, 600 and 800 microg x kg(-1) min(-1) (Group 2); or combinations of nitrous oxide and propofol at 10 + 100, 20 + 200, 30 + 300 and 40 % + 400 microg x kg(-1) x min(-1) (Group 3). Systolic blood pressure was recorded from immediately before to maximal increase following nerve stimulation. Probit analysis was used to obtain ED(50) values for 50% suppression of blood pressure elevation. Isobolographic analysis was used to evaluate the interaction between nitrous oxide and propofol. RESULTS: ED(50) values are 52.9% for nitrous oxide (Group 1), 464.1 microg x kg(-1) min(-1) for propofol (Group 2), 21.7 % + 217.1 microg x kg(-1) min(-1) for nitrous oxide and propofol combination (Group 3) and 24. 7 % + 247.1 microg x kg(-1) x min(-1) for the theoretically additive combination of nitrous oxide and propofol, respectively. CONCLUSION: The interaction between nitrous oxide and propofol for the suppression of blood pressure elevation following electrical stimulation of the mental nerve is additive. 相似文献
Stem cell factor (SCF) has crucial roles in proliferation, survival, and differentiation of hematopoietic stem cells and mast cells through binding to c-Kit receptor (KIT). Chemotaxis is another unique function of SCF. However, little is known about the intracellular signaling pathway of SCF/KIT-mediated cell migration. To investigate the signaling cascade, we made a series of 22 KIT mutants, in which tyrosine (Y) residue was substituted for phenylalanine (F) in the cytoplasmic domain, and introduced into BAF3 cells or 293T cells. On stimulation with SCF, BAF3 expressing KIT(WT)(WT) showed cell migration and Ca(2+) mobilization. Among 22 YF mutants, Y567F, Y569F, and Y719F showed significantly reduced cell migration and Ca(2+) mobilization compared to WT. In Y567F, Lyn activation on SCF stimulation decreased and C-terminal Src kinase (Csk) suppressed KIT-mediated Ca(2+) influx and cell migration, suggesting that Y567-mediated Src family kinase (SFK) activation leads to Ca(2+) influx and migration. Furthermore, we found that p38 mitogen-activated protein kinase (p38 MAPK) and Erk1/2 were also regulated by Y567/SFK and involved in cell migration, and that p38 MAPK induced Ca(2+) influx, thereby leading to Erk1/2 activation. In Y719F, the binding of phosphatidylinositol 3'-kinase (PI3K) to KIT was lost and KIT-mediated cell migration and Ca(2+) mobilization were suppressed by PI3K chemical inhibitors or dominant-negative PI3K, suggesting the involvement of Y719-mediated PI3K pathway in cell migration. Combination of Csk and the PI3K inhibitor synergistically reduced cell migration, suggesting the cooperation of SFK and PI3K. Taken together, these results indicate that 2 major KIT signaling pathways lead to cell migration, one is Y567-SFK-p38 MAPK-Ca(2+) influx-Erk and the other is Y719-PI3K-Ca(2+) influx. 相似文献
Priming of cytotoxic T lymphocytes (CTLs) by dendritic cells (DCs) is crucial for elimination of pathogens and malignant cells. To activate CTLs, DCs present antigenic peptide-complexed MHC class I molecules (MHC-I) that will be recognized by the CTLs with T cell receptors and CD8 molecules. Here we show that paired Ig-like receptor (PIR)-B, an MHC-I receptor expressed on antigen-presenting cells, can regulate CTL triggering by blocking the access of CD8 molecules to MHC-I. PIR-B-deficient DCs evoked CTLs more efficiently, leading to accelerated graft and tumor rejection. PIR-B(+) non-DC transfectant cells served as less efficient stimulators and targets for CTLs than PIR-B(-) cells at the effector phase in vitro. On surface plasmon resonance analysis, PIR-B and CD8alpha alpha were revealed to compete in binding to MHC-I. Our results may provide a novel strategy for regulating CTL-mediated immunity and diseases in a sterical manner. 相似文献
It was reported that neuronal nitric oxide synthase (nNOS) was expressed only in gonadotrophs and folliculo-stellate cells
in the anterior lobe of the pituitary gland. However, recent studies have demonstrated the occurrence of nNOS in the somatotrophs
and lactotrophs. In the present study, we investigated effects of growth hormone-releasing hormone (GHRH), gonadotropin-releasing
hormone (GnRH), and 17β-estradiol on nitric oxide (NO) release in cultured rat anterior pituitary cells in vitro. The NO
2−
level in the incubation medium of the rat anterior pituitary cells was dependent on the cell density. Pretreatment with 10
μM 17β-estradiol resulted in an increase in medium NO
2−
level. GHRH and GnRH failed to change medium NO
2−
levels, but they elicited increases in medium NO
2−
levels in estrogen-treated cells. The GHRH-induced increase in NO
2−
level was inhibited by Nχ-nitro-l-arginine methyl ester, a NOS inhibitor. These findings suggest that GnRH and GHRH could activate nNOS in the gonadotrophs
and the somatotrophs, respectively. 相似文献