脂多糖和同型半胱氨酸对人脐静脉内皮细胞单核细胞趋化蛋白1 mRNA表达的影响

目的探讨脂多糖和同型半胱氨酸是否诱导培养的人脐静脉内皮细胞表达单核细胞趋化蛋白1(MCP-1) mRNA及其机制.方法将生长至汇合的人脐静脉内皮细胞分为对照组、脂多糖组,脂多糖+SB203580组,同型半胱氨酸组,同型半胱氨酸+SB203580组,脂多糖+同型半胱氨酸组.采用斑点杂交和RT-PCR检测其MCP-1 mRNA的表达.用免疫细胞化学法检测对照组、脂多糖组和同型半胱氨酸组P38蛋白激酶蛋白的表达.结果培养的人脐静脉内皮细胞能表达较低水平的MCP-1 mRNA.斑点杂交和RT-PCR均显示各实验组的MCP-1 mRNA明显高于对照组.免疫细胞化学显示,P38蛋白激酶蛋白在对照组的细胞核阳性表达率为9.6%,当人脐静脉内皮细胞暴露于脂多糖或同型半胱氨酸后,细胞核阳性表达率升至46.7%或57.7%.结论脂多糖和同型半胱氨酸能诱导人脐静脉内皮细胞表达单核细胞趋化蛋白1 mRNA,P38蛋白激酶可能参与了该过程.     

Different effects of halothane, isoflurane and sevoflurane on sarcoplasmic reticulum of vascular smooth muscle in dog mesenteric artery

Background: The direct effect of halothane on vascular smooth muscle is mediated in part via its effects on the sarcoplasmic reticulum (SR). Little information is available concerning the effects of other volatile anesthetics including isoflurane and sevoflurane, whose vascular effects differ from those of halothane. The aim of the present study was to compare the effects of halothane, isoflurane and sevoflurane on the SR by testing the contraction induced by caffeine in vascular smooth muscle. Methods: Rings without endothelium from isolated canine mesenteric artery were mounted in physiological saline solution (PSS) for isometric tension recording. After complete depletion of Ca²⁺ from the SR by adding 35 mM caffeine, the rings were exposed to normal Ca²⁺ containing PSS (Ca²⁺ loading), to Ca²⁺-free PSS for 10 min, and then to 15 mM caffeine to induce contraction. Anesthetics were administered during Ca²⁺ loading, the Ca²⁺-free phase and simultaneously with caffeine administration. Results: Halothane (0.5-2%) attenuated the caffeine-induced contraction of canine mesenteric artery when administered during Ca²⁺ loading in the SR (P<0.001), whereas isoflurane and sevoflurane (1–4%) failed to affect the contraction. When given simultaneously with caffeine, halothane (1–2%) potentiated the caffeine-induced contraction (P<0.05), but isoflurane and sevoflurane had no effect. When given before caffeine administration, halothane (0.5-2%), isoflurane (24%) and sevoflurane (4%) all potentiated the caffeine-induced contraction (P<0.05). Conclusion: It has been shown that halothane not only potentiates caffeine- induced Ca²⁺ release from the SR, but also induces contraction by releasing Ca²⁺ from the SR. We conclude that halothane decreases Ca²⁺ accumulation in the SR while exerting facilitative and additive effects on caffeine-induced Ca²⁺ release from the SR when applied before caffeine administration and simultaneously with caffeine, respectively, whereas isoflurane and sevoflurane lack both the ability to decrease Ca²⁺ accumulation and an additive effect on caffeine-induced Ca²⁺ release from the SR, but are able to facilitate Ca²⁺ release by caffeine.     

Changes in the microcirculation in rats with experimental trigeminal neuralgia

Laboratory of Pathophysiology of Pain and Laboratory of General Pathology of the Microcirculation, Research Institute of General Pathology and Pathological Physiology, Academy of Medical Sciences of the USSR, Moscow. Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 111, No. 1, pp. 9–11, January, 1991.     

Effects of zymosan-activated plasma and phorbol myristate acetate on isolated, perfused rabbit lungs

The effects of complement activation on pulmonary vascular permeability are disputed. In rabbit lungs perfused with autologous blood, zymosan activated plasma (ZAP) induced a moderate increase in pulmonary vascular resistance (PVR), but did not detectably change the vascular permeability within 2 h. The stronger neutrophil granulocyte (PMN) activator, phorbol myristate acetate (PMA), usually gave larger PVR increases and also increased pulmonary vascular permeability. Lungs from neutropenic animals, similarly perfused and given PMA, showed unchanged PVR reactions but had no apparent increase in vascular permeability. Lungs perfused with cell-free medium and given PMA displayed modest PVR increases, and no measurable permeability change. The lung preparatory procedure itself markedly influenced leukocyte circulation. Exsanguination of lung donors decreased the concentration of circulating PMN significantly, and they virtually disappeared from the perfusate within minutes after start of lung perfusion. PMN-mediated effects must therefore have been caused by cells already sequestered in the lungs. We conclude that ZAP does not induce an increased pulmonary vascular permeability in isolated, perfused rabbit lungs, in contrast to PMA. The permeability effects of PMA appear to be PMN dependent.     

Hepatic falciform artery

The hepatic falciform artery is an occasional terminal branch of the left or middle hepatic artery, and may provide an uncommon but important collateral route when the principal visceral arteries are occluded.     

3,6-(二甲氨基)-二苯骈碘杂六环葡萄糖酸盐对AGEP引起的大鼠主动脉平滑肌细胞增殖及牛主动脉内皮细胞内皮素和一氧化氮改变的影响

目的 :观察 3 ,6 (二甲氨基 ) 二苯骈碘杂六环葡萄糖酸盐对AGEP引起的大鼠主动脉平滑肌细胞增殖及牛主动脉内皮细胞内皮素和一氧化氮改变的影响。方法 :采用牛血清白蛋白 (BSA)与不同浓度葡萄糖 (0 ,2 0 ,5 0 ,80mmol·L-1)体外孵育制备糖基化终产物 (AGEP) ,应用 [3 H] TdR掺入法和MTT比色法观察I-93对重度糖化的AGEP诱导的大鼠主动脉平滑肌细胞 (ASMC)增殖的影响 ;应用放射免疫技术及Greiss法观察I -93对AGEP引起的牛主动脉内皮细胞 (BAEC)释放内皮素 1(ET 1)和一氧化氮 (NO)的影响。结果 :I-93 10 -7～ 10 -5mol·L-1能明显抑制AGEP引起的ASMC增殖 ,其 [3 H] TdR掺入量和MTT比色法的最大抑制率分别为79 .4%和 44 .2 %。随AGEP糖浓度的增加 (2 0～ 80mmol·L-1) ,BAEC培养液中ET 1含量亦逐渐上升 [(4 93± 63 )～ (779± 10 5 )ng·L-1] ,I -93 10 -7～ 10 -5mol·L-1能明显抑制重度糖化的AGEP促进ET 1释放的作用 ;I -93对AGEP灭活NO的作用有剂量依赖性抑制效应。结论 :I -93有抑制ASMC增殖的作用 ;对AGEP诱导的BAEC释放ET 1和NO间平衡失调有调节作用 ,在防治阻塞性血管疾病方面I -93具有潜在的应用价值     

血管内皮功能障碍对肥胖伴高血糖患者胰岛分泌功能的影响

目的　探讨血管内皮功能障碍对胰岛 β细胞分泌功能的影响。 　方法　正常体重(NW )组 81例 ,单纯肥胖 (Ob)组 14 0例 ,肥胖伴高血糖 (Ob HG)组 97例。测定体质指数 (BMI)、腰臀围比 (WHR)、血压、血脂、空腹血糖和胰岛素 (FBG和FIns)及餐后血糖和胰岛素 (2hBG和 2hIns)。采用稳态模式法评价胰岛素抵抗 (HOMA IR)和 β细胞功能 (HOMA β)。用高分辨率血管外超声测定肱动脉对血流介导的内皮依赖性血管扩张 (EDD)及硝酸甘油的扩张反应。　结果　与Ob组比较 ,Ob HG组WHR、血压、甘油三酯 (TG)、FIns、2hIns和HOMA IR等显著升高 ,HOMA β明显降低 ,并伴有EDD所标志的血管内皮功能显著下降。相关分析显示 ,β细胞功能与EDD在Ob HG组呈显著正相关 (r=0 2 5 9,P <0 0 5 ) ,在Ob组和NW组无显著相关。在对Ob HG组影响EDD的因素进行控制后 ,EDD仍与 β细胞功能显著相关 (r =0 4 5 8,P <0 0 1)。多元逐步回归分析表明影响 β细胞功能的主要因素在Ob HG组为FBG、FIns和EDD ,在Ob组为FBG和HOMA IR。　结论　内皮依赖性舒张功能障碍可能是导致肥胖者 β细胞功能衰退 ,引发 2型糖尿病 (T2DM )的重要危险因素。     

Effect of lactate and bicarbonate on human peritoneal mesothelial cells, fibroblasts and vascular endothelial cells, and the role of basic fibroblast growth factor.

BACKGROUND: In patients on long-term continuous ambulatory peritoneal dialysis (CAPD), peritoneal dysfunction may occur due to loss of peritoneal mesothelial cells, peritoneal fibrosis and neovascularization. Lactate, long used as a buffer in peritoneal dialysates, has been substituted by bicarbonate in recent years. However, their effects on the peritoneum of CAPD patients are unknown. This study investigated the influence of lactate and bicarbonate on peritoneal dysfunction in CAPD patients. METHODS: The mitochondrial activity of human peritoneal mesothelial cells (HPMCs) and their expression of basic fibroblast growth factor (bFGF) were studied after culture under various conditions. We also assessed the mitochondrial-activating effect of the supernatant of those cultures on human peritoneal fibroblasts (HPFBs) and human umbilical vein endothelial cells (HUVECs) and the effect of recombinant human bFGF on the mitochondrial activity of HPFBs and HUVECs. We used the WST-1 assay to determine mitochondrial activity in HPMC. RESULTS: At pH 7.4, the mitochondrial activity of HPMCs was lowest in a medium containing 40 mM (Lac), intermediate in a lactate (15 mM) plus bicarbonate (25 mM) medium (Lac/Bic), and highest in a 40 mM bicarbonate medium (Bic). In culture supernatant, the increase of bFGF was: Lac > Lac/Bic > Bic. Mitochondrial activation of HPFBs and HUVECs was stimulated by HPMC culture supernatants in the following decreasing order: Lac > Lac/Bic > Bic. The effects of these supernatants were suppressed by a bFGF-neutralizing antibody, while recombinant bFGF caused concentration-dependent mitochondrial activation in HPFBs and HUVECs. CONCLUSIONS: The role of bFGF in peritoneal fibrosis and neovascularization may be important. A bicarbonate-containing medium is better than a lactate-containing medium for preserving cell viability in HPMCs and preventing bFGF expression by these cells.