101例尿毒症相关性肺水肿的特殊护理措施

目的 探讨尿毒症相关性肺水肿的特殊护理措施。方法 对尿毒症相关性肺水肿的护理除常规护理措施外，应做到以下几点特殊护理：①密切观察血压、血氧饱和度、近期尿量变化；②有效控制血压；③采取不同的透析方式适时适量透析超滤、加强透析中的护理；④改善全身营养状况，防止肺部感染；⑤牢记护理程序体位-吸氧-血管扩张药-血液透析；⑥严格控制入量。结果 101例病人中抢救成功84例，死亡13例，自动出院3例。结论 采取治疗和特殊护理对抢救尿毒症相关性肺水肿患者有较好效果。     

不同光凝接触镜填充液对中央角膜厚度的影响

目的　比较在行氩激光全视网膜光凝治疗中使用不同接触镜填充液对中央角膜厚度的影响 ,以寻找最适用于该治疗的填充液。方法　对 4 6例 (5 2眼 )患者进行氩激光全视网膜光凝治疗 ,每次分别随机使用 0 2 5 %氯霉素、1%羧甲基纤维素及医用透明质酸钠组作为安放全眼底激光角膜接触镜填充液 ,在治疗前及治疗后均用角膜测厚仪测量患者中央角膜厚度。结果　治疗后使用 0 2 5 %氯霉素组中央角膜平均增厚 (31 4± 10 2 ) μm ,1%羧甲基纤维素组中央角膜平均增厚 (10 6± 4 3) μm ,医用透明质酸钠组中央角膜平均增厚 (8 0± 3 5 ) μm。方差分析显示 :氯霉素组与另两组差异有极显著性意义 (P <0 0 1) ,羧甲基纤维素组与透明质酸钠组差异无显著性意义 (P >0 0 5 )。结论　 1%羧甲基纤维素及医用透明质酸钠作为安放全眼底激光角膜接触镜的填充液对角膜水肿程度的影响明显小于0 2 5 %氯霉素 ,是可供选用的优良填充液     

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by α-adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.     

细胞黏附分子(ICAM-1)在大鼠弥漫性脑损伤中的表达意义

目的探讨ICAM—1在大鼠弥漫性脑损伤中的表达及意义。方法采用Marmarou方法获得大鼠弥漫性脑损伤模型．实时定量RT—PCR、S—P免疫组化法分别测定ICAM—1蛋白和mRNA在外伤后不同时间点的表达变化．干湿重法测脑组织含水量．组织切片苏木精一伊红染色观测炎性细胞浸润情况。结果外伤组与假手术对照组比较，ICAM—1蛋白表达分别于伤后6h明显升高．72h达到高峰（P〈0.05），ICAM—ImRNA表达3h即明显升高，72h达最高峰，其后下降。7d时仍高于假手术对照组（P〈0．01）。伤后脑组织含水量较假手术对照组高，同时炎性细胞大量聚集。结论大鼠脑外伤诱导了ICAM—1的表达．ICAM—1通过介导炎性细胞的浸润可能参与了伤后脑水肿的形成过程．     

大鼠脑缺血再灌注后水孔蛋白-4的免疫组化表达与脑水肿关系的研究

目的　研究大鼠脑缺血再灌注后脑组织中水孔蛋白 - 4 (AQP- 4 )的表达与脑水肿的关系。方法　采用大鼠大脑中动脉栓塞 (MCAO)模型 ,经免疫组化法测定 AQP- 4表达阳性细胞数 ,干、湿重法测定脑水含量 ,脑水肿以脑水含量评价。结果　脑缺血再灌注后 12 h,脑缺血坏死周边区 AQP- 4表达阳性细胞及脑水含量增加 ,于 4 8～ 12 0 h 达到高峰 ,16 8h后仍处于较高水平 ,两者之间呈正相关 (r=0 .95 8,P<0 .0 1)。结论　脑缺血再灌注后AQP- 4参与脑水肿的发生 ,为脑缺血再灌注损伤的重要因素之一。     

星形细胞瘤瘤周水肿区立体定向活检组织的超微结构研究

目的探讨星形细胞瘤瘤周脑水肿的发生机制。方法对15例星形细胞瘤瘤周脑水肿的宽度进行分级：一级0～20mm、二级21～40mm、三级〉40mm。结合CT平扫及增强扫描的影像，应用立体定向技术，对15例星形细胞瘤瘤体、瘤周水肿区及正常脑组织的活检标本进行电镜观察比较。结果CT增强扫描可强化，瘤周脑水肿明显的病人，其瘤体及瘤周水肿区毛细血管超微结构均有不同程度的改变。毛细血管的分布和结构变化，影响着瘤周水肿区的形态，瘤体毛细血管的明显异常，出现于大范围瘤周水肿区的病例。CT增强扫描无强化，瘤周脑水肿不明显的病人，毛细血管超微结构与正常脑组织相似。结论伴有明显瘤周脑水肿的星形细胞瘤，其瘤体及瘤周水肿区毛细血管超微结构均有不同程度的改变，而瘤周水肿的产生，是瘤体及瘤周水肿区毛细血管超微结构改变共同作用的结果。     

Comparison of the enzymatic and edema-produscing activities of two venom phospholipase A2 enzymes

The edema-producing activity of NNAVPLA₂, an acidic phospholipase A₂ (PLA₂) enzyme from Naja naja atra venom (NNAV), was less potent than that of TMVPLA₂ II, a basic PLA; from Trimeresurus mucrosquamatus venom (TMV). These edema-forming effects were greatly suppressed by pretreatment of rats with diphenhydramine/ methysergide or compound 48/80, which reduced the tissue content of histamine and serotonin. Heparin abolished and suppressed the paw edema caused by protamine and TMVPLA₂ II, respectively, but had no effect on the NNAVPLA₂-induced response. In isolated rat peritoneal mast cells, both PLA₂ concentration dependently induced the release of histamine and β-glueuronidase. Again, TMVPLA₂ II was more potent than NNAVPLA₂. This degranulation effect of mast cells caused by TMVPLA₂ II and protamine was inhibited by heparin, while that caused by NNAVPLA₂ was unaffected. The edema-forming and mast cell degranulation effects were greatly decreased in both PBPB-modified NNAVPLA₂ and PBPB-modified TMVPLA₂ II, in which the catalytic activity of the enzymes was completely lost. PBPB-modified TMVPLA₂ II-induced paw edema was also suppressed by heparin. Furthermore, this edematous response was totally reversed in rat pretreated with aspirin in combination with diphenhydramine and methysergide. These results suggest that the edema-forming effect of PLA₂ is probably dependent on the presence of catalytic, positive charge and pharmacological sites on its molecule.     

Effect of external high-frequency oscillation on severe cardiogenic pulmonary edema

Effective gas exchange can be maintained in animals without endotracheal intubation using external high-frequency oscillation (EHFO). The aim of this study was to evaluate the effect of EHFO in patients with respiratory failure due to severe cardiogenic pulmonary edema. Seven patients were ventilated with EHFO for 2h at 60 oscillations·min⁻¹, with a cuiras pressure of 36 cmH₂O (−26 to +10) and an inspiratory to expiratory ratio of 1:1, with EHFO. Blood gas values and hemodynamic parameters were measured. Significant increases were noted in cardiac index (2.3±0.5 to 2.5±0.5 l·m⁻²;P<0.05), stroke volume index (24±7 to 28±8 ml·m⁻²;P<0.05), and arterial O₂ pressure (Pao₂) (70±4 to 95±23 mmHg;P<0.01) without a change in pulmonary artery wedge pressure at 1 h after EHFO. The respiratory rate decreased from 28±3 to 22 ±3 breaths·min⁻¹ at 5 min after the termination of EHFO (P <0.01). Arterial CO₂ pressure (Paco₂) did not, however, decrease. Increased stroke volume without a change in pulmonary artery wedge pressure (preload) suggests either improved inotropic function of the left ventricle or reduced left ventricular afterload with EHFO. The use of EHFO may be effective not only for gas exchange but also for left ventricular function in patients with severe cardiogenic pulmonary edema.     

急性高血压脑出血的治疗体会

本文对62例急性高血压脑出血进行了着重于治疗的分析。脑出血病严重威胁患者生命,死亡率高,病残率高。治疗的关键是绝对卧床,避免搬动;积极治疗及控制脑水肿、降低颅内压;头置冰帽以减低脑耗氧量,减轻脑水肿,促进脑细胞功能的恢复;加强护理,预防及治疗并发症是提高患者生存时间及存活率的重要环节;对出血量多、患者一般情况较好者,作者主张手术治疗,清除颅内血肿,可减轻症状,提高存活率及降低病残率。     

小鼠暴露在不同海拔梯度下脑含水量改变及其与脑水肿的关系

观察了小鼠暴露在不同海拔梯度下脑含水量改变及其与脑水肿的关系。实验结果表明，小鼠由低海拔区快速进入高海拔区后脑组织的湿干比值和含水量均有增高（Ｐ＜００１），以进入高海拔区后的第７ｄ为最高峰。组织学观察表明，此时脑神经细胞肿胀，胞浆内有空泡变性，胶质细胞和微血管周围有明显空晕。以上结果揭示，由低海拔区快速进入高海拔区后可致脑水肿形成。