重症急性高原病患者电解质代谢紊乱与多脏器功能障碍的关系

重症急性高原病患者电解质紊乱可引发机体的钠水潴留,血管活性物质及自由基的大量产生,从而加重各脏器的损害,导致多脏器功能障碍(MODS),甚至危及患者生命.在高原现场救治过程中应加强电解质的监测.     

两种不同方式治疗视网膜分支静脉阻塞继发黄斑水肿的meta分析

目的系统评价激光联合玻璃体腔注射雷珠单抗与单独玻璃体腔注射雷珠单抗治疗视网膜分支静脉阻塞(BRVO)继发黄斑水肿的疗效及安全性。方法通过检索PubMed、CNKI、万方等数据库收集有关治疗BRVO继发黄斑水肿的随机对照试验研究(RCT)。检索时间为建库至2019年5月。采用RevMan 5.3软件对纳入文献进行meta分析。结果共纳入12篇文献,包括1081例患者。meta分析结果显示:与单纯注药组相比,联合治疗组黄斑中心凹厚度(CMT)在随访1、3、6个月时均降低,差异有统计学意义[95%CI(-135.44^-15.54),P<0.001];但对于最佳矫正视力(BCVA)的提高,2组间无统计学差异[95%CI(-1.75~0.80),P>0.05];2组不良反应的发生率无统计学差异[OR=1.50,95%CI(0.97~2.30),P=0.07]。结论激光联合玻璃体腔注射雷珠单抗能够显著降低BRVO继发黄斑水肿患者的CMT,早期疗效优于单纯注药组。但两种方式对于治疗后BCVA的影响及不良反应的发生尚需要大样本的随机对照双盲研究加以验证。     

鬼针草总黄酮对实验性脑出血大鼠脑损伤的保护作用

[摘要] 目的：观察鬼针草总黄酮（TFB）对大鼠实验性脑出血后脑组织损伤的影响,探讨其对大鼠脑损伤的保护机制。方法：采用大脑立体定位技术,取不抗凝血液50ul缓慢注入尾状核建立大鼠实验性脑出血模型,观察TFB对脑组织含水量、全血粘度及脑匀浆中超氧化物歧化酶（SOD）、丙二醛（MDA）、一氧化氮（NO）等生化指标的影响。结果：TFB高、中、低剂量组均能显著改善脑出血大鼠脑含水量、全血粘度,高、中剂量组能明显升高脑组织SOD活性,降低MDA、NO含量(P〈0.05)。结论：TFB对实验性脑出血大鼠脑损伤的保护作用可能与其减轻脑水肿、改善血肿周围组织的微循环状态、减轻细胞膜脂质过氧化损伤、抑制NO的产生有关。     

重型颅脑损伤并发神经源性肺水肿的诊断和治疗

目的：探讨重型颅脑损伤并发神经源性肺水肿（NPE）的临床特点和治疗方法。方法：分析24例并发急性神经源性肺水肿患者的早期临床表现、治疗方法及与患者预后的关系。结果：本组24例NPE患者中死亡12例（50.0%）,存活12例（50.0%）,其中,轻残1例（4.2%）,中残4例（16.7%）,重残6例（25.0%）,恢复良好1例（4.2%）。结论：早期诊断,迅速降低颅内高压,及时行气管切开,呼吸机辅助呼吸,激素等综合治疗可降低患者的死亡率,改善预后。     

Reversible attenuation of voltage of QRS complexes and P waves and shortening of QRS duration and QTc interval consequent to large perioperative intravenous fluid infusions

A 39-year-old woman with a gangrenous pyelonephritis and septic shock underwent a nephrectomy, in preparation for which, she received large preoperative fluid resuscitation. Quantitative evaluation of her serial standard electrocardiograms (ECGs) revealed reversible attenuation of voltage in association with peripheral edema (PERE), with the latter being eventually completely abolished. The transient low-voltage ECG (LVECG) (attenuated amplitudes of QRS complexes) was associated with parallel transient attenuation of the amplitude of P waves and shortening of the QRS duration and QTc, whereas the P-wave duration increased. Awareness of these ECG changes with PERE of varying pathophysiologic mechanisms is useful, ensuring avoidance of improper procedural and laboratory testing and correct measurement of wave amplitudes and ECG time intervals for proper ECG diagnosis. In addition, these ECG associations can be used as indices of the presence and course of PERE postoperatively, as well as in a large variety of medical settings.     

Heterogeneous pulmonary blood flow in response to hypoxia: a risk factor for high altitude pulmonary edema?

High altitude pulmonary edema (HAPE) is a rapidly reversible hydrostatic edema that occurs in individuals who travel to high altitude. The difficulties associated with making physiologic measurements in humans who are ill or at high altitude, along with the idiosyncratic nature of the disease and lack of appropriate animal models, has meant that our understanding of the mechanism of HAPE is incomplete, despite considerable effort. Bronchoalveolar lavage studies at altitude in HAPE-susceptible subjects have shown that mechanical stress-related damage to the pulmonary blood gas barrier likely precedes the development of edema. Although HAPE-susceptible individuals have increased pulmonary arterial pressure in hypoxia, how this high pressure is transmitted to the capillaries has been uncertain. Using functional magnetic resonance imaging of pulmonary blood flow, we have been able to show that regional pulmonary blood flow in HAPE-susceptible subjects becomes more heterogeneous when they are exposed to normobaric hypoxia. This is not observed in individuals who have not had HAPE, providing novel data supporting earlier suggestions by Hultgren that uneven hypoxic pulmonary vasoconstriction is an important feature of those who develop HAPE. This brief review discusses how uneven hypoxic pulmonary vasoconstriction increases regional pulmonary capillary pressure leading to stress failure of pulmonary capillaries and HAPE. We hypothesize that, in addition to the well-documented increase in pulmonary vascular pressure in HAPE-susceptible individuals, increased perfusion heterogeneity in hypoxia results in lung regions that are vulnerable to increased mechanical stress.     

双水平正压通气在急性心源性肺水肿中的应用

目的探讨急性心源性肺水肿（ACPE）使用经鼻/面罩双水平正压通气（BiPAP）的救治方法。方法分析42例ACPE并发呼吸衰竭患者,经鼻/面罩连接呼吸机BiPAP无创通气救治,据患者反应调节呼吸机参数,2h好转后,分析比较治疗前后心功能分级改善情况,平均动脉压（MAP）、心率（HR）、呼吸频率（RR）、SpO2和动脉血气：PH、氧分压（PaO2）、二氧化碳分压（PaCO2）的变化。结果 BiPAP治疗2h后患者的MAP、HR、RR、SpO2和动脉血气中PH、PaO2较治疗前均改善显著,差异有统计学意义（P〈0.05）。结论经鼻/面罩连接BiPAP无创通气可作为ACPE合并呼吸衰竭患者的首选治疗措施之一。尽早正确使用可以使许多ACPE患者避免有创通气。     

Spinal cord injury induced heat shock protein expression is reduced by an antioxidant compound H-290/51. An experimental study using light and electron microscopy in the rat

Summary. The possibility that oxidative stress participates in heat shock protein 72 kD (HSP 72) expression following a focal trauma to the spinal cord was examined using a potent antioxidant compound H-290/51 in a rat model. A focal spinal cord injury (SCI) inflicted by making a longitudinal incision on the right dorsal horn of the T10–T11 segment under equithesin anaesthesia resulted in profound upregulation of HSP 72 expression in the adjacent spinal cord segments T9 and T12. This expression of HSP was most marked in the ipsilateral cord at 5 h after SCI. Pretreatment with H-290/51 (50 mg/kg, p.o.) 30 min before SCI markedly attenuated HSP expression in the spinal cord seen at 5 h. The motor functions of traumatized rats were also improved in the drug treated group. At this time, structural changes in the spinal cord and edema formation were considerable reduced compared to the untreated traumatized rats. Taken together, these observations suggest that (i) oxidative stress participates in HSP response following trauma, and (ii) the antioxidant compound H-290/51 attenuates cellularstress, improves motor functions and induces considerable neuroprotection in the early phase of SCI. Further studies using post-injury treatment with H-290/51 is needed to explore its therapeutic potentials in clinical settings.     

Effect of Phenylephrine on Alveolar Fluid Clearance in Ventilator-induced Lung Injury

Objective To investigate the effect of phenylephrine(an α-adrenergic agonist) on alveolar fluid clearance(AFC) in ventilator-induced lung injury and the possible mechanism involved.Methods A total of 170 male Wistar rats were randomly allocated into 17 groups(n=10) using random number tables.Short-term(40 minutes) mechanical ventilation with high tidal volume(HVT) was performed to induce lung injury,impair active Na + transport and lung liquid clearance in the rats.Unventilated rats served as controls.To demonstrate the effect of phenylephrine on AFC,phenylephrine at different concentrations(1×10-5,1×10-6,1×10-7,1×10-8,and 1×10-9 mol/L) was injected into the alveolar space of the HVT ventilated rats.To identify the influence of adrenergic antagonists,Na + channel,and microtubular system on the effect of phenylephrine,phenylephrine at 1×10-5 mol/L combined with prazosin(an α 1-adrenergic antagonist,1×10-4 mol/L),yohimbine(an α 2-adrenergic antagonist,1×10-4 mol/L),atenolol(a β 1 adrenergic antagonist,1×10-5 mol/L),ICI-118551(an β 2-adrenergic antagonist,1×10-5 mol/L),amiloride(a Na + channel blocker,5×10-4 mol/L),ouabain(a Na + /K +-ATPase blocker,5×10-4 mol/L),colchicine(a microtubular disrupting agent,0.25 mg/100 g body weight),or β-lumicolchicine(an isomer of colchicine,0.25 mg/100 g body weight) were perfused into the alveolar space of the rats ventilated with HVT for 40 minutes.AFC and total lung water content were measured.Results Basal AFC in control rats was(17.47±2.56)%/hour,which decreased to(9.64± 1.32)%/hour in HVT ventilated rats(P=0.003).The perfusion of phenylephrine at 1×10-8,1×10-7,1×10-6,and 1×10-5 mol/L significantly increased the AFC in HVT ventilated rats(all P<0.05).This effect of phenylephrine on AFC was suppressed by prazosin,atenolol,and ICI-118551 in HVT ventilated rats by 53%,31%,and 37%,respectively(all P<0.05).The AFC-stimulating effect of phenylephrine was lowered by 33% and 42% with amiloride and ouabain,respectively(both P<0.05).Colchicine significantly inhibited the effect of phenylephrine(P=0.031).Conclusion Phenylephrine could increase the AFC in HVT-ventilated rats and accelerate the absorption of pulmonary edema.