Cerebral energy metabolism in patients with brain lesions at normo- and hyperbaric oxygen pressures

Summary The object of this study was to ascertain the oxygen tolerance limit and the oxygenation state of the injured brain in man. While breathing air, oxygen and hyperbaric oxygen at pressures of 1.5 and 2.0 atmospheres absolute (ATA), the cerebral arteriovenous differences (AVD) for O₂, glucose, lactate, pyruvate and blood gas pressures and pH values were measured. The balance of the cerebral glucose metabolism was calculated. The results showed that the injured brain did not tolerate the exposure to an oxygen pressure of 2.0 ATA for 10 to 15 min, but exposure to 1.5 ATA for 35–40 min was tolerated and had a favorable effect on the glucose or energy metabolism of the brain as well as on the clinical course. There was a distinctly increased cerebral glycolysis while breathing air indicating insufficient oxygen delivery to the brain. The change from breathing air to oxygen resulted in a distinct inhibition of cerebral glycolysis, which indicated improved cerebral oxygenation and energy production and gave evidence for a Pasteur effect regulating the glucose metabolism of the injured brain in man. At an inspiratory oxygen pressure of 1.5 ATA we had a nearly balanced cerebral glucose metabolism indicating an adequate cerebral oxygenation and energy formation. Further increase in inspiratory oxygen pressure to 2.0 ATA (performed only in group A) increased cerebral glycolysis considerably. This was assumed to be due to cerebral oxygen poisoning resulting in disturbed oxidative energy formation. Following this alteration an extreme reduction of the cerebral glucose uptake appeared, probably due to a disturbance of the specific glucose transport system. These metabolic alterations were not accompanied by seizures or any other clinical neurological manifestation. In group B, exposed to 1.5 ATA, such alterations of the cerebral glucose metabolism did not appear. A nearly balanced cerebral glucose metabolism was found at inspiratory oxygen pressures of 1.0 and particularly of 1.5 ATA, indicating an improved oxygenation and energy production of the affected brain. Finally, a renewed increase of the cerebral glycolysis occurred following the change from breathing oxygen to air. This again indicated an insufficient oxygen delivery to the affected brain.

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Zusammenfassung Ziel dieser Arbeit war es, die Wirkung verschiedener inspiratorischer O₂-Drucke auf den zerebralen Glukose- bzw. Energiestoffwechsel zu untersuchen. Dabei sollte insbesondere die Sauerstoff-Toleranzgrenze und der Zustand der Oxygenierung des geschädigten Hirns bestimmt werden. Unter Luft-, Sauerstoff und hyperbarer Sauerstoffatmung, d. h. bei Drucken von 1,5 und 2,0 Atmosphären, wurden die arterio-hirnvenösen Differenzen (AVD) für O₂, Glukose, Laktat, Pyruvat sowie die Blutgasdrucke und die pH-Werte gemessen. Die Bilanz des zerebralen Glukosestoffwechsels wurde bestimmt. Die Ergebnisse zeigten vor allem, daß das geschädigte Hirn eine Sauerstoffbelastung von 2,0 Atmosphären mit einer Expositionszeit von 10 bis 15 min nicht toleriert. Dagegen wurde eine Sauerstoffbelastung von 1,5 Atmosphären mit einer Expositionszeit von 35–40 min vertragen und hatte einen günstigen Einfluß auf den zerebralen Glukose- bzw. Energiestoffwechsel sowie auf den Krankheitsverlauf von traumatischen oder ischämischen Hirngewebsveränderungen. Während der Luftatmung fand sich eine erhebliche Steigerung der zerebralen Glykolyse, was auf eine mangelhafte O₂-Versorgung des Hirngewebes hinwies. Der Wechsel von Luft- auf Sauerstoffatmung führte zu einer deutlichen Hemmung der zerebralen Glykolyse. Dies zeigte eine Besserung der zerebralen Sauerstoffversorgung und Energieproduktion an und wies auf einen Pasteur Effekt bei der Regulation des Glukosestoffwechsels des geschädigten Hirns hin. Bei einem inspiratorischen Sauerstoffdruck von 1,5 Atmosphären war eine praktisch ausgeglichene Bilanz des zerebralen Glukosestoffwechsels nachweisbar, was für eine ausreichende Sauerstoffversorgung und Energiebildung des Hirns sprach. Der weitere Anstieg des inspiratorischen Sauerstoffdruckes auf 2,0 Atmosphären, der nur in Gruppe A durchgeführt wurde, bewirkte jedoch eine erhebliche Steigerung der zerebralen Glykolyse. Es ist anzunehmen, daß diese Stoffwechseländerung durch eine zerebrale Sauerstoffvergiftung hervorgerufen wurde, die vor allem zu einer Störung der oxydativen Energiegewinnung führte. Anschließend trat eine extreme Reduzierung der zerebralen Glukoseaufnahme auf, die am ehesten durch eine Störung des spezifischen Glukosetransportsystems des Hirns bedingt war. Diese Stoffwechselstörungen gingen nicht mit epileptischen Anfällen oder sonstigen klinisch-neurologischen Veränderungen einher. Bei den Patienten der Gruppe B, die nur mit einem Sauerstoffdruck von 1,5 Atmosphären belastet wurden, traten derartige Veränderungen des zerebralen Glukosestoffwechsels nicht auf. Eine praktisch ausgeglichene Bilanz des zerebralen Glukosestoffwechsels wurde bei inspiratorischen Sauerstoffdrucken von 1,0 und vor allem von 1,5 Atmosphären nachgewiesen und zeigte eine Besserung der Sauerstoffversorgung und Energiebildung des geschädigten Hirns an. Schließlich beobachteten wir nach dem Wechsel von Sauerstoff- auf Luftatmung einen erneuten Anstieg der zerebralen Glykose, was wiederum auf eine insuffiziente Sauerstoffversorgung des Hirns hinwies.

     

Current therapy of retrolental fibroplasia. Retinopathy of prematurity

Retrolental fibroplasia, frequently referred to now as the "retinopathy of prematurity," has shown an increased incidence in recent years. This is apparently due to advances in neonatal care, which have resulted in a four- to five-fold improvement in the survival of the extremely low birthweight infants and it is these infants who are at the highest risk of developing retrolental fibroplasia. The use of large supplements of vitamin E, a known antioxidant, is discussed along with other forms of therapy.     

An acute fatal occupational cadmium poisoning by inhalation

Summary A 43-year-old male smelter was admitted to a hospital on account of severe dyspnea about 2 days after exposure to brownish-yellow smoke produced by melting of copper scrap. On admission pronounced hypoxemia was revealed, and an oxygen-enriched gas was administered after intubation. Although inspired oxygen concentration was gradually increased, hypoxemia progressed and he died on day 11 in hospital.The principal autopsy finding was chiefly confined to the lungs. Both lungs were heavy (the left weighing 1,470 g; the right 1,710 g) and firm to the touch. Histologically, no normal alveoli were found throughout the entire lung. Some alveolar spaces were occupied by pneumocytes, others by organized exudate with fibrosis. Interstitial fibrosis was present. Patchy areas of inflammatory cell infiltrations as well as intra-alveolar hemorrhages were observed. On the basis of the above findings a diagnosis of diffuse alveolar damage was made.Based on the available evidence (presence of cadmium in the copper scrap, feature of the smoke, clinical signs with latent time, and high cadmium concentration of the lung), the diffuse alveolar damage was considered to have been caused by inhaled cadmium. The pulmonary change of the present case was more advanced in pathologic stage in comparison with those reported in the literature.     

Pulse oximetry and capnography in anaesthetic practice: an epidemiological appraisal

In the evaluation of any medical technology the efficacy, effectiveness, and efficiency must each be considered before routine deployment is recommended. Since the widespread practice of patient monitoring by pulse oximetry and capnography has occurred before the performance of rigorously controlled trials, definitive proof of worth is lacking. The purpose of this review is to appraise critically the effectiveness of this technology. The assessment was performed using concepts developed in epidemiology and community medicine to establish a given factor to be causative to a given outcome. The current literature pertaining to anaesthetic adverse outcomes was reviewed, and the use of monitors evaluated against the criteria of a causal relationship. While the conclusions are based more on the absence of positive data (owing to low frequency of adverse anaesthetic occurrences) rather than negative results, it must be concluded that the effectiveness of such monitoring has yet to be demonstrated. Such a conclusion should not detract from their use, for the role of an individual factor in the complex chain of accident evolution will seldom be demonstrable. Rather, such an appraisal should encourage a clear perspective of the depth of our clinical science, and encourage more rigorous critical evaluation in the future.     

纳洛酮加清开灵治疗野生蕈中毒30例疗效观察

目的：观察纳洛酮与清开灵合用治疗急性野生蕈中毒的临床疗效。方法：采用随机数字表法将86例患者随机分为3组。治疗组30例以纳络酮加清开灵治疗，纳洛酮组26例单用纳洛酮治疗，清开灵组30例单用清开灵治疗。观察3组患者症状好转时间、症状消失时间、重症清醒时间。治疗5天为1疗程，共治2－8疗程。结果：治疗组在症状好转时间、症状消失时间、清醒时间均明显短于纳洛酮组和清开灵组（P＜0．05，P＜0．01）。结论：纳洛酮与清开灵合用，可以从不同途径作用于脑组织，尽快改善中毒症状，减少脑损伤，二者合用尚可减少纳洛酮的用量，从而减少纳洛酮的心血管效应。     

Study on Metabolites of Aconitum Alkaloids in Human Urine

TheaconitebelongstoplantsofgenusAconituminfamilyofRanunculaceaandhavenotableclinicalfunctionsintreatingrheumaticarthritis ,heartfailure ,etc .However,accidentsofaconitine(fromaconite)poisoningfrequentlyoccurtomanypeopletakingtheseherbs .Theplantsofthisfamilycontainaconitine ,mesaconitine ,hypaconitineandotheraco nitumalkaloids .Theyarehighlytoxic ,andtheirtreatmentdoseapproachestothetoxicdoseorlethaldose .Duringtheperiodfrom 1989- 1995 ,morethan 30casesofpoisoningcausedbyaconitineinsometradit…     

高压氧治疗对脑外伤患者血糖影响的比较研究

目的 探讨高压氧治疗对脑外伤患者血糖的影响。方法 将100例脑外伤患者随机分为治疗组和对照组，分别测量治疗前后两组患者血糖浓度。结果 高压氧治疗后脑外伤患者血糖浓度较对照组明显降低。结 论高压氧治疗能使脑外伤后升高的血糖降低，促进受损伤脑组织修复。     

Low-dose dopexamine in patients undergoing hemihepatectomy: an evaluation of effects on reduction of hepatic dysfunction and ischaemic liver injury

BACKGROUND: Hepatic dysfunction is a common problem in patients after hemihepatectomy. Treatment with low-dose dopamine has been shown to be beneficial in hemihepatectomy patients. We hypothesized that dopexamine, a synthetic vasoactive catecholamine, due to its specific pharmocodynamic profile may be more effective in reducing hidden ischaemic episodes in the hepato-splanchnic region during and after temporary total cross-clamping of hepatic inflow in these patients. METHODS: The effects of low-dose dopexamine on hepatic venous haemoglobin oxygen saturation (ShvO2), hepatic venous lactate level, monoethylglycinxylid (MEGX) formation, hepatic synthetic function and indicators for hepatic cell damage were studied during hemihepatectomy and for 16 h postoperatively in hemihepatectomy patients and compared to those of low-dose dopamine. In a prospective, double-blind clinical study 20 patients received randomly either dopexamine (DPX) 0.5 microg kg(-1) min(-1) (n=10) or dopamine (DO) 2.5 microg kg(-1) min(-1) (n= 10). Infusions were started after induction of anaesthesia and continued 16 h postoperatively. Hepatic vein, radial and pulmonary artery were catheterized. Measurements were carried out after induction of anaesthesia, after total cross-clamping of hepatic inflow, and at 2 h and 16 h postoperatively. RESULTS: There were no differences in systemic haemodynamics, oxygenation, ShvO2, serum aminotransferases or MEGX levels between the groups. At 16 h postoperatively prothrombin and antithrombin III levels were significantly lower while hepatic venous lactate was significantly higher in the DPX group compared to the DO group. CONCLUSION: In patients undergoing hemihepatectomy, we could not reveal superior hepatoprotective effects of low-dose dopexamine compared to low-dose dopamine.     

芦荟对大鼠肝微粒体脂质过氧化损伤体外模型的影响

目的: 探讨芦荟的抗氧化作用及其剂量效应关系。方法: 通过大鼠微粒体的提取,制备了VC/Fe2+和过氧基异丙苯(CHP)脂质过氧化损伤模型,检测不同剂量芦荟轧汁干预对丙二醛(MDA)含量变化的影响,观察芦荟清除活性氧的抗氧化作用。结果: 在CHP微粒体脂质过氧化激发模型中,各芦荟干预组的MDA含量均较对照组显著降低(P﹤0.01),在VC/Fe2+模型中,低剂量芦荟轧汁干预组与高剂量干预组MDA含量较阳性对照组显著下降(P﹤0.05),并且高剂量组降低更加明显(P﹤0.01)。但中剂量芦荟轧汁组MDA含量反而较阳性对照组有一定的升高。结论: 芦荟轧汁在抗氧化方面存在着双向效应,在一定剂量范围内有着较好的抗氧化作用,可能是芦荟的医疗保健功效的机制之一;但特定的剂量又可激发活性氧的生成。