The diffusion of carbon dioxide in erythrocytes and hemoglobin solutions

Summary The CO₂ diffusion constant (Krogh's diffusion constant) has been estimated from the CO₂ flux across layers with defined thickness under steady state conditions.At 22°C and in hemoglobin solutions with a concentration of 33 g% the diffusion constant for CO₂ was found to be 3.3×10^–4 cm² min^–1 atm^–1. This value is about 40% of the diffusion constant for CO₂ in water. The relationship between the diffusion constant and the hemoglobin concentration was approximately linear in a concentration range of 10–40 g%. The temperature coefficient of the diffusion constant was –0.5%/°C both in water and hemoglobin solutions. At 38°C and in a hemoglobin solution with a concentration of 33 g%, the diffusion constant for CO₂ was therefore 3.0×10^–4 cm² min^–1 atm^–1, the diffusion coefficient 11×10^–6 cm² s^–1.A general theory for the diffusion of CO₂ in hemoglobin solutions has been derived. According to this theory the diminution of the CO₂ diffusion in hemoglobin solutions in comparison to water can be explained quantitatively by a reduction of the water space by the hemoglobin molecules.The diffusion constant for CO₂ in layers of erythrocytes was insignificantly (0–3%) smaller than in hemoglobin solutions with the same hemoglobin concentration. It is concluded that the erythrocyte membrane does not offer a considerable resistance for the CO₂ diffusion.     

HO-1/CO径路在肺缺血-再灌注损伤中的作用

目的：探讨血红素氧合酶-1（HO-1）/一氧化碳（CO）径路在肺缺血-再灌注损伤中的作用。 方法： 采用在体兔单肺原位缺血-再灌注模型。实验兔40只，随机均分为假手术对照（C）组、肺缺血-再灌注（I-R）组、肺缺血-再灌注加氯铁血红素(H)组和肺缺血-再灌注加锌原卟啉(Z)组。分别在缺血前、缺血后、再灌注1 h、2 h、3 h抽血，检测一氧化碳血红蛋白(COHb)浓度。实验结束时取肺组织检测湿干重比（W/D）、肺泡损伤率（IAR），观察肺组织超微结构的改变、HO-1的活力、表达部位及强度。 结果： 血浆COHb浓度，I-R组、H组明显高于C组，以H组为著（P<0.01）；H组、Z组显著高于、低于I-R组（P<0.01）。肺组织HO-1活力H组最高，其次是I-R组，Z组和C组最低（P<0.05和P<0.01）。I-R组、H组、Z组HO-1在肺血管内皮、部分血管平滑肌、外膜层及部分气道上皮均有阳性表达，明显高于C组，尤以H组最为明显（P<0.01）。W/D、IAR值，I-R组和Z组均明显高于C组，尤以Z组为著，H组虽较C组为高，但显著低于IR组和Z组（P<0.05和P<0.01）。肺组织形态学异常改变，以Z组为著，H组较轻。 结论： HO-1/CO径路对缺血-再灌注肺发挥积极的保护作用。     

Ventilatory and upper-airway resistance responses to upper-airway cooling and CO2 in anaesthetised rats

The effects of upper airway (UA) cool air and CO₂ on breathing and on laryngeal and supraglottic resistances were studied in anaesthetised rats breathing spontaneously through a tracheostomy. Warm, humidified air containing 0, 5 and 9–10% CO₂ and cool, room-humidity air were delivered at constant flow to either the isolated larynx to exit through a pharyngotomy or to the supraglottic UA to exit through the mouth and/or nose (nose open or sealed). Spontaneous tracheal airflow and UA airflows, temperatures and pressures were recorded. CO₂ had no effect on breathing but caused a slight increase in laryngeal resistance which was abolished by cutting the superior laryngeal nerves (SLN). Cool air caused a decrease in respiratory frequency and/or peak inspiratory flow when applied to the isolated larynx or to the supraglottic airway with the nose closed. These effects were abolished by SLN section. With the nose open, the ventilatory inhibition was not abolished by SLN section. Cool air also caused substantial decreases in laryngeal and supraglottic resistances which were attenuated by SLN section and which persisted following recurrent laryngeal nerve section. In conclusion, whilst UA cooling inhibits breathing and decreases UA resistances, UA CO₂ has minimal effects.     

The relationship between exposure duration,carboxyhemoglobin, blood glucose,pyruvate and lactate and the severity of intoxication in 39 cases of acute carbon monoxide poisoning in man

The relationship between exposure duration, COHb, blood glucose, pyruvate and lactate and the severity of intoxication was investigated in a group of 39 cases of acute CO poisoning treated in the Clinical Toxicology Center in ód, Poland.On the basis of clinical criteria the patients were classified into cases of mild, moderate, severe and very severe CO poisoning. COHb and carbohydrate metabolites were estimated in venous blood taken immediately after admission of the patient to hospital prior to treatment.The severity of intoxication did not correlate with blood COHb; variation in exposure duration seems to be responsible for this phenomenon. Severe and very severe poisonings were associated with longer exposures and were accompanied by a markedly higher blood lactate level, compared to mild and moderate cases. Blood pyruvate depended less than lactate on the severity of intoxication. Blood glucose depended neither on exposure duration nor on the severity of intoxication.Among the carbohydrate metabolic parameters studied, blood lactate determination can be helpful in the evaluation of the severity of CO poisoning in man.     

In vivo inhibition of dopamine-β-hydroxylase in rat adrenals during exposure to carbon disulphide

Male rats were exposed for a maximum of 4 h to carbon disulphide at atmospheric levels of 1.0—4.0mg/l and the turnover rates of adrenal dopamine was determined by injecting -methyl-p-tyrosine and measuring the rate at which dopamine disappears. Although the level of exposure was significantly higher than the 30.0 g/l permissible limit, or the average occupational exposure, similar or even higher peak exposure values were reported from the viscose rayon industry.After inhibition of tyrosine hydroxylase by -methyl-p-tyrosine, adrenal dopamine contents declined at a slower rate in rats exposed to carbon disulphide than in controls. The reduced rate of dopamine metabolism during exposure to carbon disulphide indicates inhibition of dopamine--hydroxylase in vivo. The size of this effect, which could be detected as soon as 30 min after starting the exposure to carbon disulphide, was dose dependent. The rate of dopamine turnover was still reduced 2 h after the end of a single exposure. However at that time, because of the larger dopamine pool present in the adrenals, the amount of dopamine converted per unit of time was again at pre-exposure levels.S. C. was supported during these studies by grants from the British Wellcome Trust and from the European Medical Research councils.     

Ultrastructure of carbon disulphide neuropathy

Summary Adult Wistar rats were exposed to carbon disulphide (CS₂) vapour at a concentration of 2.4 mg/l of air for 5 days a week (6h a day), and the ultrastructure of peripheral nerves, neuromuscular junctions and muscles was investigated after 6 months of exposure to CS₂. Numerous giant axons, i.e. paranodal or internodal swellings, were seen in the peripheral nerves. At the swollen paranodes, the myelin sheath was thinned, in other regions large intramyelinic vacuoles indicative of more dramatic demyelination were observed at axonal enlargements. Axonal enlargements consisted essentially of whorls of tightly packed neurofilaments. A number of nerve fibres underwent complete degeneration, but at the same time there was evidence of nerve regeneration. Nerve terminals were affected in a similar way following CS₂ exposure. At neuromuscular junctions, filamentous swellings of nerve terminals preceded their degeneration and eventual denudation of synaptic gutters. As a rule, the postsynaptic part of neuromuscular junctions remained unimpaired by CS₂ treatment. Muscles were affected by both atrophy and degeneration. Clusters of dense and lamellar bodies and numerous autophagosomes indicative of direct myotoxic effect of CS₂ were frequently encountered in the investigated muscles. Some muscle fibres apparently underwent necrosis judging from the occurrence of myotubes characteristic of muscle degeneration and regeneration.The pathomorphology of CS₂ neuropathy resembles that of other toxic neuropathies which presumably have a common origin in impaired energy metabolism.     

阻塞性呼吸睡眠暂停综合征与中枢呼吸驱动

目的阐明不同浓度的CO     

Exocrine ductalpCO2 in the rabbit pancreas

An improvedpCO₂ microelectrode has been evaluated and used to investigate whether a significant barrier to diffusion of CO₂ exists in the rabbit pancreas. The results of this study show the improved Carter and CaflischpCO₂ microelectrode to be an accurate and reliable tool for measuring pancreatic venous and ductalpCO₂. The similarities betweenpCO₂ values from the pancreatic ducts and small pancreatic veins suggest that there is no barrier to CO₂ diffusion between small veins and exocrine ducts in the rabbit pancreas, and that ductalpCO₂ is probably strongly influenced by the CO₂ tension of the small pancreatic blood vessels.     

Investigations into the effects of various hepatotoxic compounds on urinary and liver taurine levels in rats

The effect of various hepatotoxicants on urinary taurine and urinary creatine has been studied in the rat. Several hepatotoxic agents, carbon tetrachloride, thioacetamide, galactosamine and allyl alcohol which all caused hepatic necrosis (sometimes accompanied by steatosis), resulted in a rise in urinary taurine and in some cases creatine, when administered to rats. Ethionine and hydrazine also raised urinary taurine but caused only steatosis and did not raise urinary creatine. Therefore urinary taurine and possibly creatine may be useful markers of liver injury and dysfunction. Liver taurine levels were also affected by some of the hepatotoxicants but in those cases where there was a rise in urinary taurine this could not be accounted for by the loss in liver taurine. It is suggested that the increase in urinary taurine is partly due to changes in protein synthesis and hence in sulphur amino acid metabolism caused by hepatotoxic agents. However, bromobenzene did not increase urinary taurine and-naphthylisothiocyanate and lithocholate caused reduced levels. It is suggested that this lack of increase in urinary taurine may be due to depletion of glutathione or interference with the biliary system.     

单肺通气时肺内分流与PETCO2的相关性研究

目的：研究单肺通气时PETCO2和Qs/Qt之间的关系。方法：选择28例择期开胸手术的患者分别于TLV 20min、OLV 5min、15min、30min、60min测动脉血和混合静脉血气并同时记录PETCO2,计算Qs/Qt,进行统计学处理。结果：OLV时不同时段PETCO2、PaCO2、Qs/Qt比TLV时增大(P＜0.05),TLV时PETCO2与Qs/Qt不相关(r=-0.0230,P=0.9077)。OLV时PETCO2与Qs/Qt相关(r=0.4739,P=0.00001),其直线回归方程为y=3.4862+0.0147x(y=PETCO2,x=Qs/Qt)。结论：OLV时PETCO2与Qs/Qt呈直线相关,PETCO2随Qs/Qt增加而增大。