Ventral medulla pHi measured in vivo by 31P NMR is not regulated during hypercapnia in anesthetized rat

Chemoreceptors in the ventral medulla contribute to the respiratory response to hypercapnia. Do they ‘sense’ intracellular pH (pH_i)? We measured pH_i in the ventral medulla or cortex (control) using ³¹P-NMR obtained via a novel 3×5 mm² surface coil in anesthetized rats breathing air or 7% CO₂. During air breathing over 240 min, pH_i decreased slightly from 7.13±0.02 to 7.05±0.02 (SEM; n=5; 2 cortex, 3 ventral medulla). During 180 min of hypercapnia, cortical pH_i (n=4) decreased from 7.17±0.02 to 6.87±0.01 by 90 min and recovered by 150 min. Ventral medulla pH_i showed no such regulation. It decreased from 7.11±0.02 to 6.88±0.02 at 90 min and recovered only after cessation of hypercapnia (n=5), results consistent with pH_i being the chemoreceptor stimulus. However, non-chemoreceptor neurons that contribute to our medullary NMR signal also do not appear to regulate pH_i in vitro. Regional differences in pH_i regulation between cortex and ventral medulla may be due to both chemosensitive and non-chemosensitive neurons.     

The direct effect of carbon monoxide on KCa channels in vascular smooth muscle cells

 The vasorelaxation induced by carbon monoxide (CO) has been demonstrated previously. Both a guanosine cyclic monophosphate (cGMP) signalling pathway and cGMP-independent mechanisms have been proposed to be responsible for the vascular action of CO. A direct effect of CO on the activity of calcium-activated K (K_Ca) channels in vascular smooth muscle cells (SMCs) and the underlying mechanisms were investigated in the present study. It was found that CO hyperpolarized single SMCs isolated from rat tail arteries. The whole-cell outward K⁺ channel currents in vascular SMCs, but not in neuroblastoma cells, were enhanced by CO. Extracellularly or intracellularly applied CO increased the open probability of single high-conductance K_Ca channels concentration-dependently without affecting the single channel conductance. Although it did not increase the resting level of intracellular free calcium concentration, CO significantly enhanced the calcium sensitivity of single K_Ca channels in SMCs. Furthermore, the effect of CO on K_Ca channels was not mediated by cGMP or guanine nucleotide-binding proteins (G proteins, G_i/G_o or G_s) in excised membrane patches. Our results suggest that the direct modulation of high-conductance K_Ca channels in vascular SMCs by CO may constitute a novel mechanism for the vascular effect of CO. Received: 9 January 1997 / Received after revision: 21 February 1997 / Accepted: 10 March 1997     

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.     

Recreational gasoline sniffing: acute gasoline intoxication and latent organolead poisoning. Case reports and literature review

Gasoline is a readily obtainable intoxicant that unfortunately lends itself to habitual abuse by sniffing, a practice found particularly among children and adolescents. The concerted effects of the multiple hydrocarbon and other constituents of gasoline result in a predictable acute toxic syndrome. Organoleads, primarily tetraethyl lead (TEL), cause a separate toxicologic symptom-sign complex that overlaps with the initial acute toxic syndrome. The different clinical symptomatology, effects on hemoglobin synthesis, and response to chelation therapy are all in keeping with the view that organolead poisoning is a separate and distinct toxicologic entity from that of classical elemental lead poisoning or "plumbism".     

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.     

2010—2020年云南省学校食源性疾病暴发事件流行病学分析

目的 了解云南省学校食源性疾病暴发事件流行病学特征和趋势。 方法 收集2010—2020年云南省各地报告的学校食源性疾病暴发资料,并进行描述性流行病学分析。 结果 2010—2020年共发生学校食源性疾病暴发260起,发病6 600人,死亡2人,总体呈下降趋势。学校食源性疾病暴发高峰期为第二、四季度,占总起数的66.54%(173/260);暴发场所多发生在小学,占总起数的58.08%(151/260)。报告明确或可疑致病因子的185起事件中由微生物或可疑微生物引起的占40.00%(74/185),毒素引起的占46.49%(86/185);明确致病因子的118起暴发事件中,60.17%(71/118)是由4种致病因子引起的,其中蓖麻毒素导致的最多,达22起(18.64%),发病人数428人,其次是蜡样芽孢杆菌20起(16.95%),原因食品被归因为一类食品植物类,主要是大米、三明治、面包。导致暴发污染环节最多的是生产加工环节(50.77%,132/260)。 结论 关注学校食源性疾病暴发事件流行特征,在学生开学季时,加强对小学食堂植物类食品的生产加工环节管理和监督。微生物、毒素感染是学校食源性疾病主要的致病因素,且原因查明率低,进一步强化医疗机构食源性疾病微生物、毒素检测能力,提高原因查明率,最大限度地降低学校食源性疾病的发病率。