Biomedical subjects
J Meulenbelt
Publications and source records attributed to J Meulenbelt.
Rat model to investigate the treatment of acute nitrogen dioxide intoxication.
1. The pulmonary toxic events induced by acute nitrogen dioxide (NO)2 exposure were studied in the rat to develop an inhalation model to investigate therapeutic measures. 2. A good correlation was observed between the lung weights and severity of the atypical pneumonitis. The pulmonary effects observed, became more pronounced with increasing NO2 concentrations (0, 25, 75, 125, 175 or 200 ppm, 1 ppm NO2 = 1.88 mg m-3 NO2) and exposure times (5, 10, 20 or 30 min). 3. An adequate NO2 concentration is 175 ppm, because it can induce a severe lung injury without mortality. This makes it possible to investigate suitable therapeutic interventions for several days. 4. Following acute inhalatory NO2 intoxication, transformation of NO2 to nitrate is presumably more notable than transformation to nitrite. 5. The transformation of NO2 to nitrate in lung tissue causes a slight increase in the serum nitrite concentration, which does not induce measurable formation of methaemoglobin. 6. Presumably, methaemoglobin does not contribute to the toxicity of NO2 intoxication.
Biochemical and histological alterations in rats after acute nitrogen dioxide intoxication.
1. In previous studies a rat inhalation model was developed to investigate the treatment of acute nitrogen dioxide (NO2) intoxication. 2. Biochemical parameters, which may be important for the evaluation of lung injury and repair, were reviewed and compared with the histology. 3. After exposure to high NO2 concentrations (75 ppm, 125 ppm or 175 for 10 min) the lung injury observed by light microscope was most pronounced after 24 h and became worse with increasing concentration. 4. The most sensitive indicators for lung injury in the broncho-alveolar lavage fluid (BAL) were protein and albumin concentrations, angiotensin converting enzyme activity, beta-glucuronidase activity and the presence of neutrophil leucocytes. The changes observed in these variables were dose-dependent. Following exposure to 175 ppm the protein and albumin concentrations and the angiotensin converting enzyme activity showed a 100-fold increase, while the beta-glucuronidase activity showed a 10-fold increase. 5. Glucose-6-phosphate dehydrogenase and glutathione peroxidase in the supernatant of lung homogenate and gamma-glutamyl transferase activity in BAL are likely to be the most practical parameters for monitoring the phase of repair because their activities were maximal at the moment histological changes were reduced in intensity. 6. Repair was almost complete 7 d following exposure.
Two cases of acute toluene intoxication.
Two patients exposed to high concentrations of toluene in air (greater than 7000 mg/m3) were found at the bottom of a small swimming pool under construction. Their symptoms were stupefaction, paresis, and amnesia. Patient A had been exposed for three hours and patient B for two hours. Ninety minutes after the exposure, the toluene blood concentration in patient A was 4.1 mg/l and in patient B 2.2 mg/l. Urinary ortho-cresol secretion was shown to be a good index of exposure to toluene. After high level exposure, urinary meta-cresol excretion may also be used to monitor toluene exposure.
Acute nitrous oxide intoxication: clinical symptoms, pathophysiology and treatment.
Nitrogen dioxide is a representative of the group of compounds which may cause pulmonary symptoms after a symptom free interval. Even when there are no symptoms immediately following exposure to nitrogen dioxide, clinical observation is advisable, because severe pulmonary involvement can be the result. The present paper discusses the clinical symptoms which are observed in man after acute exposure to nitrogen dioxide, as well as the pathophysiological mechanisms involved. Practical therapeutic guidelines are given for dealing with the diagnostic difficulties concerning this type of intoxication.
[Acute cyanide poisoning in an infant].
An infant of 9 months was admitted to hospital in comatose condition; cyanide poisoning was suspected. This poisoning was caused by the desorption of hydrocyanic acid from building materials after the house had been fumigated with hydrocyanic acid under strict supervision and observed safety measures. Administration of 4-dimethyl-aminophenol, a methaemoglobin inducer, and sodium thiosulphate together with supportive measures, led to complete recovery of the infant, although the general hypotony persisted for a few weeks.
Renal failure associated with the use of dextran-40.
A typical case of dextran-40 associated acute renal failure is presented. In this patient a single plasma exchange was successful in considerably lowering the plasma dextran concentration. At the same time the elevated plasma oncotic pressure was reduced to normal values. Diuresis returned within 12 h. Several possible explanations of the mechanism of renal failure associated with the use of dextran-40 are discussed. While the mechanism of dextran-associated renal failure remains unsolved, plasma exchange seems to be effective therapy.
Acute MCPP intoxication: report of two cases.
1. Two cases of serious intoxication with phenoxy herbicides (MCPP) are reported. 2. Both patients had central nervous system involvement, became unconscious and had an inadequate respiration. Muscle cramps and rhabdomyolysis with renal failure were noted in both. Shortly after admission both patients developed a serious decrease in arterial blood pressure (160/80 mmHg to 80/45 mmHg). In one patient this was demonstrated to be caused by a reduction in peripheral vascular resistance. 3. Plasma concentration of MCPP in patient 2 was 298 mg/l (3-4 h after ingestion). The plasma t1/2 was about 17 h. MCPP plasma elimination probably follows first-order kinetics.
Skin lesions due to exposure to methyl bromide.
Six patients were occupationally exposed to high concentrations of methyl bromide during a fumigation procedure using adequate airway protection. Within a few hours all patients developed skin lesions, consisting of sharply demarcated erythema with multiple vesicles and large bullae. There was a striking predisposition for parts of the skin that were relatively moist or subject to mechanical pressure, such as axillae, groin, and abdomen. Microscopically, early skin lesions revealed necrosis of keratinocytes, severe edema of the upper dermis, subepidermal blistering, and diffuse infiltration of neutrophils and, to a lesser degree, eosinophils. Two patients developed an urticarial rash approximately one week after the exposure. On histologic examination, these late lesions showed combined features of a spongiotic dermatitis and urticaria. No immunopathologic manifestations were observed. In all patients, the skin returned to normal after four weeks, except for some residual hyperpigmentation. Plasma bromide levels after exposure strongly suggested percutaneous absorption of methyl bromide.
Acute pulmonary intoxications. Overview and practical guidelines.
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Exposure of the skin to methyl bromide: a study of six cases occupationally exposed to high concentrations during fumigation.
1 The effects of exposure of the skin to high concentrations of methyl bromide were studied in 6 cases, who had been unintentionally exposed. 2 Exposure to high concentrations of methyl bromide (approximately 40 g/m3) for 40 min can lead to redness and blistering of the skin. This cannot be prevented by wearing standard protective clothing. 3 Skin lesions show a preference for relatively moist skin areas. 4 Plasma bromide levels were highest immediately following exposure (mean 9.0 +/- 1.4 mg/l) and fell in subsequent hours (mean 6.8 +/- 2.3 mg/l 12 h after the exposure), suggesting absorption of (methyl) bromide through the skin. 5 No systemic effects were noted in this series. 6 Fumigation with methyl bromide should not be done in such a way as to require the presence of workers inside closed areas, where methyl bromide is released.
[Acute disease with fever, headache, exanthema and diminished kidney function: an emergency case].
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[Treatment of a renal artery occluded by an embolism with low-dose streptokinase].
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