Search PubMed⌕ Search

Biomedical subjects

B Sangster

Publications and source records attributed to B Sangster.

At least 19 recordsLinked to original sources
PubMed1992

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.

Administration, Inhalation↗
PubMed1992

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.

Administration, Inhalation↗
PubMed1992

In vitro binding characteristics for cesium of two qualities of prussian blue, activated charcoal and Resonium-A.

The in vitro binding characteristics of radioactive 137Cs to two forms of Prussian blue [colloidally (soluble) K3Fe[Fe(CN)6] and insoluble Fe4[Fe(CN)6]3] and to activated charcoal and sodium polystyrene sulfonate (Resonium-A) were investigated by constructing Langmuir isotherms at pH = 1.0, 6.5 and 7.5 at 37 degrees C. At the three pHs investigated, 137Cs binding to activated charcoal and sodium polystyrene sulfonate was negligible. Binding of 137Cs to insoluble Prussian blue exceeded that for the soluble form and was pH dependent for both formulations. Maximum binding capacities were 87 mg/g (pH = 1.0), 194 mg/g (pH = 6.5) and 238 mg/g (pH = 7.5) for the insoluble form and 48 (pH = 1.0), 73 (pH = 6.5) and 78 (pH = 7.5) for the soluble form. As activated charcoal did not bind 137Cs, charcoal hemoperfusion is of no value. This has been confirmed by an in vitro experiment, using a Gambro Adsorbs 300 C cartridge.

Cesium Radioisotopes↗
PubMed1992

Intoxication with beta-sympathicolytics.

Based on the review of available literature, this article states the possible clinical problems with beta-blocker intoxication. Some 26% of severe cases of intoxication will die. This fact stimulated the attempt, using animal experiments, to gain an insight into the pathophysiological profile of this intoxication. The results of these animal experiments led to the following conclusion: toxic doses of beta-blockers result in a dose-dependent decrease of myocardial contractility. This negative inotropic effect is not related to the antagonizing effects of the beta-blocker at the beta-adrenergic receptor level, nor to the additional properties of this group of drugs, but is influenced by a combination of other factors. These include (1) a direct negative inotropic effect on the myocardium, probably caused by a calcium dependent mechanism; (2) a decrease in serum calcium concentration, probably caused by a decreased parathormone production; (3) a centrally mediated hypotensive action. Toxic doses of beta-blockers do not only affect the myocardium and the haemodynamic system, they can also lead to respiratory arrest. This arrest is caused by the direct effect of these drugs on the central nervous system and can, in itself, be the cause of death. Such results lead to the following therapeutic advice: patients with severe beta-blocker intoxication must be admitted to an Intensive Care Unit, as early initiation of ventilation, as well as administration of beta-antagonist can be essential; the drop in serum calcium concentration must be corrected; drugs which can improve myocardial contractility, other than via the beta-adrenergic receptor, such as phosphodiesterase inhibitors and glucagon, should be administered.

Adrenergic beta-Antagonists↗
PubMed1991

Effects of chlorthalidone and mechanical ventilation on hydroxyprolinuria during immobilization by means of muscle relaxants.

The influence of chlorthalidone on bone resorption in immobilized patients treated with mechanical ventilation was studied. Bone resorption was measured by means of urinary excretion of hydroxyproline and calcium. Blood pH was measured because of a possible effect of mechanical ventilation on calcium metabolism. Twenty-five patients were examined, 14 receiving and 11 not receiving chlorthalidone. Patients receiving chlorthalidone over a period of at least five and a maximum of 27 days showed lower hydroxyprolinuria and a higher blood pH value than the non-users. No differences were observed concerning calcium and phosphate metabolism. It is suggested that this slight alkalosis resulting from chlorthalidone may inhibit bone resorption.

Adolescent↗
PubMed1990

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 Disease↗
PubMed1979

Severe extrapyramidal syndrome in a dog caused by a haloperidol (Serenase) intoxication.

The case history of a one-year-old male mongrel dog intoxicated with 120 mg haloperidol is described. The dog showed a coma with a severe extrapyramidal syndrome and was treated with orphenadrine. Symptoms, occurrence, and therapy of the extrapyrmidal syndrome are discussed. Emphasis is laid on the importance to differentiate this syndrome from epilepsy and other neurological disorders.

Animals↗
PubMed1979

The influence of biperiden in overdose on respiration and circulation in the dog.

Biperiden lactate was administered intravenously in overdose to dogs under general anaesthesia. Biperiden appeared to have a toxic influence on respiration and circulation independently. Respiratory arrest occurred at a dose of 33 +/- 10 mg/kg and has probably a central origin. When artificial ventilation was instituted circulatory standstill occurred at a dose of 45 +/- 5 mg/kg. The toxic influence of biperiden is characterised by a decrease of heart rate and of left ventricular contractility resulting in cardiogenic shock. Biperiden is compared with orphenadrine as far as its potential hazard is concerned for patients trying to commit suicide by ingesting an overdose.

Animals↗
PubMed1979

The influence of orphenadrine HCl in overdose alone and in combination with droperidol on respiration and circulation in the rat.

Orphenadrine HCL was intravenously administered to rats under urethane anesthesia to investigate whether the primary cause of death in orphenadrine intoxication is respiratory arrest or cardiac standstill. The spontaneously breathing animals died from apnoe after a mean dose of 63 + 11 mg/kg. The artificially ventilated animals died from cardiac arrest after a mean dose of 144 +/- 47 mg/kg. It was concluded that primary cause of death is respiratory insufficiency and that hypoventilation can mask the cardiotoxicity of orphenadrine. On the analogy of earlier experiments in dogs the ability of droperidol to counteract the influence of orphenadrine was investigated. Droperidol enhanced the influence of orphenadrine on respiration and had no influence on the cardiotoxic influence of orphenadrine in the rat.

Animals↗