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Biomedical subjects

P Harry

Publications and source records attributed to P Harry.

At least 37 records · Page 2Linked to original sources
PubMed1994

Efficacy of 4-methylpyrazole in ethylene glycol poisoning: clinical and toxicokinetic aspects.

Potentially fatal ethylene glycol intoxication in an adult with normal renal function was treated with 4-methylpyrazole administered three hours after the incident occurred. The plasma ethylene glycol concentration was 3.5 g l-1 on admission. The metabolic acidosis present on admission resolved within four hours, and the subsequent clinical course was uneventful. The apparent plasma half-life of ethylene glycol was 16 h and the mean renal and plasma clearances of ethylene glycol were 24 and 25 ml min-1, respectively. These results support the hypothesis that complete blockade of hepatic metabolism of ethylene glycol is achieved by 4-methylpyrazole. The only side-effect observed as a result of treatment was a transient slight increase in serum transaminase activity.

Adult↗
PubMed1993

Simultaneous determination of ethylene glycol, propylene glycol, 1,3-butylene glycol and 2,3-butylene glycol in human serum and urine by wide-bore column gas chromatography.

A method has been developed for the separation and measurement of ethylene glycol and three other glycols (propylene glycol, 1,3-butylene glycol and 2,3-butylene glycol) in biological samples by wide-bore column gas chromatography with a flame ionization detector. The method used 1,3-propylene glycol (1,3-propanediol) as an internal standard. The method was linear at least from 2 to 1000 micrograms/ml, with a detection limit of 1 microgram/ml. Analytical recoveries were 89-98% for the different concentrations. Precision studies showed coefficients of variation of 1.5-7.7% for the different concentrations. The assay was applied to the analysis of biological samples from two patients who had ingested ethylene glycol and/or other glycols in a suicide attempt.

Adult↗
PubMed1992

[Metabolic acidosis in severe acute asthma. Effect of alkaline therapy].

Respiratory acidosis of severe acute asthma is a severity factor. In this paper the treatment of associated metabolic acidosis is discussed. Among 34 consecutive episodes of severe acute asthma with acidosis (pH < 7.35) treated with continuous adrenaline perfusion, theophylline and hydrocortisone hemisuccinate, respiratory acidosis was observed in 12, metabolic acidosis in 2 and mixed respiratory and metabolic acidosis in 20. The association of hypercapnic acidosis with hypochloraemic acidosis reflected a time of installation longer than when respiratory acidosis only was present (p < 0.05). Among the 22 patients who had metabolic acidosis on admission, 14 were treated with 168 +/- 82 mmol of sodium bicarbonate, the remaining 8 patients being untreated and acting as controls. The rapidity with which pH was corrected was the same in the treated and untreated groups (9.1 +/- 5.5 hours vs 6.7 +/- 3.7 hours), whereas dyspnoea (respiratory rate < 18/min) was more rapidly corrected in the treated group that in controls (11.6 +/- 5.7 hours vs 5.9 +/- 5.9 hours; p < 0.05). It is concluded that in more than 50% of the cases respiratory acidosis of severe acute asthma is associated with a metabolic acidosis. Correcting this metabolic acidosis with sodium bicarbonate results in improvement of respiration, perhaps by facilitating the action of bronchodilator catecholamines.

Acidosis↗
PubMed1992

[Torsades de pointes during sultopride poisoning].

A case of sultopride poisoning (ingested dose 16 g) in a 35-year-old, 65 Kg man is described. On admission myoclonus, mydriasis, vomiting and cardio-respiratory arrest were observed. Torsades de pointes were treated with potassium chloride infusion and pace maker stimulation. Plasma sultopride concentration was 25 mg/l and urinary concentration 12 g/l. A prolongation of Q-T interval may announce severe arrhythmias in sultopride poisoning.

Adult↗
PubMed1992

[Iodoform poisoning. 3 cases].

Three cases of iodoform poisoning are described following dressings with 10% iodoform gauze (0.10 x 5 m) on extended wounds. Five, ten and sixteen days after the beginning of dressings, the patients became confuse, hallucinated, and one of them was subsequently comatose. Vomiting, fever, tachycardia with premature ventricular beats and shortening of P-R interval, slight increase of transaminases and proteinuria were observed. Within a few days (3 to 8) after the iodoform dressings were discontinued, the signs of iodoform toxicity disappeared. The toxicity of iodoform is probably unrecognized if the rarity of the observations published and the amount of iodoform gauzes annually sold are compared.

Adult↗
PubMed1992

[Use of intravenous adrenalin in severe acute asthma].

The efficacy of and tolerance to intravenous Adrenaline (IV) have been assessed in cases of acute severe asthma (AAG). From January 1983 to March 1990 there were 56 episodes of AAG treated by intravenous Adrenaline using an average dose of 0.33 microgram per kilogramme per minute, in association with intravenous steroid therapy and Aminophylline (0.6 mg/kg per hour). A group of 12 patients were ventilated before admission and were excluded from the study. Two groups were defined on the basis of their admission PaCO2: Group A with 30 episodes of AAG and a PaCO2 above 45 mm of mercury, Group B with 14 episodes of AAG and a PaCO2 of less than 45 mm of mercury. The clinical improvement was equally rapid in both groups on average 8.7 (plus or minus 8.2) hours in Group A and 14.6 (plus or minus 15.7) hours in Group B. Artificial ventilation was only required in 2.3% of cases (7% in Group A and none in Group B). Treatment using intravenous Adrenaline is well tolerated as is shown by the absence of any worsening of the tachycardia, the significant fall in blood pressure after correcting the PaCO2 in Group A and the absence of any raised blood pressure in Group B. In conclusion, treatment with intravenous Adrenaline associated with IV Theophylline and IV corticosteroids based on the fact of its rapid action and that it is well tolerated, means that this drug should be considered as part of the therapeutic arsenal during acute severe asthmatic attacks in patients who are breathing spontaneously.

Acute Disease↗
PubMed1991

[Electroencephalographic silence after intoxication with a carbamate tranquilizer].

A case of acute meprobamate poisoning in a 43 year-old-woman is reported. Twenty five hours after admission in the intensive care unit, deep coma and cerebral electrical silence were observed whereas the meprobamate plasmatic concentration was 250 mg/l. The patient recovery was uneventful. Meprobamate analysis must be performed for unexplained coma with isoelectric EEG.

Adult↗
PubMed1989

[Sinusitis during nasotracheal intubation].

Sinusitis is mentioned as one complication of nasotracheal intubation. 30 patients admitted to the I.C.U. and prolonged intubated (+5 days) underwent clinical examination and C.T. scan: 23 C.T. scan revealed anomalies and 5 sinusitis. One patient had blood cultures positive for the organism present on nasal cultures. Patients nasally intubated are at risk for sinusitis which can have adverse effects.

Cross Infection↗
PubMed1983

Evidence for two structurally related progesterone receptors in chick oviduct cytosol.

The existence of two progesterone receptor forms present in crude cytosol of chick oviduct has been demonstrated by photoaffinity labelling using [3H]R5020. On SDS-polyacrylamide gels these two forms exhibit app. Mr-values of 79000 and 109000 corresponding to the progesterone receptor forms A and B. Peptide maps of photoaffinity-labelled steroid receptors have been established by limited proteolysis with alpha-chymotrypsin. The peptide map obtained for chick oviduct cytosol progesterone receptor crosslinked with [3H]R5020 proved to be the sum of peptides obtained from partially purified preparations of forms A and B. The peptide maps of both progesterone receptor forms were identical for peptides below the Mr-value of form A, indicating extensive homology of the two forms. A significantly different peptide pattern was observed for the rat liver glucocorticoid receptor crosslinked with [3H]triamcinolone acetonide. Prolonged proteolysis with chymotrypsin gave rise to peptides with Mr-values of 6000 and 10000 from the hormone-binding domain of progesterone and glucocorticoid receptors, respectively.

Animals↗
PubMed1983

A reappraisal of ecdysteroid binding in Drosophila.

Ecdysteroid binding was investigated in Kc cells and larval fat body of Drosophila. After incubation of intact Kc cells, 200-300 specific binding sites were detected for both 20-OH ecdysone and ponasterone A. However, if cells were fractionated prior to incubation with 20-OH ecdysone, no specific binding was observed. In the fat body the number of specific nuclear binding sites appears to be enhanced by the factor of polyteny if compared with Kc cells. Both systems displayed a high degree of non-specific cytoplasmic binding. The intracellular distribution of specifically bound ponasterone A was different from that of the physiological hormones. In fat body, even after an incubation of 60 min at 22 degrees C, the majority of specifically bound ponasterone A was located in the cytoplasm. Differences between the results of this study and previous reports on ecdysteroid binding are discussed.

Adipose Tissue↗
PubMed1981

Ecdysteroids are bound to vitellin in newly laid eggs of Locusta.

The follicle cells of vitellogenic ovaries of Locusta migratoria have been reported to synthesize impressive amounts of ecdysteroids which accumulate inside the oöcytes where they persist during egg-laying; these ecdysteroids are conjugated to more than 95%, and it is believed that their hydrolysis in the egg is the source of the peaks of free ecdysone observed in early embryonic development. The present paper shows that, in the eggs, the ecdysteroid conjugates are bound to a 520 000-dalton macromolecule which shares several characteristics with the major yolk protein vitellin and is precipitated by an anti-vitellin antibody. The physiological relevance of the binding of ovarian ecdysteroid conjugates is discussed in respect to the transfer of maternal ecdysteroids to the embryo.

Animals↗