Browsing by Author "Mouton, W. L."

Now showing 1 - 4 of 4
  • Thumbnail Image
    Item
    Experimental evaluation of the prophylactic and therapeutic effects of hydrocortisone in haemorrhagic shock
    (Health & Medical Publishing Group, 1985) Engelbrecht, F. M.; Mattheyse, F. J.; Mouton, W. L.
    The prophylactic and therapeutic effects of hydrocortisone (50mg/kg) in severe haemorrhagic shock were evaluated by metabolic, biochemical and haematological investigations in a rabbit model. It was found that administration of hydrocortisone prior to severe haemorrhage had no beneficial effect on any of the values measured. Owing to haemoconcentration and marked mobilization of leucocytes it would appear that in pretreated animals the magnitude of the hypoxia was increased and led to greater tissue damage and higher levels of lysosomal enzymes than in rabbits which had not received pretreatment with hydrocortisone. On the other hand, hydrocortisone therapy combined with volume replacement 1 hour after the haemorrhagic insult had several beneficial effects. The metabolic capacity of liver and kidney tissues was improved, the lysosomal concentration remained within normal limits, and normal limits, and the mean blood pressure and pulse pressure were maintained better than in controls. However, it would appear that this beneficial effect is only exerted on tissue still in a reversible state of shock. There is therefore no beneficial effect on lung tissue metabolism, the lungs being more sensitive to hypoxic damage than either liver or kidney tissue. Administration of hydrocortisone results in the immediate release of endotoxins into the circulation. This might be due to its vasodilatory action on the microcirculation of the intestinal viscera.
  • Thumbnail Image
    Item
    Haemorrhagic shock : metabolic parameters for the assessment of damage in lung, liver and kidney tissue
    (Health & Medical Publishing Group, 1984) Engelbrecht, F. M.; Mattheyse, F. J.; Mouton, W. L.
    Changes in catabolic and biosynthetic parameters measured in vitro were used as criteria to assess the degree of damage in tissues after an animal was exposed to severe haemorrhagic shock for periods of 1 and 2 hours (blood loss 36.8%, blood pressure 30 ± 5 mmHg). The biosynthetic capacity of lung tissue, as determined by the incorporation of 1-14C-palmitate into total lung lipids, declined significantly with time. This reduction correlates well (r = 0.99) with the rate of decline in 14CO2 production from 1-14C- and 6-14C-glucose oxidation as well as with the decline in the rate of oxygen uptake. Any one of these parameters could therefore be used as an index of the degree of tissue damage due to haemorrhagic shock. Comparing the rates of decline in 14CO2 production from 1-14C-glucose by lung, liver and kidney tissue from the same animal after haemorrhagic insult for 1 hour, lung tissue appeared to be the most sensitive to hypoxia and kidney the least so. However, 2 hours after severe haemorrhage, i.e. near the terminal phase, the rate of 14CO2 production from 6-14C-glucose by liver tissue decreased dramatically by more than 53% of the control value. Apart from kidney and lung dysfunction, irreparable liver damage probably plays a major role in the fatal course of severe haemorrhage.
  • Thumbnail Image
    Item
    A prospective study of long-term use of amikacin in a paediatrics department : indications, administration, side-effects, bacterial isolates and resistance
    (Health & Medical Publishing Group, 1990) Hesseling, P. B.; Mouton, W. L.; Henning, P. A.; Kirsten, G. F.; Spruyt, L. L.; Schraader, E. B.; Wessels, G.; Grassman, R.
    Amikacin (Amikin; B-M) was used as the only aminoglycoside for 18 months in a paediatric department within a general hospital because of high levels of resistance of Klebsiella pneumoniae, Pseudomonas aeruginosa and Enterobacter cloacae isolates to tobramycin, gentamicin and netilmicin. Between 1 February 1987 and 31 July 1988, 816 children were treated with a slow intravenous injection at a standardised dose adjusted for weight and age. Respiratory disease was present in 35,8% of 537 neonates, 56,4% of 190 infants and 70,9% of 89 older children. Escherichia coli (65 isolates), Klebsiella species (59 isolates), Enterobacter species (26 isolates) and P. aeruginosa (22 isolates) constituted the most common Gram-negative pathogens. The positive blood culture yield was 7,8%. Satisfactory median peak and trough serum amikacin levels were achieved. No significant renal side-effects were noted. Severe bilateral hearing loss in 1 low-birthweight infant resulted from inadvertent overdosage. At the end of this 18-month surveillance period 97,7% of E. coli, 98,6% of K. pneumoniae, 96,3% of E. cloacae, and 98,0% of P. aeruginosa isolates remained sensitive to amikacin, while resistance of K. pneumoniae to tobramycin, netilmicin and gentamicin decreased significantly (P < 0,003, P < 0,001 and P < 0,007 respectively; chi-square test).
  • Thumbnail Image
    Item
    Shock lung : experimental studies on a haemorrhagic hypovolaemic rabbit model
    (Health & Medical Publishing Group, 1983) Engelbrecht, F. M.; Mouton, W. L.; Van Schalkwyk, L. J.
    An experimental model of haemorrhagic hypotension was standardized using rabbits to investigate the shock lung syndrome over a period of 120 minutes. Acute hypovolaemia was induced by withdrawal of blood under anaesthesia to a mean arterial pressure of 30 ± 5 mmHg within 10 minutes. The mean leucocyte counts and the release of lysosomal enzymes (acid phosphatase and β-glucuronidase) in the blood and in lung tissue, as well as the metabolic capacities of lung tissue in terms of protein and lipid biosynthesis, were investigated at set intervals after 30, 60, 90 and 120 minutes. The results indicate a progressive decline in leucocyte numbers over 120 minutes to about 40% of the original. An immediate granulocytopenia was observed with a relative lymphocytosis within 30 minutes. The β-glucuronidase and acid phosphatase contents of the plasma increased with time; β-glucuronidase activity increased progressively as leucocytes disappeared from the circulation. Concomitantly, the capacity of the lung tissue to synthesize protein and lipids was retarded with time, becoming significantly lower than baseline values after 60 minutes of hypovolaemia. The decline in leucocyte numbers in the circulation correlated well with the increase in β-glucuronidase activity and the retarded metabolic capacity of the lung tissue.