[Studies on the toxicokinetics of 3H-sulfolane in rat after oral administration].
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Biomedical subjects
Publications and source records attributed to Z C Yang.
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A first-order difference equation which constitutes a simple model for a lethal parasite-host interaction is studied. Completing a study initiated by May and Anderson, the dynamics are shown to be completely chaotic.
Chronic lung lymph fistulae were produced in six goats according to Winn's and Stothert's methods with our modification to define the pathophysiology of pulmonary oedema after severe steam inhalation injury. Arterial blood gas, lung lymph flow (QLym), lymph/plasma total protein concentration ratio (L/P), and beta-glucuronidase (beta-G) in plasma and lung lymph were monitored for 24 h post-injury. The pathological changes in the lung tissues were also determined at the end of the study. It was found that directly after injury, QLym increased steadily to a peak value at 6 h, followed by declining values at 18 and 24 h. L/P decreased promptly during the 60 min after injury and then also steadily increased to a peak value at 4 h (P less than 0.05). A significant increase in plasma beta-G was only observed at 4 h post-burn. However, lung lymph beta-G activities and lymph beta-G transport increased immediately after injury, reaching a peak at 4 h (5 and 12 times above baseline values, respectively, P less than 0.01). Significant hypoxaemia and hypocapnia occurred at 2 h post-burn and deteriorated progressively throughout the study. There were obvious pulmonary interstitial and alveolar oedema microscopically. This study demonstrates that the increase in transvascular fluid and protein flux after steam inhalation injury is mainly due to increased pulmonary microvascular permeability. Nevertheless, a hydrostatic pressure effect can not be completely excluded, especially in the first hour post-burn. Lysosomal enzyme release is considered to be one of the important factors which damage lung microvascular elements and induce an increase in their permeability.
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Last year, after a systematic search of pathological and patho-physiological changes of inhalation injury in dogs, we recorded severe pulmonary oedema as early as 2 h postburn (the earliest monitoring time designed in experiment) on dogs inflicted with both body surface and severe respiratory burns without any fluid replacement during the whole course of experiment. In an analysis of cases admitted into our burn centre in the past ten years, we also found that there was no definite relationship between the incidence and severity of pulmonary oedema occurring in severe burn patients and the amount of fluid infused in the early burn phase. These facts led us to the following experiment designed to study the effect of intravenous infusion on development of pulmonary oedema after severe burns complicated with inhalation injuries.