Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs
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Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs
Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs
解放军医学杂志(英文版)1987年第4期 页码:328-334
Affiliations:
Department of Pulmonary Diseases Second Teaching Hospital Third Military Medical College Chongqing
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纸质出版:1987
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Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs[J]. 解放军医学杂志(英文版), 1987,(4):328-334.
[1]文富强,毛宝龄,郭先健,张楚毅.Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs[J].Journal of Medical Colleges of PLA,1987(04):328-334+392.
Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs[J]. 解放军医学杂志(英文版), 1987,(4):328-334.DOI:
[1]文富强,毛宝龄,郭先健,张楚毅.Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs[J].Journal of Medical Colleges of PLA,1987(04):328-334+392.DOI:
Pathogenesis and Therapeutic Effect of Anisodamine on Experimental Respiratory Distress Syndrome in Dogs
摘要
Abstract
<正> Respiratory distress syndrome was inflicted on 30 dogs with anintravenous injection of oleic acid of the dose 0.06ml/kg. Half of theanimals were treated with anisodamine. Another 5 dogs were injected withsaline to serve as control. The dynamic changes of total hemolyticcomplement activity
neutrophil aggregation rate
platelet aggregation rate
fibrin degradation products
white cell count and platelet count in both theperipheral arterial and venous blood
and blood gas analysis were tested.The pathological and clinical changes were also observed. The results ofthe study suggest that the pathogenesis of respiratory distress syndromewas apparently related to the increase of complement activation
neutrophilaggregating activity
and blood coagulation. The therapeutic effect ofanisodamine can be enhanced if the complement-neutrophil-fibrindegradation products pathway is blocked.
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