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Changes of pulmonary surfactant-associated protein A in rats after freshwater drowning

Jin Fa-guan

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Abstract

Objective To observe the changes of pulmonary surfactant-associated protein A(SP-A)in rats after freshwater drowning.Methods Twenty-four rats were randomly divided into the control group(n=6)and the drowning group(n=18).The drowning rat model was established by intratracheally instilled with freshwater(8 mL/kg).Arterial blood gases was examined and respiratory rates were recorded.Six rats were randomly sacrificed 2,4,6 h after drowning respectively and the lungs were sampled for histopathology examination.Meanwhile the expression of SP-A was detected by immunohistochemistry.Results Compared with the control group,the respiratory rates accelerated significantly,then slowed gradually but always faster than normal range in the drowning group.PaO2 decreased significantly 5 min after instillation then elevated but remained at a low level[(48.7±3.93)mm Hg vs(93.65±6.02)mm Hg,P0.05].PaCO2 increased significantly 5 min after instillation then decreased and remained below normal level[(36.20±4.41)mm Hg vs(55.96±4.60)mm Hg,P0.05].In the control group,SP-A was distributed in a consecutive linear fashion on the intra-alveolar interior surface.In the drowning group,alveolar wall collapse,alveolar and interstitial edema and focal atelectasis were observed Meanwhile SP-A was demonstrated on the alveolar interior surface and the interface of the intra-alveolar effusion in a granular deposit fashion with the quantity decreased gradually compared to the control group.Conclusion Freshwater drowning might result in lung injure and abnormalities in the quality and quantity of SP-A.

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Objective To observe the changes of pulmonary surfactant-associated protein A(SP-A)in rats after freshwater drowning.Methods Twenty-four rats were randomly divided into the control group(n=6)and the drowning group(n=18).The drowning rat model was established by intratracheally instilled with freshwater(8 mL/kg).Arterial blood gases was examined and respiratory rates were recorded.Six rats were randomly sacrificed 2,4,6 h after drowning respectively and the lungs were sampled for histopathology examination.Meanwhile the expression of SP-A was detected by immunohistochemistry.Results Compared with the control group,the respiratory rates accelerated significantly,then slowed gradually but always faster than normal range in the drowning group.PaO2 decreased significantly 5 min after instillation then elevated but remained at a low level[(48.7±3.93)mm Hg vs(93.65±6.02)mm Hg,P0.05].PaCO2 increased significantly 5 min after instillation then decreased and remained below normal level[(36.20±4.41)mm Hg vs(55.96±4.60)mm Hg,P0.05].In the control group,SP-A was distributed in a consecutive linear fashion on the intra-alveolar interior surface.In the drowning group,alveolar wall collapse,alveolar and interstitial edema and focal atelectasis were observed Meanwhile SP-A was demonstrated on the alveolar interior surface and the interface of the intra-alveolar effusion in a granular deposit fashion with the quantity decreased gradually compared to the control group.Conclusion Freshwater drowning might result in lung injure and abnormalities in the quality and quantity of SP-A.

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Available abstract

Objective To observe the changes of pulmonary surfactant-associated protein A(SP-A)in rats after freshwater drowning.Methods Twenty-four rats were randomly divided into the control group(n=6)and the drowning group(n=18).The drowning rat model was established by intratracheally instilled with freshwater(8 mL/kg).Arterial blood gases was examined and respiratory rates were recorded.Six rats were randomly sacrificed 2,4,6 h after drowning respectively and the lungs were sampled for histopathology examination.Meanwhile the expression of SP-A was detected by immunohistochemistry.Results Compared with the control group,the respiratory rates accelerated significantly,then slowed gradually but always faster than normal range in the drowning group.PaO2 decreased significantly 5 min after instillation then elevated but remained at a low level[(48.7±3.93)mm Hg vs(93.65±6.02)mm Hg,P0.05].PaCO2 increased significantly 5 min after instillation then decreased and remained below normal level[(36.20±4.41)mm Hg vs(55.96±4.60)mm Hg,P0.05].In the control group,SP-A was distributed in a consecutive linear fashion on the intra-alveolar interior surface.In the drowning group,alveolar wall collapse,alveolar and interstitial edema and focal atelectasis were observed Meanwhile SP-A was demonstrated on the alveolar interior surface and the interface of the intra-alveolar effusion in a granular deposit fashion with the quantity decreased gradually compared to the control group.Conclusion Freshwater drowning might result in lung injure and abnormalities in the quality and quantity of SP-A.

Key concepts: Atelectasis, Medicine, Pulmonary surfactant, Lung, Respiratory system, Histopathology, Immunohistochemistry, Pulmonary edema

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