Abstract

Numerous literature has been accumulated on the inter-face action or pulmonary surfactant material, however, only few papers are dealt with the physiological aspect of this material or inter-face action in asthmatic bronchitis. This communication is concerned with the alteration of the surfactant and interface action of the lung in experimentally induced asthmatic bronchitic condition in guinea pigs. The alteration of the interface action is quantitatively determined by the measurement of the phosphatidyl choline. The state of the anaphyractoid condition in asthmatic bronchitic change in passively sensitized and then locally desensitized guinea pigs had been clinically and anatomically observed.The lung wash solution which was obtained through airway was subjected for determining surface tension and quantitative determination of the phosphatidyl choline. The maximum surface tension and minimum surface tension were calibrated from the hysteresis curve, namely diagram of the surface tension and area ratio which was drawn by X-Y axis curve, being connected by modified wilhelmy balance which was widely used for determination of the interface action of the lung.The stability index was also caliculated from the given formula as follows :The phosphatidyl choline was purified from the specimen and identified by the two dimensional paper chromatography and semi-quantitative determination of this substance was performed.The results obtained were as follows :(1) Actively sensitized guinea pigs with airsole exposure of the antigen led to cause slight degree of anaphyractic state. In this circumstance, the lungs were edematous with overexpansion and presence of occasional hemorrhagic foci.On the other hand, local desensitized guinea pigs with repeated airsole exposure to the antigen turned out to be devoid of the anaphyractic reaction. The pathological findings of the lungs remained to be a lesser extent and were essentially identical with those of the control group.(2) The elevation of the maximum and minimum surface tension was observed in the passively sensitized guinea pigs and contrary, locally desensitized guinea pigs with repeated airsole exposure to the antigen remained in normal range as of the control group. As the matter of fact, the stability index was lowered in the former group and returned to the range of the control group.(3) The semi-quantitative determination of the phosphatidyl choline disclosed decrease in the former group and increase to the normal range as of the control group respectively. Therefore, it is postulated that the pulmonary surface tension is elevated at the sequence of the repeated attacks of the asthmatic condition and is lowered at recovery from the state. It is also reasonable to assume the alteration of the pulmonary surface tension is based on the quantitative changes of the pulmonary surfactant.

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