Experimental Production of Pulmonary Infarct

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  • 肺硬塞症の成因に関する実験的研究
  • Viewed in the Coagulo-Fibrinolytic Activity
  • 凝固線溶能の立場から

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Abstract

In the course of experimental production of the pulmonary infarct, observations were made upon variation of the coagulo-fibrinolytic activity in the blood and the lung tissue.<br>1) Over-coagulative state in the blood provoked by injection of the human serum disappears usually within 2 minutes, and then, in the contrary, a state of prolongation in clotting produced by consumption of the coagulation factors appears thereafter.<br>2) In this stage, tissue activator and anti-thrombin effect in the lung show an increase in comparison with that in the normal lungs.<br>3) Injection of lycopodium spores produce a gradual change in blood coagulability and tissue fibrinolytic activity, showing manifest hypercoagulable and lowered fibrinolytic activity 2 days later.<br>4) In additon to the hypercoauglable state, paroxysmal occurrence of thrombembolism and consequent depressive state in the fibrinolytic activity give rise pulmonary infarct.<br>5) The optimum method for experimental production of lung infarct is to inject blood clots, t-AMC-HA, and human serum injection for consequtive four days.<br>6) Three factors, closure of the pulmonary arterial trees by large thrombus, presence of sustained hypercoagulable state, and depression in the fibrinolytic activity, appears sine qua non for occurrence of the pulmonary infarct. Repeated microembolization, inflammatory change in the tissue, and alveolar bleeding are considered to be additional promotive factors.

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