DURING the past few years, there has been an increasing interest in fibrinolytic enzymes and their relationship to the development or progression, or both, of hyaline membrane disease (HMD) in premature infants, as well as in their therapeutic use in this syndrome. Fluorescent-labeled antibody techniques1and electron microscopic studies2have shown that the hyaline membranes are composed of fibrin and resemble a plasma clot. The fibrin probably originates from plasma which has leaked from the capillaries to the air spaces of the lung.1,2Craig et al3postulated that hyaline membrane formations obstruct air flow to the alveoli, prevent their expansion, and decrease lung compliance. However, there is controversy regarding the pathogenesis as well as the significance of the membranes.3-12 Comparison of previous studies if often difficult because of the various terms used for the same substance, as well as different methods which report fibrinolytic activity
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Marguerite Markarian (1967) studied this question.