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The formation and effect of stored platelet concentrate microemboli on pulmonary ultrastructure.

作者信息

Bisio J M, Connell R S, Harrison M W

出版信息

Surg Gynecol Obstet. 1982 Mar;154(3):342-7.

PMID:7064069
Abstract

The formation of microaggregates of platelets and leukocytes and the infusion of these aggregated blood elements in pulmonary ultrastructure and function have been extensively studied. This study was undertaken to document the formation of platelet microaggregates during storage of platelet concentrate and to determine what effect the infusion of stored platelets has on pulmonary ultrastructure. The screen filtration pressure of platelet concentrate stored at 4 degrees C. for a period of 48 hours was measured after six, 24 and 48 hours of storage. Screen filtration pressure progressively rose from a mean of 47.20 millimeters of mercury to a mean of 237.40 millimeters of mercury at 48 hours, p less than 0.02 between six and 48 hours of storage. Specimens of the lung taken for biopsy from ten patients undergoing open heart operations were examined for ultrastructural alterations. Those specimens obtained following cardiopulmonary bypass, but prior to the infusion of platelet concentrate, showed only mild ultrastructural abnormalities. Those specimens obtained for pathologic study following the infusion of platelet concentrate exhibited extensive accumulations of platelet aggregates in the pulmonary microcirculation and widespread degenerative changes in the capillary endothelial cells, intra-alveolar septae and alveolar epithelial cells. In areas in which cellular discontinuities occurred, protein exudates, fibrin clumps and red blood cells were observed in the interstitium and in the alveolar air spaces. The storage of platelet concentrate results in the formation of aggregate material. The infusion of platelet concentrate results in the formation of aggregate material. The infusion of platelet concentrate results in the formation of ultrastructural lesions, similar to those observed in situations known to lead to pulmonary dysfunction, such as following massive transfusion, hypovolemia, sepsis and hypoxia.

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