White blood cell deformability and plugging of skeletal muscle capillaries in hemorrhagic shock.

The cause of maldistributed capillary perfusion in hemorrhagic shock was investigated in a combined in vivo and in vitro study. The cat tenuissimus muscle was observed by vital microscopy before and after withdrawal of 45% of the blood volume. The induced shock conditions reduced the number of perfused capillaries about 50%. Close examination of the scattered, nonperfused capillaries showed that they remained open and almost invariably contained one or several leukocytes. These cells were usually located at the bulgings of endothelial cell nuclei, and when occasionally dislodged, recirculation immediately occurred. Platelet or erythrocyte aggregates were not seen in the microvasculature in shock. To test whether the trapping of leukocytes reflected an impaired deformability of these cells in shock or was merely a pressure dependent phenomenon, deformability studies were performed on leukocytes in vitro. Central venous blood was drawn before and 2 h after bleeding and leukocytes were separated by sedimentation. The passage-time of single leukocytes through a glass capillary stenosis at constant driving pressures was used as an index of cell deformability. No qualitative changes in stiffness were found after shock. The distribution of cell passage-times indicated, however, that the stiffest portion of the leukocyte population was removed from the circulation in shock.