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.

No abstract

In order to investigate possible differences in the reaction to hypoxic conditions between "red" and "white" skeletal muscle, cats were subjected to a 2 h period of either hemorrhagic shock or hind limb tourniquet ischemia, and the hypoxia induced changes were studied in the soleus and lateral gastrocnemius muscles. Muscle biopsies were analysed for ATP, CP, glucose, G 6-P and lactate. Using microelectrodes, the resting membrane potential was repeatedly measured. Both experimental models resulted in increased tissue lactate levels and a successive decrease in the membrane potential of both muscles studied. No reduction of the high energy phosphagen content (ATP + CP) occurred in any of the muscles during shock. The tourniquet ischemia resulted in a 40% reduction of the ATP + CP content in the soleus muscle, whereas in the gastrocnemius muscle no significant reduction occurred. A significant correlation was found between the tissue lactate content and the membrane potential under both conditions and in both muscles studied. It is concluded that "red" muscles are more susceptible to metabolic derangement than "white" muscles during total ischemia, whereas during hypovolemia "red" muscles appear to be protected from early hypoxic damage, probably due to a redistribution of skeletal muscle blood flow.

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Skeletal muscle reactions to hemorrhagic shock were investigated in anesthetized cats (n = 23). The tenuissimus muscle was exposed for vital microscopy and shock was induced by single-withdrawal of 45% of the blood volume. Muscle microcirculation, energy metabolism and cell membrane potentials were followed over a 2 h period along with blood pressure, hematocrit and blood leukocyte, platelet, glucose, pyruvate and lactate contents. Bleeding usually caused complete cessation of muscle blood flow for 5--20 min, while the animal compensated the blood pressure. Reflex constriction occurred in medium-sized but not in terminal arterioles. When flow reappeared a marked maldistribution was evident in the capillary bed. Flow remained in 30--50% of the capillaries, permanently or intermittedly. Leukocytes could be found lodged in many arrested capillaries and also adhering to venules in large numbers. Erythrocyte or platelet plugs were not seen in the muscle microvasculature. Glucose and G6-P contents doubled and lactate increased 5-fold in muscle tissue during shock. CP was reduced by about 25% while the ATP-level remained unchanged. Membrane potentials declined 12% in shock and the spread in potentials from adjacent fibers increased.