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The intracerebral microcirculation of the rat in hemorrhagic shock
The intracerebral microcirculation of the isocortex was studied in unanesthetized rats under hemorrhagic shock. To observe the microvessels, three markers were separately injected intravenously during the shock period: (a) Evans blue for fluorescence microscopic visualization of the vessels. (b) India ink for gross and light microscopic evidence of retention of carbon. (c) Horseradish peroxidase (HRP) for light and electron microscopic study. Lack of spontaneous recovery from shock was associated with: (a) 55-65% blood loss, a low blood pressure (30-40 mm Hg), and a dramatic increase in pulse rate; (b) marked Evans blue fluorescence along the vessels; (c) no retention of India ink in the microcirculation; (d) peroxidase activity on the luminal surface of the endothelium. Absence of India ink in the microcirculation of the isocortex during the shock period, as shown by light and electron microscopy, suggests that there is sufficient cerebral blood flow to clear the carbon particles from the blood stream and that there are no openings greater than 30 nm in the endothelial layer allowing seepage of carbon particles through or between endothelial cells. Vascular Evans blue fluorescence and peroxidase activity were both demonstrated on the luminal surface of the endothelial cells, by light microscopy, indicating that these markers are abnormally retained. Ultrastructural demonstration of increased HRP uptake and adherence onto the endothelial cells confirms these observations. These results show that regional endothelial alterations occur in this model of hemorrhagic shock.
The intracerebral microcirculation of the isocortex was studied in unanesthetized rats under hemorrhagic shock. To observe the microvessels, three markers were separately injected intravenously during the shock period: (a) Evans blue for fluorescence microscopic visualization of the vessels. (b) India ink for gross and light microscopic evidence of retention of carbon. (c) Horseradish peroxidase (HRP) for light and electron microscopic study. Lack of spontaneous recovery from shock was associated with: (a) 55-65% blood loss, a low blood pressure (30-40 mm Hg), and a dramatic increase in pulse rate; (b) marked Evans blue fluorescence along the vessels; (c) no retention of India ink in the microcirculation; (d) peroxidase activity on the luminal surface of the endothelium. Absence of India ink in the microcirculation of the isocortex during the shock period, as shown by light and electron microscopy, suggests that there is sufficient cerebral blood flow to clear the carbon particles from the blood stream and that there are no openings greater than 30 nm in the endothelial layer allowing seepage of carbon particles through or between endothelial cells. Vascular Evans blue fluorescence and peroxidase activity were both demonstrated on the luminal surface of the endothelial cells, by light microscopy, indicating that these markers are abnormally retained. Ultrastructural demonstration of increased HRP uptake and adherence onto the endothelial cells confirms these observations. These results show that regional endothelial alterations occur in this model of hemorrhagic shock.