No abstract

Contractile events during wound healing. During granulation tissue contraction, fibroblasts develop characteristics typical of smooth muscle; (1) they contain an extensive cytoplasmic fibrillar system, (2) they show immunofluorescent labeling of anti-actin antibodies, (3) there are cell and cell to stroma attachments, (4) strips of granulation tissue, when tested pharmacologically in vitro, behave similarly to smooth muscle. These data support the view that under certain conditions, fibroblasts can differentiate into a cell type structurally and functionally similar to smooth muscle and this cell, the 'myofibroblast', plays an important role in connective tissue contraction. During epithelialization, epidermal cells develop an extensive cytoplasmic contractile apparatus which has morphological and immunological characteristics similar to those of myofibroblasts. Such apparatus disappears as soon as epithelialization is completed. It is proposed that such a contractile apparatus plays a role in cell motility enabeling individual cells to rearrange themselves in an appropriate pattern. In conclusion, significant amounts of contractile proteins may be synthetized by fibroblasts and epithelial cells during wound healing and may play an important role in this process.

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.

No abstract

SummaryNormal platelets incubated with anti-actin autoantibodies (AAA) (from the serum of patients with chronic aggressive hepatitis) do not show binding of these antibodies as seen by indirect immunofluorescence. AAA serum does not inhibit thrombin-induced clot retraction, despite the binding of the antibodies to platelets in the clot. Similarly, AAA serum does not affect “reversible” or “irreversible” aggregation (induced by ADP, collagen or epinephrine), despite the binding of the antibodies to platelet actin under such circumstances. AAA also bind to platelets when aggregation is inhibited by EDTA. The incubation of “reversibly” aggregated platelet with AAA results in a small but definite binding of AAA to platelets. These findings suggest that during “irreversible” and/or “reversible” aggregation, changes take place at the surface of platelets which expose the antigen at the surface of the cell.