Pathophysiology of shock.

Abstract

Pathophysiology of shock was fundamentaly investigated in several different ways. 1. Fractional distribution of cardiac output was measured, using radioactive microsphere technique. Hemorrhagic, endotoxin and trime-thapan hypotension were compared to each other in their fractional distribution of cardiac output. As a whole, cardiac output was distributed in the way to maintain cerebral or coronary blood flow, whatever the cause of shock may be. This centralization was rather well maintained even shock progressed. Splanchinic blood flow, especially the pancreas flow were decreased significantly. This may be related to the production of vasoactive or toxic substances from these organs. 2. Myocardial depressant factor was identified both in plasma and pancreas in advanced shock. Gel-chormatographic analysis was applied to separate the myocardial depressant factor. It is also demonstrated that myocardial depressant factor was produced in pancreas, transported via blood stream to the hear and caused cardiac depression. 3. In vivo cardiac contractility was measured by the change of Vmax sequentially as shock advanced. Left ventricular pressure was measured, using catheter tip transducer. In hemorrhagic shock, cardiac contractility began to decrease 4 hours after bleeding and continued to deteriorate progressively thereafter. 4. Regional coronary blood flow distribution was also measured by radioactive microsphere method. 2 hours after bleeding, endocardial fractional distribution already began to decrease and remained in the same distributional pattern even 4 hours after bleeding, while the myocardial contractility did not show any deterioration in 2 hours after bleeding. So it may be said that endo-cardial ischemia had no significant relationship with this cardic dysfunction. 5. Phagocytic function was decreased progressively when shock advanced. Reticuloendothelial depressing substance was also analyzed using gel-chromatographic method. Bioassay of RDS was shown by the decrease of phagocytic index after administering this fraction to healthy rats. 6. Closed loop, negative feed back mechanism (Fig.24) was suggested with relation to the above mentioned results. Decrease of cardiac output, followed by decrease of splanchinic blood flow, might cause the production of myocardial depressant factor. And this MDF might exert again decrease of cardiac contractility, thus closed negative feed-back loop was established. This mechanism might be called as peripheral theory for cardiac deterioration in shock. MDF, lysozomal enzymes or other vasoactive substances could not be phagocytized because of the reticuloendothelial system dysfunction, which may be caused by the decrease in opsonin activity or the release of reticuloendothelial depressing substance.