Graded intestinal vascular obstruction. IV. An analysis of the pathophysiology in the development of refractory shock.
Pathophysiological mechanisms of importance for mortality in shock were studied using different modes of treatment in a standardized intestinal vascular obstruction model. In an untreated series the degree of intestinal mucosal damage, but not the increase in hematocrit, correlated to mortality. The importance of hypovolemia, instability of membranes, and metabolic blockage were studied in several series by giving saline, dextran 40, dextran 70, albumin, methylprednisolone, glucose, and glucose-insulin-potassium. Dextran 70 was the only agent which significantly reduced mortality--from 88 to 58%. This effect was, however, not due to hemodilution nor to prevention of mucosal lesions. In an additional series the effects of dextran 70 on intestinal electrolyte concentration, on pulmonary trapping of platelets, and on cardioinhibitory effects in vitro of intestinal venous plasma were evaluated in comparison with untreated shock. Dextran 70 prevented the electrolyte changes and platelet trapping in the lung, and the cardioinhibitory effect of intestinal venous plasma was reduced. A combination of these mechanisms may be of importance in producing mortality in this shock model.
D000818:Animals; D001826:Body Fluids / Q000378:metabolism; D003911:Dextrans / Q000627:therapeutic use; D004195:Disease Models, Animal; D004573:Electrolytes / Q000097:blood; D005260:Female; D006400:Hematocrit; D007413:Intestinal Mucosa / Q000473:pathology; D007422:Intestines / Q000098:blood supply*; D007511:Ischemia / Q000503:physiopathology; D008168:Lung / Q000098:blood supply; D008297:Male; D009200:Myocardial Contraction; D051381:Rats; D011919:Rats, Inbred Strains; D012769:Shock / Q000188:drug therapy / Q000401:mortality / Q000503:physiopathology*
D003911:Dextrans; D004573:Electrolytes