Host Resistance to Hemorrhagic Shock. XI. Role of Deficient Flow Through Intestine in Development of Irreversibility. ∗

Abstract

Summary and conclusions

1 Transient ischemia of the gut in rabbits produced a type of shock that is similar to the state of hemorrhagic shock which is irreversible to transfusion. Since the shock was as profound and as lethal whether a substantial plasma volume loss did or did not occur, hypovolemia was not an essential feature. This is further demonstrated by the observation that plasma volume therapy delayed but did not prevent death, and by the observation that dibenaminized animals and animals given antibiotics developed an equal degree of hypovolemia, but survived without blood volume therapy. Bacterial cultures were sterile, and the only notable gross lesion at death was intramural hemorrhage in the gut wall. 2) Dibenamine given in advance of the occlusion prevented the development of irreversible shock and resulted in recovery without therapy. When killed before or after recovery from shock these rabbits did not show a visible injury to the gut. 3) Non-absorbable antibiotics given in advance achieved the same protection as dibenamine. 4) Dibenamine prevented and the antibiotics reduced the degree and duration of the granulocytopenia which occurs in untreated animals. 5) A fall in rectal temperature occurred in all rabbits exposed to the vascular occlusion of the gut whether they developed shock or not, and whether they survived or not. 6) Transient ischemia of the gut produces an endotoxemia derived from the intraintestinal flora sufficient to overwhelm the normal detoxifying potential, and so induces irreversible shock. 7) These observations are in conformity with prior evidence that irreversibility to transfusion in hemorrhagic shock is due to endotoxins derived from the intestinal flora, and suggest further that deficient flow through the intestine accounts for the invasion of circulation by these endotoxins in sufficient quantity to produce irreversibility.