Small intestinal mucosal lesions in feline septic shock: a study on the pathogenesis.
The pathogenesis of small intestinal mucosal damage in septic shock was explored in experiments on 15 cats given live E coli i.v. Villous (absorptive site) blood flow was studied by the carbon monoxide uptake technique using isolated small intestinal segments. In eight of the cats, segments were perfused intraluminally with oxygenated or nitrogenated saline. The main part of the small intestine was unperfused and served as control. Nine cats (60%) developed mucosal damage. They had significantly lower arterial blood pressure at the end of septicemia (56 +/- 6) than cats without mucosal damage (76 +/- 3 mmHg). Total intestinal blood flow was similar before or during septicemia. Villous blood flow before septicemia was 3.7 +/- 0.5 ml/min X 100 g intestine and 5.1 +/- 1.0 (n.s.) in the two groups, respectively, and remained unchanged. Intraluminal perfusion with oxygenated but not with nitrogenated saline prevented the development of mucosal damage. It was concluded that the small intestinal mucosal damage is due to hypoxia in spite of unchanged villous blood supply.
D000136:Acid-Base Equilibrium; D000818:Animals; D002415:Cats; D006439:Hemodynamics; D006454:Hemoglobins / Q000032:analysis; D007022:Hypotension / Q000209:etiology; D007413:Intestinal Mucosa / Q000473:pathology*; D007421:Intestine, Small / Q000098:blood supply / Q000473:pathology*; D012772:Shock, Septic / Q000473:pathology* / Q000503:physiopathology; D013997:Time Factors
D006454:Hemoglobins