title: The fall of cardiac output in endotoxemic rats cannot explain all changes in organ blood flow: a comparison between endotoxin and low venous return shock.
abstract: During endotoxin shock mean arterial pressure (MAP) and cardiac output (CO) fall, and the latter is redistributed. To evaluate whether these changes are solely caused by the low output, or are also based on endotoxin itself, we compared regional hemodynamic changes during endotoxemia with those in a nonendotoxemic state of decreased CO in anesthetized rats. In group E (n = 10) endotoxin Escherichia coli O127:B8 (8 mg.kg-1) was infused from t = 0 till t = 60 min. In group B (n = 10) the same decrease of CO and MAP was obtained as in group E by inflating a balloon in the inferior caval vein, distal to the renal veins, from t = 0 till t = 60 min. We measured MAP, CO (thermodilution), central venous pressure, heart rate, organ blood flow, and redistribution of CO (microspheres), arterial lactate and glucose, and hematocrit. MAP and CO decreased (p < .05) in both groups (by 30 and 50%, respectively at t = 60). Heart rate, hematocrit, arterial lactate, and arterial glucose were significantly higher (p < .05) in group E (by 17, 12, 180, and 55%, respectively). Blood flow to most organs had similarly decreased in both groups. The decreased intestinal blood flow lead to macroscopic damage only in group E. Blood flows (absolute or as percentage of CO) to heart, hepatic artery, and diaphragm, however, had significantly increased in group E while blood flows to skin, skeletal muscle, and stomach had decreased more in group E. Except for the heart these differences could be explained by increased work load (detoxification: liver; hyperventilation: diaphragm, muscle) and thus to a more pronounced redistribution at the expense of skin and muscle blood flow. Regional hemodynamic changes during endotoxemia thus could largely be attributed to decrease of CO and redistribution of the circulating blood volume. In the heart, endotoxin seemed to exert effects independent of the hypodynamic state. This was also true for the intestinal damage and the rise in hematocrit and arterial lactate.
authors.affiliation: Laboratory for Physiology, Vrije Universiteit, Amsterdam, The Netherlands.
authors.forename: M F
authors.initials: MF
authors.lastname: Mulder
authors.forename: A A
authors.initials: AA
authors.lastname: van Lambalgen
authors.forename: G C
authors.initials: GC
authors.lastname: van den Bos
authors.forename: L G
authors.initials: LG
authors.lastname: Thijs
mesh_terms: D000818:Animals; D001784:Blood Gas Analysis; D001786:Blood Glucose / Q000378:metabolism; D002302:Cardiac Output / Q000502:physiology; D002404:Catheterization; D006400:Hematocrit; D006439:Hemodynamics / Q000502:physiology*; D007773:Lactates / Q000097:blood; D019344:Lactic Acid; D008070:Lipopolysaccharides; D008297:Male; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D012039:Regional Blood Flow / Q000502:physiology; D012769:Shock / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D012772:Shock, Septic / Q000097:blood / Q000209:etiology / Q000503:physiopathology*
chemical_list: D001786:Blood Glucose; D007773:Lactates; D008070:Lipopolysaccharides; D019344:Lactic Acid