title: Differential cardiovascular effects of endotoxin derived from Escherichia coli or Pseudomonas aeruginosa.
abstract: Sepsis is characterized by various symptoms, signs and underlying pathophysiology. To investigate possible mechanisms underlying this diversity, we compared the cardiovascular effects of lipopolysaccharide (LPS) derived from Escherichia coli (E-LPS) with those of LPS from Pseudomonas aeruginosa (P-LPS) in rats. We also examined the possible roles of tumor necrosis factor-alpha (TNF-alpha) and oxidative stress in LPS-induced cardiovascular damage. E-LPS (10 mg/kg body weight) or P-LPS (2 mg/kg body weight) was administered intravenously to Wistar rats. Echocardiography was serially performed. E-LPS induced an increase in left ventricular fractional shortening that persisted for at least 6 h, whereas P-LPS elicited an initial increase and a subsequent decrease in this parameter. Histological analysis revealed that P-LPS induced interstitial edema, congestion, intramyocardial bleeding, myocardial necrosis, infiltration of inflammatory cells, and formation of fibrin thrombi in the heart, whereas no pathological changes were apparent in the hearts of rats treated with E-LPS. Furthermore, the plasma concentration of TNF-alpha in rats treated with P-LPS was greater than that in rats treated with E-LPS, but the glutathione redox ratio in the heart was not affected by either type of LPS. In conclusion, E-LPS and P-LPS induced distinct patterns of functional and structural responses in the cardiovascular systems of rats. These differential responses may be attributable in part to the difference in the associated increases in the plasma concentration of TNF-alpha. The cardiovascular effects of LPS thus depend on the causative organisms.
authors: Pathophysiological Laboratory Sciences, Graduate School of Medicine, Nagoya University, Japan.
authors: Aya
authors: A
authors: Matsushita
authors: Mitsunori
authors: M
authors: Iwase
authors: Yosuke
authors: Y
authors: Kato
authors: Sahoko
authors: S
authors: Ichihara
authors: Gaku
authors: G
authors: Ichihara
authors: Hirotaka
authors: H
authors: Kimata
authors: Keiko
authors: K
authors: Hayashi
authors: Katsunori
authors: K
authors: Hashimoto
authors: Toyoharu
authors: T
authors: Yokoi
authors: Akiko
authors: A
authors: Noda
authors: Yasuo
authors: Y
authors: Koike
authors: Mitsuhiro
authors: M
authors: Yokota
authors: Kohzo
authors: K
authors: Nagata
mesh_terms: D000818:Animals; D002319:Cardiovascular System / Q000187:drug effects*; D004452:Echocardiography; D004731:Endotoxins / Q000633:toxicity*; D005978:Glutathione / Q000378:metabolism; D008070:Lipopolysaccharides / Q000633:toxicity; D008297:Male; D008565:Membrane Proteins / Q000633:toxicity*; D009206:Myocardium / Q000378:metabolism / Q000473:pathology; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology; D011550:Pseudomonas aeruginosa; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume / Q000187:drug effects; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000502:physiology
chemical_list: D004731:Endotoxins; D008070:Lipopolysaccharides; D008565:Membrane Proteins; D014409:Tumor Necrosis Factor-alpha; C025357:endotoxin binding proteins; D005978:Glutathione