Articles: sepsis.
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Clinical Trial Controlled Clinical Trial
Alterations in coagulation and fibrinolysis during sepsis.
Circulating levels of thrombin-antithrombin III complex (TAT) and plasmin-alpha 2 plasmin inhibitor complex (PIC) in 49 septic patients (23 patients with organ dysfunction (OD), 26 without OD) and 11 postgastrectomy patients were measured to determine the significance of the coagulation-fibrinolytic systems in the development of OD. Tissue plasminogen activator (t-PA), plasminogen activator inhibitor 1 (PAI-1), and thrombomodulin were also measured. The mean level of TAT on the day when OD occurred was significantly higher compared with the maximum level of TAT in septic patients without OD (P < .01) or postoperative patients (P < .01). ⋯ Septic patients with OD showed higher levels of PAI-1 (P < .001) but not of t-PA. Thrombomodulin levels were significantly higher in the septic patients with OD compared with the others (P < .001). We conclude that suppression of the fibrinolytic system contributes to the imbalance between coagulation and fibrinolysis, and that this hypercoagulable millieu on the endothelial surface leads to the onset of OD.
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Journal of anesthesia · Mar 1996
Alterations in the myocardial β-adrenergic system during experimental endotoxemia.
In this study to investigate whether β-adrenergic receptor systems in the heart are impaired during endotoxemia, we examined two models of septic shock in rats, each of which has a different time course for the shock state. Male Wistar rats were divided into two groups: (1) the LPS (lipopolysaccharide) iv group (Escherichia coli endotoxin 1.0 mg·kg(-1) iv bolus administration), and (2) the CLP (cecal ligation and puncture model) group. As a control group for each model, a 0.9% saline injection group and a sham-operated group were also prepared. ⋯ The alteration in hemodynamics of septic-shock rats observed in this study was linked to the change in heart β-receptor density rather than the change in plasma CA. These observations suggested that the alterations which occur in the β-receptor system during endotoxemia depend upon the model of animal sepsis that is employed, and the time course of the septic-shock state. These alterations in the β-adrenergic system are thought to cause myocardial dysfunction during endotoxemia.