Microdialysis-evaluated myocardial cyclooxygenase-mediated inflammation and early circulatory depression in porcine endotoxemia

Abstract

Endotoxemia induced a myocardial COX-mediated inflammation without signs of ischemia. In parallel, a depletion of myocardial energy substrates and a deterioration in myocardial performance were seen.

Type 1 Diabetes Is Associated With Increased Cyclooxygenase- and Cytokine-Mediated Inflammation

“…Prostaglandins are well-known mediators of inflammation, and 15-ketodihydro-PGF 2␣ , a major metabolite of bioactive PGF 2␣ , is a potent indicator of in vivo inflammatory processes (14,15,22,23). Thus, the results from this study suggest ongoing COX-mediated low-grade inflammatory processes among patients with type 1 diabetes.…”

“…Prostaglandin F 2␣ (PGF 2␣ ) is a potent vasoconstrictive compound (11). Moreover, prostaglandins are important mediators of the inflammatory process (12,13), and 15-keto-dihydro-PGF 2␣ , a major metabolite of PGF 2␣ , has been shown to be a reliable indicator of in vivo COX-mediated inflammation (14,15). In a recent study, 15-keto-dihydro-PGF 2␣ , high-sensitivity C-reactive protein (CRP), and serum amyloid protein A (SAA), which are all inflammatory indicators, were increased in men with type 2 diabetes in a population-based cross-sectional study (16).…”

Endotoxic shock model with fluid resuscitation in Macaca mulatta: The authors' reply

“…However, only a few of these authors studied signs of early-phase septic shock (Hinshaw et al 1983, Mutschler et al 2003 because it was difficult to clearly define the concept of early-phase septic shock. In 2000, a clinical protocol was publicized in which sepsis, septic shock, hypotension and multiple organ system failure were defined and the diagnostic criteria of septic shock were determined.…”

Effects of olprinone on hepatosplanchnic circulation and mitochondrial oxidation in a porcine model of endotoxemia

“…A recent investigation suggested that myocardial dysfunction could actually occur early (<30 min) in septic shock [12]. Furthermore, Mutschler et al [13] have reported that endotoxin caused a rapid cyclooxygenase (COX)-mediated inflammatory response in the myocardium (within 1 h) and that this early inflammation may have been a mediator of myocardial dysfunction in porcine endotoxemia. In the present study, this hypodynamic model was therefore adopted in order to avoid: (a) massive fluid challenge in septic shock, which may contribute to overpermeability pulmonary edema, causing severe respiratory failure [14]; and (b) aggressive fluid replacement, such as is used clinically, which may mask the pathophysiological Sepsis is characterized by the excessive production of inflammatory mediators and by the excessive activation of inflammatory cells, thus resulting in metabolic anarchy, including increased lactate concentration and metabolic acidosis, even during a hyperdynamic state with high CO.…”