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Saving the heart 30 beats/min did not demonstrate adverse impact on global haemodynamics in rates above 110/min. Using well titratable betablocker seems to be safe and cardioprotective in septic shock patients with high cardiac output.

Colonic inflammation induces local glucocorticoid activation via 11betaHSD1 and impairs glucocorticoid inactivation via 11betaHSD2. The observed changes indicate a role for local metabolism of glucocorticoids in the control of colonic inflammation.

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Background: The regional citrate anticoagulation (RCA) induces changes in total (Ca^tot) and ionized (Ca²⁺) calcium. As of now, we do not have much information about parallel changes of total (Mg^tot) and ionized (Mg²⁺) magnesium. Methods: The authors compared changes of Mg²⁺ and Mg^tot with changes of Ca²⁺ and Ca^tot in 32 critically ill patients on 4% trisodium citrate (4% TSC) with calcium-free fluids. Results: The median continuous venovenous hemodiafiltration balance of Mg^tot was -0.91 (-1.18 to -0.53) mmol/h compared to the median balance of Ca^tot 0.86 (0.08-1.55) mmol/h. Postfilter Mg²⁺ decreased by 68.3% (70.8-65.6) in parallel (r = 0.41, p = 0.03) to decrease of postfilter Ca²⁺ (by 70.2% (73.0-66.1)) and was significantly related to the postfilter Ca²⁺ (r = 0.50, p < 0.001). The decrease of prefilter to postfilter Ca²⁺ correlated to a dosage of 4% TSC per blood flow (r = 0.37, p = 0.04). Conclusions: The loss of Mg^tot during RCA is not covered by magnesium concentration in ordinary dialysis/substitution fluid and may lead to the depletion of total body magnesium. The postfilter Mg²⁺ is significantly related to the postfilter Ca²⁺. Video Journal Club “Cappuccino with Claudio Ronco” at http://www.karger.com/?doi = 440972.

Recent in vitro studies have shown the involvement of pro-inflammatory cytokines in the regulation of the local metabolism of glucocorticoids via 11beta-hydroxysteroid dehydrogenase type 1 and type 2 (11HSD1 and 11HSD2). However, direct in vivo evidence for a relationship among the local metabolism of glucocorticoids, inflammation and steroid enzymes is still lacking. We have therefore examined the changes in the local metabolism of glucocorticoids during colonic inflammation induced by TNBS and the consequences of corticosterone metabolism inhibition by carbenoxolone on 11HSD1, 11HSD2, cyclooxygenase 2 (COX-2), mucin 2 (MUC-2), tumor necrosis factor alpha (TNF-alpha), and interleukin 1beta (IL-1beta). The metabolism of glucocorticoids was measured in tissue slices in vitro and their 11HSD1, 11HSD2, COX-2, MUC-2, TNF-alpha, and IL-1beta mRNA abundances by quantitative reverse transcription-polymerase chain reaction. Colitis produced an up-regulation of colonic 11HSD1 and down-regulation of 11HSD2 in a dose-dependent manner, and these changes resulted in a decreased capacity of the inflamed tissue to inactivate tissue corticosterone. Similarly, 11HSD1 transcript was increased in colonic intraepithelial lymphocytes of TNBS-treated rats. Topical intracolonic application of carbenoxolone stimulated 11HSD1 mRNA and partially inhibited 11HSD2 mRNA and tissue corticosterone inactivation and these changes were blocked by RU-486. The administration of budesonide mimicked the effect of carbenoxolone. In contrast to the local metabolism of glucocorticoids, carbenoxolone neither potentiates nor diminishes gene expression for COX-2, TNF-alpha, and IL-1beta, despite the fact that budesonide down-regulated all of them. These data indicate that inflammation is associated with the down-regulation of tissue glucocorticoid catabolism. However, these changes in the local metabolism of glucocorticoids do not modulate the expression of COX-2, TNF-alpha, and IL-1beta in inflamed tissue.

Background: Testing metabolic effects of a novel calcium-free, magnesium, phosphate and lactate containing solution (Lactocitrate) in combination with citrate anticoagulation. Methods: Patients on CRRT (2,000 ml/h, blood flow (Qb) 100 ml/min, trisodium citrate (4% TSC)) with arterial lactate <3 mmol/l were included. At start, bicarbonate-buffered fluid was changed to Lactocitrate and the substitution of magnesium and phosphorus ceased. At 9 h the Qb was increased to 150 ml/min. At 18 h the CRRT dosage was increased to 3,000 ml/h. Results: In 22 CVVHDF patients and another 23 on CVVH the pH, aHCO₃ and Na (all p > 0.05) showed no significant changes regardless of the increased dosage of 4% TSC at 9 h (p < 0.001). Mg_tot and phosphorus stabilised within normal range. Arterial lactate increased to 1.9 (1.6-2.6) mmol/l at 3,000 ml/h, p < 0.001). Citrate- and lactate-related energetic gains were up to 74 (61-86) kJ/h. Conclusions: The fluid performed well within ordinary CRRT dosage and Qb up to 150 ml/min. Lactate levels mildly increased and no magnesium and phosphorus replenishments were necessary.

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