Shock : molecular, cellular, and systemic pathobiological aspects and therapeutic approaches : the official journal the Shock Society, the European Shock Society, the Brazilian Shock Society, the International Federation of Shock Societies
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Comparative Study
Pathophysiologic and clinical correlates of hypophosphatemia and the relationship with sepsis and outcome in postoperative patients after hepatectomy.
Hypophosphatemia in critically ill and postoperative (p.o.) patients is a multifactorial event, and is also related to severity of illness. This study was conducted to assess pathophysiologic correlates of hypophosphatemia and the simultaneous relationship with clinical events after hepatectomy. A total of 333 measurements were obtained in 59 patients: these were performed preoperatively and at p.o. days 1, 3, and 7 in all patients, and subsequently, until recovery or death, only in those with complications. ⋯ Plasma phosphate at p.o. day 1 was related inversely to APACHE II score (r2 = 0.4, P < 0.001), and levels lower than 1.5 mg/dL were associated with an almost 4-fold increase in the rate of complications compared with cases with higher phosphate (P < 0.001). The best single variable bridging early evidence of hypophosphatemia to subsequent development of complications was plasma cholesterol, which fell significantly from p.o. day 3 onward in patients with complications compared with those recovering normally (P < 0.01), and in nonsurvivors compared with survivors (P < 0.01). Hypophosphatemia may anticipate clinical evidence of complications by reflecting an early stronger acute-phase response, with shift of phosphate from intra- to extravascular space, or true phosphorus deficiency, which may favor development of complications by impairing high-energy substrate availability for host defense and other cell functions.
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Frequent hypokalemia was noted immediately after trauma, and it was hypothesized that hypokalemia occurred more frequently in the more severely injured. A retrospective trauma registry and chart review was done on 546 trauma patients looking at admission potassium, a variety of lab tests related to potassium, specific injuries, hospital/ICU lengths of stay, and general patient demographics. Admission hypokalemia (K < 3.6 meq/l) was more frequent in those with closed head injuries (41.1% vs. 27.5%, P < .001) and in those who suffered spinal cord injuries (54.5% vs. 33.6%, P < .05). ⋯ Hypokalemic patients more likely needed a ventilator, (26.6% vs. 16.5%, P < .01) but did not have significantly more ventilator days (P > .05). Subsequently, hypokalemic patients had longer ICU lengths of stay (LOS) (2.6 vs. 1.5 days, P < .005) and longer hospital LOS (8.5 vs. 5.6 days, P < .001). When stratified into categories of "severe": (K < 3.1 meq/l), "moderate": (K = 3.1-3.3 meq/l), and "mild": (K = 3.4-3.5 meq/l) hypokalemia, those with severe hypokalemia had significantly lower GCS (10.0 vs. 13.1, p < .05), higher serum glucose levels (167 vs. 137 mg/dl, P < .05), lower creatinine levels (.77 vs. .95 mg/dl, P < .05), and longer hospital lengths of stay (13.1 days vs. 7.6 days, P < .05 results).
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Comparative Study
A 4-amino analogue of tetrahydrobiopterin attenuates endotoxin-induced hemodynamic alterations and organ injury in rats.
Most recently we have shown that 4-aminotetrahydrobiopterin (4-ABH4), an analogue of tetrahydrobiopterin (cofactor of NO synthase), even administered 2 h after endotoxin challenge, improves survival rate in rats. The following experiment was performed to examine the effects of 4-ABH4 with respect to endotoxin-induced hemodynamic alterations and organ failure. At 2 h after endotoxic challenge (10 mg kg(-1) body weight) animals received 4-ABH4 at a dose of 1, 10, or 100 mg kg(-1) body weight. ⋯ Moreover, endotoxin-induced lung edema and intestinal necrosis were significantly reduced by 4-ABH4. Our study provides information that tetrahydrobiopterin analogue, 4-ABH4, improves LPS induced hemodynamic conditions and organ injury. This may, at least in part, account for the previously observed protection of rats by 4-ABH4 against endotoxin-induced mortality in the same endotoxic shock model.
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Hypertonic saline (HTS) resuscitation inhibits acute lung injury in animal models of shock, but some argue this may simply represent more efficient fluid resuscitation. Inflammatory mediators within mesenteric lymph have been identified as a link between splanchnic hypoperfusion and acute respiratory distress syndrome (ARDS). We hypothesize that HTS resuscitation abrogates post-shock lymph-mediated neutrophil (PMN) priming and PMN-mediated human endothelial cell cytotoxicity. ⋯ Hypertonic resuscitation (HTS) abrogates PHSML pniming of the PMN and PMN-mediated HMVEC cytotoxicity. Furthermore, incubation of PMNs in clinically relevant HTS (180 mM NaCl) prevents PHSML PMN priming and PMN:HMVEC interactions. These studies suggest inhibition of PMN signal transduction is a mechanism whereby HTS resuscitation abrogates acute lung injury.
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Comparative Study
Effects of dopamine on systemic and regional blood flow and metabolism in septic and cardiac surgery patients.
Dopamine is used in the clinical setting to support cardiac output and blood pressure and to improve diuresis. Experimental studies suggest that dopamine may reduce splanchnic perfusion and redistribute blood flow locally. To assess the effects of dopamine on splanchnic perfusion, we used dopamine to increase cardiac output by 25% in nine septic patients and 11 patients after cardiac surgery. ⋯ Dobutamine in these patients [6.4 (4.2-9.5) microg x kg(-1) x min(-1)] increased splanchnic blood flow from 1.20 (0.44) L x min(-1) x m(-2) to 1.43 (0.57) L x min(-1) x m(-2) (P = 0.008), while splanchnic oxygen consumption did not change 72 (25) mL x min(-1) x m(-2) vs. 76 (22) mL x min(-1) x m(-2) (not significant)]. The reduction of splanchnic oxygen consumption by dopamine in sepsis suggests an impairment of hepatosplanchnic metabolism despite an increase in regional perfusion. The safety and indications of dopamine use in sepsis should be re-evaluated.