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Objective: Controlled mechanical ventilation can impair systemic and renal blood flow and function, which may be aggravated by respiratory acidosis. We hypothesized that partial ventilatory support using airway pressure release ventilation (APRV) with spontaneous breathing provides better cardiopulmonary and renal function than full ventilatory support using APRV without spontaneous breathing., Design: Prospective randomized study., Setting: Intensive care unit of a university hospital., Patients: Twelve patients with acute lung injury (ALI)., Interventions: Airway pressure release ventilation with and without spontaneous breathing, maintaining either the same minute ventilation (V(E)) or the same airway pressure (Paw) limits., Measurements: Systemic hemodynamics were estimated by double-indicator dilution, effective renal blood flow (ERBF) by para-aminohippurate, and glomerular filtration rate (GFR) by inulin clearance., Results: Compared to APRV with spontaneous breathing, cardiac index (CI) was decreased when the upper Paw limit was increased to provide the same V(E) (4.26+/-1.21 l min(-1) m(-2)vs 3.72+/-0.99 l min(-1) m(-2); p<0.05) while CI was increased when Paw limits were held constant (4.91+/-1.41 l min(-1) m(-2); p<0.05). Effective renal blood flow and GFR were higher during APRV with spontaneous breathing (858+/-388 ml min(-1) m(-2) and 94+/-47 ml min(-1) m(-2)) than during APRV without spontaneous breathing and the same V(E) (714+/-236 ml min(-1) m(-2)and 82+/-35 ml min(-1) m(-2)) or the same Paw (675+/-287 ml min(-1) m(-2) and 80+/-41 ml min(-1) m(-2); p<0.05). Urine volume did not change., Conclusions: Spontaneous breathing during APRV was associated with better renal perfusion and function than APRV without spontaneous breathing applying either the same V(E) or the same Paw limits. Maintaining spontaneous breathing during ventilatory support may, therefore, be advantageous in preventing deterioration of renal function in patients with ALI.

Objective: To investigate the effects of prone positioning on systemic hemodynamics, intra-abdominal pressure (IAP), plasma disappearance rate of indocyanine green (PDR(ICG)), and gastric intramucosal to arterial PCO2 difference (Pi-aCO2)., Design and Setting: Prospective randomized study in the intensive care unit of a university hospital., Patients: 12 mechanically ventilated, hemodynamically stable patients with acute lung injury., Intervention: Positioning supine and prone for 3 h in random order., Measurements: Systemic hemodynamics were determined by transpulmonary double-indicator dilution technique using an integrating fiberoptic monitoring system. The same monitoring system was used to measure PDR(ICG). IAP was measured in the urinary bladder and gastric intramucosal PCO2 was evaluated by automated recirculation gas tonometry., Results: IAP increased from 10 +/-3 in the supine to 13+/-4 mmHg in the prone position. Cardiac index increased from 3.8+/-0.9 (supine) to 4.2+/-0.6 l/m(2) per minute (prone), mean arterial pressure from 75+/-10 (supine) to 81+/-11 mmHg (prone), PaO2/FIO2 from 194+/-66 (supine) to 269+/-68 mmHg (prone), and oxygen delivery from 558+/-122 (supine) to 620+/-74 ml/m(2) per minute (prone). No other parameters, including PDR(ICG) and Pi-aCO2, differed between the two positions., Conclusions: Prone positioning in mechanically ventilated patients with acute lung injury, despite a small increase in IAP, does not negatively affect the hepatic capacity to eliminate ICG and gastric intramucosal energy balance when systemic blood flow and oxygenation are improved.

Objective: To investigate the role of macrophage migration inhibitory factor (MIF) as a marker of severity of systemic inflammation in patients with severe sepsis and critically ill postsurgical patients., Design: Prospective observational study in consecutive patients with severe sepsis, critically ill nonseptic postsurgical patients, and healthy blood donors., Setting: A surgical intensive care unit of a university hospital., Patients and Participants: 19 patients with severe sepsis, 18 critically ill nonseptic postsurgical patients, and 10 healthy blood donors., Measurements and Results: MIF plasma levels of patients and participants were measured. Interleukin 6 plasma levels were monitored as a control marker of inflammation. The median MIF plasma level was four to five times higher in patients with severe sepsis (2.70 ng/ml, range 0.31-19.59) and in critically ill nonseptic postsurgical patients (2.43 ng/ml, range 0.49-4.31) than in healthy blood donors (0.56 ng/ml, range 0.16-1.68). MIF plasma levels did not differ between the patient groups., Conclusions: MIF serves as a general marker for systemic inflammation in septic and nonseptic acute critical illness, but MIF does not discriminate for severity or differentiate between infectious and noninfectious origins of an acute critical illness.

Objective: To investigate the ex vivo endotoxin-inducible heat shock protein 70 (HSP70) expression in the peripheral blood mononuclear cells (PBMC) of patients with severe sepsis in order to assess the capacity of this potentially protective response during systemic inflammation., Design: Prospective observational study in consecutive patients with severe sepsis and healthy blood donors., Setting: Surgical intensive care unit in a university hospital., Patients and Participants: Eleven patients with the diagnosis of severe sepsis, one patient who had recovered from severe sepsis and 13 healthy blood donors., Interventions: None., Measurements and Results: We studied the inducibility of HSP70 expression in the PBMC of patients with severe sepsis and healthy blood donors ex vivo. Human whole blood was incubated with variable lipopolysaccharide (LPS from Salmonella minnesota Re 595) concentrations (0; 0.1; 10; 100 ng/ml) for different periods of time (0.5; 2; 4; 10 h). The PBMC were separated by Ficoll density gradient and then disrupted by hypotonic lysis. HSP70 was measured by means of enzyme-linked immunosorbent assay (ELISA). We found a LPS dose- and time-dependent inhibition of ex vivo HSP70 expression in the PBMC of both patients with severe sepsis and healthy individuals. However, the levels of HSP70 expression in patients were significantly lower compared to those of healthy individuals at all LPS concentrations and incubation times. On average, HSP70 expression in the PBMC of healthy controls was 2.8 (range 1.2-3.9) times higher than in patients. HSP70 expression was inducible by thermal heat shock in the PBMC of both patients and healthy individuals., Conclusions: Endotoxin inhibits HSP70 expression in PBMC ex vivo. In vivo, the suppression of HSP70 expression induced by endotoxin and high levels of proinflammatory cytokines may contribute to the cellular dysfunction of immunocompetent cells concerning antigen presentation, phagocytosis and antibody production associated with decreased resistance to infectious insults during severe sepsis.