[Influence of pressure- and volume-controlled ventilation on pulse pressure variations: randomized study]. / Influence du mode de ventilation sur la variation respiratoire de la pression pulsée artérielle: étude randomisée.

OBJECTIVE: Pulse pressure variation (ΔPP) has been demonstrated to be an accurate dynamic parameter to predict fluid responsiveness. However, the impact of different ventilator modes on this parameter is unknown. We compared ΔPP values calculated alternatively during pressure- and volume-controlled ventilation. STUDY DESIGN: Double-blind randomized study, cross-over design. PATIENTS: Patients in intensive care unit after a cardiac surgery. METHOD: Patients were ventilated alternatively in both ventilator modes (according to the randomization): volume-controlled ventilation (VVC) and pressure-controlled ventilation (VPC). Other parameters of ventilation were identical. ΔPP values were calculated for each patient in both ventilator modes. RESULTS: Among the 26 patients analyzed, mean ΔPP value was de 14.0±7.3% in VVC and 11.8±6.2% in VPC (P<0,0001). On Bland-Altman representation, mean bias was +2.2±2.3% and inferior and superior limits of agreement were respectively -2.3 and 6.7%. Arterial blood pressure and central venous pressure were not modified. CONCLUSION: ΔPP values obtained with both ventilator modes were not interchangeable. On average, ΔPP decreases by more than two points in the passage VVC to VPC for a given patient, all others things being equal.

Genetically related Escherichia coli strains associated with Crohn's disease.

Escherichia coli strains isolated from patients with Crohn's disease (CD) with chronic ileal lesions (n=14), early endoscopic recurrent lesions (n=20), without endoscopic recurrence (n=7), and controls (n=21) were compared by ribotyping. The dendrogram generated by 50 ribotype profile analysis revealed a large cluster of genetically linked E coli strains isolated significantly more frequently from patients with chronic and recurrent CD (24/33 patients) than from controls (9/21) (p<0.05). Most patients operated on for chronic ileal lesions (78.5%) harboured E coli strains belonging to cluster A (p<0.002 v controls). The prevalence of patients with early recurrent lesions harbouring E coli strains belonging to this cluster was high but not significant, although 16 strains isolated from eight patients presented the same ribotype profile. In this cluster, 21 of 26 strains isolated from patients with active CD demonstrated adherent ability to differentiated Caco-2 cells, indicating that most of the genetically related strains share a common virulence trait. Comparison of E coli strains recovered from ulcerated and healthy mucosa of patients operated on for CD demonstrated in each patient that a single strain colonised the intestinal mucosa. Our results suggest that although a single E coli isolate was not found in Crohn's ileal mucosa, some genotypes were more likely than others to be associated with chronic or early recurrent ileal lesions.

Invasive ability of an Escherichia coli strain isolated from the ileal mucosa of a patient with Crohn's disease.

Crohn's disease (CD) is an inflammatory bowel disease in which Escherichia coli strains have been suspected of being involved. We demonstrated previously that ileal lesions of CD are colonized by E. coli strains able to adhere to intestinal Caco-2 cells but devoid of the virulence genes so far described in the pathogenic E. coli strains involved in gastrointestinal infections. In the present study we compared the invasive ability of one of these strains isolated from an ileal biopsy of a patient with CD, strain LF82, with that of reference enteroinvasive (EIEC), enteropathogenic (EPEC), enterotoxigenic (ETEC), enteraggregative (EAggEC), enterohemorrhagic (EHEC), and diffusely adhering (DAEC) E. coli strains. Gentamicin protection assays showed that E. coli LF82 was able to efficiently invade HEp-2 cells. Its invasive level was not significantly different from that of EIEC and EPEC strains (P > 0.5) but significantly higher than that of ETEC (P < 0.03), EHEC (P < 0. 005), EAggEC (P < 0.004) and DAEC (P < 0.02) strains. Strain LF82 also demonstrated efficient ability to invade intestinal epithelial cultured Caco-2, Intestine-407, and HCT-8 cells. Electron microscopy examination of infected HEp-2 cells revealed the presence of numerous intracellular bacteria located in vacuoles or free in the host cell cytoplasm. In addition, the interaction of strain LF82 with epithelial cells was associated with the elongation of microvillar extensions that extruded from the host cell membranes and engulfed the bacteria. This internalization mechanism strongly resembles Salmonella- or Shigella-induced macropinocytosis. The use of cytochalasin D and colchicine showed that the uptake of strain LF82 by HEp-2 cells was mediated by both an actin microfilament-dependent mechanism and microtubule involvement. In addition, strain LF82 survived for at least 24 h in HEp-2 and Intestine-407 cells and efficiently replicated intracellularly in HEp-2 cells. PCR and hybridization experiments did not reveal the presence of any of the genetic determinants encoding EIEC, EPEC, or ETEC proteins involved in bacterial invasion. Thus, these findings show that LF82, which colonized the ileal mucosa of a patient with CD, is a true invasive E. coli strain and suggest the existence of a new potentially pathogenic group of E. coli, which we propose be designated adherent-invasive E. coli.