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Biomedical subjects

Charis Roussos

Publications and source records attributed to Charis Roussos.

At least 19 recordsLinked to original sources
PubMed2007

Soluble guanylyl cyclase expression is reduced in LPS-induced lung injury.

Soluble guanylyl cyclase (sGC) is a cGMP-generating enzyme implicated in the control of smooth muscle tone that also regulates platelet aggregation. Moreover, sGC activation has been shown to reduce leukocyte adherence to the endothelium. Herein, we investigated the expression of sGC in a murine model of LPS-induced lung injury and evaluated the effects of sGC inhibition in the context of acute lung injury (ALI). Lung tissue sGC alpha1 and beta1 subunit protein levels were determined by Western blot and immunohistochemistry, and steady-state mRNA levels for the beta1 subunit were assessed by real-time PCR. LPS inhalation resulted in a decrease in beta1 mRNA levels, as well as a reduction in both sGC subunit protein levels. Decreased alpha1 and beta1 expression was observed in bronchial smooth muscle and epithelial cells. TNF-alpha was required for the LPS-triggered reduction in sGC protein levels, as no change in alpha1 and beta1 levels was observed in TNF-alpha knockout mice. To determine the effects of sGC blockade in LPS-induced lung injury, mice were exposed to 1H-[1,2,4]oxodiazolo[4,3-a]quinoxalin-l-one (ODQ) prior to the LPS challenge. Such pretreatment led to a further increase in total cell number (mainly due to an increase in neutrophils) and protein concentration in the bronchoalveoalar lavage fluid; the effects of ODQ were reversed by a cell-permeable cGMP analog. We conclude that sGC expression is reduced in LPS-induced lung injury, while inhibition of the enzyme with ODQ worsens lung inflammation, suggesting that sGC exerts a protective role in ALI.

Aerosols↗
PubMed2007

Angiopoietin-2 is increased in severe sepsis: correlation with inflammatory mediators.

OBJECTIVE: Angiopoietin (Ang)-2 is an endothelium-specific growth factor, regulated by proinflammatory stimuli, that destabilizes vascular endothelium and increases vascular leakage; consequently, Ang-2 may contribute to sepsis pathophysiology. We have studied 1) serum Ang-2 levels in critically-ill patients and investigated potential relationships with inflammatory mediators and indices of disease severity and 2) the effect of sepsis-related inflammatory mediators on Ang-2 production by lung endothelium in vitro. DESIGN: Prospective clinical study followed by cell culture studies. SETTING: General intensive care unit and research laboratory of a university hospital. SUBJECTS: Human and bovine lung microvascular endothelial cells and 61 patients (32 men). Patients were grouped according to their septic stage as having: no systemic inflammatory response syndrome (n = 6), systemic inflammatory response syndrome (n = 8), sepsis (n = 16), severe sepsis (n = 18), and septic shock (n = 13). INTERVENTIONS: Cells were exposed to lipopolysaccharide, tumor necrosis factor-alpha, and interleukin-6. MEASUREMENTS AND MAIN RESULTS: Patients' serum Ang-2 levels were significantly increased in severe sepsis as compared with patients with no systemic inflammatory response syndrome or sepsis (p < .05 by analysis of variance). Positive linear relationships were observed with: serum tumor necrosis factor-alpha (rs = 0.654, p < .001), serum interleukin-6 (rs = 0.464, p < .001), Acute Physiology and Chronic Health Evaluation II score (rs = 0.387, p < .001), and Sequential Organ Failure Assessment score (rs = 0.428, p < .001). Multiple regression analysis revealed that serum Ang-2 is mostly related to serum tumor necrosis factor-alpha and severe sepsis. Treatment of human lung microvascular endothelial cells with all mediators resulted in a concentration-dependent Ang-2 reduction. Treatment of bovine lung microvascular endothelial cells with lipopolysaccharide and tumor necrosis factor-alpha increased Ang-2 release, and interleukin-6 reduced basal Ang-2 levels. CONCLUSIONS: First, patients' serum Ang-2 levels are increased during severe sepsis and associated with disease severity. The strong relationship of serum Ang-2 with serum tumor necrosis factor-alpha suggests that the latter may participate in the regulation of Ang-2 production in sepsis. Second, inflammatory mediators reduce Ang-2 release from human lung microvascular endothelial cells, implying that this vascular bed may not be the source of increased Ang-2 in human sepsis.

APACHE↗
PubMed2006

Pituitary-adrenal responses to human corticotropin-releasing hormone in critically ill patients.

OBJECTIVE: To investigate the pattern of pituitary-adrenal responses to human corticotropin-releasing hormone (hCRH) in critically ill patients and to examine the relation between responses and clinical outcome. DESIGN AND SETTING: Prospective study in consecutive critically ill patients in a general intensive care unit in a teaching hospital. PATIENTS: The study included 37 critically ill, mechanically ventilated patients with diverse underlying diagnoses (28 men, 9 women; median age 56 years). INTERVENTIONS: A morning blood sample was obtained to measure baseline cortisol, corticotropin (ACTH), and cytokines. Patients were then injected with 100 microg hCRH, and plasma cortisol and ACTH were measured over a period of 2 h. MEASUREMENTS AND RESULTS: In the overall patient population baseline and peak cortisol concentrations following hCRH were 16+/-5 and 21+/-5 microg/dl, respectively, and median baseline and peak ACTH levels 23 and 65 pg/ml, respectively. Higher ACTH levels and longer release of cortisol were noted in nonsurvivors (n=18) than in survivors (n=19). Furthermore, nonsurvivors had higher concentrations of interleukin 8 (115 vs. 38 pg/ml) and interleukin 6 (200 vs. 128 pg/ml) than survivors. CONCLUSIONS: Critically ill patients demonstrate altered pituitary-adrenal axis responses to hCRH. This is particularly evident in the sickest patients with the highest degree of inflammatory profile who ultimately do not survive.

Adolescent↗
PubMed2006

Successful resuscitation with thrombolysis of a patient suffering fulminant pulmonary embolism after recent intracerebral haemorrhage.

We report the life-saving administration of thrombolysis during cardiopulmonary resuscitation in a patient with recent intracerebral haemorrhage. A 53-year-old male with intracerebral haemorrhage was admitted to the intensive care unit. On the 24th day of treatment he suffered cardiac arrest with pulseless electrical activity. Transoesophageal echocardiography was performed during ongoing cardiopulmonary resuscitation. Thrombi in the right heart cavities with excessive right ventricular dysfunction confirmed the diagnosis of fulminant pulmonary embolism. Permanent restoration of a spontaneous rhythm was feasible only after administration of systemic thrombolysis with recombinant tissue plasminogen activator. Neurological examination and a computed tomogram of the brain did not show rebleeding. We conclude that under extreme circumstances absolute contraindications to thrombolysis should be weighed against the potential benefit.

Acute Disease↗
PubMed2006

Respiratory mechanics in brain-damaged patients.

OBJECTIVE: To assess respiratory mechanics on the 1st and 5th days of mechanical ventilation in a cohort of brain-damaged patients on positive end-expiratory pressure (PEEP) of 8 cmH(2)O or zero PEEP (ZEEP). DESIGN AND SETTING: Physiological study with randomized control trial design in a multidisciplinary intensive care unit of a university hospital. PATIENTS AND MEASUREMENTS: Twenty-one consecutive mechanically ventilated patients with severe brain damage and no acute lung injury were randomly assigned to be ventilated with ZEEP (n = 10) or with 8 cmH(2)O of PEEP (n = 11). Respiratory mechanics and arterial blood gases were assessed on days 1 and day 5 of mechanical ventilation. RESULTS: In the ZEEP group on day 1 static elastance and minimal resistance were above normal limits (18.9 +/- 3.8 cmH(2)O/l and 5.6 +/- 2.2 cmH(2)O/l per second, respectively); on day 5 static elastance and iso-CO(2) minimal resistance values were higher than on day 1 (21.2 +/- 4.1 cmH(2)O/l; 7.0 +/- 1.9 cmH(2)O/l per second, respectively). In the PEEP group these parameters did not change significantly. One of the ten patients on ZEEP developed acute lung injury. On day 5 there was a significant decrease in PaO(2)/FIO(2) in both groups. CONCLUSIONS: On day 1 of mechanical ventilation patients with brain damage exhibit abnormal respiratory mechanics. After 5 days of mechanical ventilation on ZEEP static elastance and minimal resistance increased significantly, perhaps reflecting "low lung volume" injury. Both could be prevented by administration of moderate levels of PEEP.

Adult↗
PubMed2006

Kinetics of progenitor hemopoetic stem cells in sepsis: correlation with patients survival?

BACKGROUND: Current theories underline the crucial role of pro-inflammatory mediators produced by monocytes for the pathogenesis of sepsis. Since monocytes derive from progenitor hemopoetic cells, the kinetics of stem cells was studied in peripheral blood of patients with sepsis. METHODS: Blood was sampled from 44 patients with septic syndrome due to ventilator-associated pneumonia on days 1, 3, 5 and 7 upon initiation of symptoms. Concentrations of tumour necrosis factor-alpha (TNFalpha), interleukin (IL)-6, IL-8 and G-CSF were estimated by ELISA. CD34/CD45 cells were determined after incubation with anti-CD45 FITC and anti-CD34 PE monocloncal antibodies and flow cytometric analysis. Samples from eight healthy volunteers served as controls. RESULTS: Median of CD34/CD45 absolute count of controls was 1.0/mul. Respective values of the total study population were 123.4, 112.4, 121.5 and 120.9/mul on days 1, 3, 5 and 7 (p < 0.0001 compared to controls). Positive correlations were found between the absolute CD34/CD45 count and the absolute monocyte count on days 1, 5 and 7. Survival was prolonged among patients with less than 310/microl CD34/CD45 cells on day 1 compared to those with more than 310/microl of CD34/CD45 cells (p: 0.022). Hazard ratio for death due to sepsis was 5.47 (p: 0.039) for CD34/CD45 cells more than 310/microl. Median IL-6 on day 1 was 56.78 and 233.85 pg/ml respectively for patients with less than 310/microl and more than 310/microl CD34/CD45 cells (p: 0.021). CONCLUSION: Stem cells are increased in peripheral blood over all days of follow-up compared to healthy volunteers. Patients with counts on day 1 less than 310/microl are accompanied by increased survival compared to patients with more than 310/microl.

Adult↗
PubMed2006

Antioxidants increase the ventilatory response to hyperoxic hypercapnia.

RATIONALE: The mechanisms by which chemoreceptors process carbon dioxide stimuli are poorly understood. Recent in vitro studies suggest a role of reactive oxygen species in central carbon dioxide chemoreception. OBJECTIVES: We tested the hypothesis that antioxidant treatment modulates the ventilatory response to carbon dioxide in healthy humans, either during unloaded breathing or after strenuous resistive breathing. METHODS: In the first experiment of this randomized, double-blind, placebo-controlled study, 14 healthy males completed hyperoxic carbon dioxide rebreathing, received either antioxidants (vitamins E, A, and C for 2 mo, allopurinol for 15 d, and N-acetylcysteine for 3 d) (n = 7) or placebo (n = 7), and repeated rebreathing 3 mo later. In the second experiment, 18 healthy males completed a series of rebreathing tests before and after strenuous resistive breathing. Subjects repeated the same protocol 3 mo later, after they had received antioxidants (n = 9) or placebo (n = 9). MAIN RESULTS: After antioxidants, the sensitivity of the ventilatory (minute ventilation) response to carbon dioxide increased (mean [+/- SEM], 3.2 +/- 0.5 vs. 1.7 +/- 0.4 L/min/mm Hg; p < 0.001). Antioxidants also increased the sensitivity to carbon dioxide before and at 5, 30, and 120 min after resistive breathing (p = 0.01). This effect was entirely due to increased tidal volume. Antioxidants did not influence the breathing pattern during resting breathing or the rapid shallow breathing response to carbon dioxide at 5 min after resistive breathing. CONCLUSIONS: Antioxidants, by augmenting the tidal volume, increase the sensitivity of the ventilatory response to carbon dioxide, either during unloaded breathing or after resistive breathing.

Adult↗
PubMed2006

Pulmonary function at peak exercise in patients with chronic heart failure.

BACKGROUND: Various respiratory abnormalities are associated with chronic heart failure (CHF). However, changes in inspiratory capacity (IC) and breathing pattern from rest to exercise in patients with CHF have not been thoroughly investigated in these patients. MATERIALS AND METHODS: Seventy seven (66 male/11 female) patients with clinical stable CHF (age: 52+/-11 years) were studied. All the patients underwent pulmonary function tests, including measurements of IC and maximal inspiratory pressure (Pimax) at rest and then a maximal cardiopulmonary exercise testing (CPET) on a treadmill. During the CPET, IC was measured every 2 min. Pimax was measured again after the end of CPET. RESULTS: Percent predicted forced expiratory volume in 1 s (FEV1) was 91+/-12, %predicted forced vital capacity (FVC) was 92+/-13, %FEV1/FVC was 81+/-4, and %predicted IC was 85+/-18. Peak exercise IC was lower than resting (2.4+/-0.6 vs. 2.6+/-0.6 l, p<0.001). Analysis of variance between Weber's groups revealed statistically significant differences in peak exercise IC (p<0.001), VE/VCO2slope (p<0.001), resting Pimax (p=0.005) and post-exercise Pimax (p<0.001). At rest, there was a statistically significant difference in end-tidal CO2 (P(ETCO2)) (p=0.002), in breathing frequency (p=0.004), in inspiratory time (Ti) (p=0.04) and in total respiratory time (T(Tot)) (p=0.004) among Weber's groups. At peak exercise there was a statistically significant decrease in minute ventilation (VE) (p<0.001), tidal volume (VT) (p<0.001), respiratory cycle (VT/TI) (p<0.001) and P(ETCO2) (p<0.001). Peak IC was correlated with peak VO2 (r=0.72, p<0.001), anaerobic threshold (r=0.71, p<0.001), VO2/t slope (r=0.54, p<0.0001), and post-exercise Pimax (r=0.62, p<0.001). CONCLUSIONS: In patients with CHF, peak exercise IC is reduced in parallel with disease severity, which is probably due to respiratory muscle dysfunction.

Anaerobic Threshold↗
PubMed2006

Inhaled activated protein C attenuates lung injury induced by aerosolized endotoxin in mice.

The serine protease activated protein C (APC) possesses prominent anticoagulant and anti-inflammatory actions. In this study, we investigated the effect of inhaled recombinant human (rh) APC in a murine lung injury model. Animals inhaled 10 mg of Pseudomonas lipopolysaccharide (LPS) in 3 mL normal saline (NS); 30 min prior to LPS, mice were pretreated with inhaled rhAPC (4 mg/3 mL NS; APC+LPS group) or NS (LPS group). A control animal group inhaled vehicle (NS) twice. 24 h later, total cells and cell-types, protein content, and the cytokines tumor necrosis factor-alpha, interleukin (IL)-6, macrophage inflammatory protein-1alpha, and mouse keratinocyte-derived chemokine (a homolog of human IL-8) were estimated in bronchoalveolar lavage fluid (BALF). Lung pathology given as total histology score (THS), wet/dry lung weight ratios, and lung vascular cell adhesion molecule (VCAM)-1 expression were additionally assessed. rhAPC inhalation attenuated the aerosolized LPS-induced increases of: total cells, neutrophils and macrophages in BALF, lung tissue VCAM-1 protein levels, and THS. Total protein levels and cytokines in BALF, and wet/dry weight ratios were increased in the LPS group, but rhAPC pretreatment did not significantly alter the LPS-induced responses. In conclusion, in this murine septic model of lung injury, inhaled rhAPC appears to attenuate lung inflammation, without reversing the observed increases in lung permeability and BALF cytokines. This effect may be associated with leukocyte trafficking modifications, related, at least in part, to VCAM-1 reduction.

Administration, Inhalation↗
PubMed2006

Vascular endothelial growth factor levels in post-CABG pleural effusions are associated with pleural inflammation and permeability.

BACKGROUND: Vascular endothelial growth factor (VEGF) participates in the pathogenesis of exudative pleural effusions (PEs). In the present study, we determined the pleural fluid (PF) and serum VEGF levels in patients with post-coronary artery by-pass grafting (post-CABG) PEs. METHODS: Thirty-eight patients with post-CABG (two with bilateral) PEs were studied. PEs were divided into "early" (occurring earlier than 30 days after surgery) and "late" ones. VEGF levels were measured using ELISA. RESULTS: (i) Serum and PF VEGF levels did not differ significantly when all the patients (P=0.053) or those with late effusions (P=0.6) were analyzed; serum VEGF levels were significantly elevated in comparison to PF VEGF levels in patients with early (P=0.007) effusions. (ii) Serum VEGF levels were significantly higher in patients with early than in those with late effusions (P=0.033), while PF VEGF levels were not significantly different between the two groups (P=0.77). (iii) PF VEGF levels were higher than corresponding serum levels in 4/24 patients with early and in 10/16 patients with late post-CABG PEs (P=0.006). (iv) In PEs VEGF levels significantly correlated with red blood cells (P=0.015), nucleated cells (P=0.003), protein levels (P=0.002) and lactate dehydrogenase (LDH) levels (P=0.04). CONCLUSION: In post-CABG PEs, preferential local production of VEGF in the pleural cavity is most commonly observed a month or later after surgery. The fact that in PEs VEGF levels correlate with markers of pleural inflammation (inflammatory cells and LDH levels) and vascular hyperpermeability (protein levels) suggests that VEGF may be involved in the pathogenesis of post-CABG PEs.

Cell Count↗
PubMed2006

Extranodal marginal zone B-cell lymphoma of the lung in Sjögren's syndrome patients: reappraisal of clinical, radiological, and pathology findings.

BACKGROUND: Primary Sjögren's syndrome (pSs) is an autoimmune rheumatic disease that may express in a small number of patients a spectrum of lymphoproliferative diseases. The aim of this study was to describe clinical, imaging and pathology features of the extranodal marginal zone B-cell lymphoma (MZCL) of the lung of mucosa-associated lymphoid tissue (MALT) type in patients with pSs. METHODS: All patients (N=10) with biopsy proven MZCL of the lung of MALT type diagnosed in a tertiary teaching hospital during the last 7 years were studied. RESULTS: Seven patients had pSs. Almost all patients presented an indolent clinical course, contrasting strongly with the spectacular radiological findings in both chest roentgenograms and computed tomography. Pathology infiltration patterns observed were either nodular, peribronchial-perivascular, alveolar, or interstitial. Immunohistochemical study in all cases showed B cell phenotypes. Immunoglobulin light chain restriction was demonstrated in all patients. Monoclonal IgM(kappa) was evident in 5/7, IgM(lambda) in 1/7 and IgG (kappa) in 1/7 of patients. CONCLUSIONS: Lung MZCL associated with pSs are characterized by an important dissociation between clinical expression and radiological pattern. Clinical presentation and imaging features are not specific. Therefore, histologic documentation is mandatory to ensure diagnosis. Various chemotherapeutic agents in combination with rituximab lead to partial or complete remission in the majority of patients.

B-Lymphocytes↗
PubMed2006

Early apoptosis of blood monocytes in the septic host: is it a mechanism of protection in the event of septic shock?

INTRODUCTION: Based on the central role of the triggering of monocytes for the initiation of the septic cascade, it was investigated whether apoptosis of blood monocytes in septic patients is connected to their final outcome. METHODS: Blood monocytes were isolated from 90 patients with septic syndrome due to ventilator-associated pneumonia on days 1, 3, 5 and 7 from the initiation of symptoms. Apoptosis was defined after incubation with annexin-V-fluorescein isothiocyanate and propidium iodine and reading by a flow cytometer. The function of first-day monocytes was evaluated from the concentrations of tumour necrosis factor alpha (TNFalpha) and IL-6 in supernatants of cell cultures after triggering with endotoxins. TNFalpha, IL-6 and IL-8 were estimated in serum by an enzyme immunoassay. RESULTS: Mortality rates of patients with apoptosis < or =50% compared with patients with apoptosis >50% were 49.12% and 15.15%, respectively (P < 0.0001). Kaplan-Meier analysis showed a 28-day survival benefit in patients with septic shock and monocyte apoptosis >50% compared with those patients with apoptosis < or =50% (P = 0.0032). Production of IL-6 by monocytes on the first day by patients with apoptosis < or =50% was similar compared with monocytes isolated from healthy controls. Serum concentrations of TNFalpha were higher in patients with monocyte apoptosis < or =50% and septic shock compared with patients with apoptosis >50% on day 7; similar findings occurred for serum IL-6 on days 1 and 7 and for serum IL-8 on days 1 and 5. CONCLUSION: Early apoptosis of monocytes upon presentation of clinical signs of sepsis is connected to a favourable outcome. These findings are of particular importance for the patient with septic shock, where they might constitute a mechanism of pathogenesis.

Adult↗
PubMed2006

The combination of the load/force balance and the frequency/tidal volume can predict weaning outcome.

OBJECTIVE: To examine whether an appropriately designed combination of an index of ventilatory endurance and the frequency divided by tidal volume ratio (f/VT) provides prognostic information for weaning outcome not offered by any index alone. DESIGN AND SETTING: Prospective study in a multidisciplinary intensive care unit, university hospital. PATIENTS: 124 consecutive mechanically ventilated patients. INTERVENTIONS: We designed an index of ventilatory endurance (load/force balance) calculated as the mean inspiratory airway pressure (PI) during controlled mechanical ventilation/maximum inspiratory pressure (MIP) [PI equals the triplicate of mean airway pressure (Paw) displayed by the ventilator] and tested its capacity in predicting weaning outcome at 48 h along with f/VT and many other indices in 75 consecutive mechanically ventilated patients ready to wean. A stepwise discriminant function analysis was used to test the performance of appropriately designed index combination. Threshold values of indices and their combination were prospectively validated in another group of 45 consecutive patients. RESULTS: Stepwise discriminant analysis showed that PI/MIP and f/VT were the only indices that remained in the model with the function D=7.628xmean Paw/MIP+0.0158xf/VT-2.374. The cutoff point of D=0.5 had 94% sensitivity, 67% specificity, and 87% correct classifications. Prospective validation demonstrated similar results. The simplified discriminant function D=15xmean Paw/MIP+0.003xf/VT-5 and the cut-off point of D=1.0 had 89% sensitivity, 67% specificity, and 85% correct classifications. CONCLUSIONS: The combination of mean Paw/MIP and f/VT in a simplified discriminant function is useful in predicting weaning outcome.

Female↗
PubMed2006

Soluble triggering receptor expressed on myeloid cells 1 as an anti-inflammatory mediator in sepsis.

OBJECTIVE: To define the significance of soluble triggering receptor expressed on myeloid cells 1 (sTREM-1) in the septic cascade by comparing its kinetics to those of other proinflammatory mediators and of interleukin (IL) 10. DESIGN: Prospective study in a tertiary unit. PATIENTS: Blood was sampled from 90 patients with septic syndrome due to ventilator-associated pneumonia for 7 days after the appearance of symptoms. Concentrations of tumor necrosis factor (TNF) alpha, IL-6, IL-8, IL-10, and sTREM-1 were determined by enzyme-linked immunosorbent assay. RESULTS: Serum levels of TNFalpha, IL-6, IL-10, and sTREM-1 were higher in nonsurvivors than in survivors; similar differences were not found for IL-8. Positive correlations were found between the ratios IL-10/TNFalpha and sTREM-1/TNFalpha, between IL-10/IL-6 and sTREM-1/IL-6, and between IL-10/IL-8 and sTREM-1/IL-8. Median values of IL-10/TNFalpha upon presentation of sepsis, severe sepsis, and septic shock were 3.21, 2.16, and 2.86, respectively (NS). Respective values for sTREM-1/TNFalpha were 21.28, 7.33, and 27.78 (p=0.047 between sepsis and severe sepsis, p=0.003 between severe sepsis and septic shock). CONCLUSIONS: sTREM-1 follows the kinetics of IL-10 and should therefore be considered an anti-inflammatory mediator in sepsis. Decreased ratios of sTREM-1/TNFalpha might determine transition from sepsis to severe sepsis and from severe sepsis to septic shock.

Aged↗
PubMed2006

Effects of exercise-induced arterial hypoxaemia and work rate on diaphragmatic fatigue in highly trained endurance athletes.

Diaphragmatic fatigue occurs in highly trained athletes during exhaustive exercise. Since approximately half of them also exhibit exercise-induced arterial hypoxaemia (EIAH) during high-intensity exercise, the present study sought to test the hypothesis that arterial hypoxaemia contributes to exercise-induced diaphragmatic fatigue in this population. Ten cyclists ( : 70.0 +/- 1.6 ml kg(-1) min(-1); mean +/-s.e.m.) completed, in a balanced ordering sequence, one normoxic (end-exercise arterial O(2) saturation (S(a,O(2))): 92 +/- 1%) and one hyperoxic (F(I,O(2)): 0.5% O(2); S(a,O(2)) : 97 +/- 1%) 5 min exercise test at intensities equal to 80 +/- 3 and 90 +/- 3% of maximal work rate (WR(max)), respectively, producing the same tidal volume (V(T)) and breathing frequency (f) throughout exercise. Cervical magnetic stimulation was used to determine reduction in twitch transdiaphragmatic pressure (P(di,tw)) during recovery. Hyperoxic exercise at 90% WR(max) induced significantly (P= 0.022) greater post-exercise reduction in P(di,tw) (15 +/- 2%) than did normoxic exercise at 80% WR(max) (9 +/- 2%), despite the similar mean ventilation (123 +/- 8 and 119 +/- 8 l min(-1), respectively), breathing pattern (V(T): 2.53 +/- 0.05 and 2.61 +/- 0.05 l, f: 49 +/- 2 and 46 +/- 2 breaths min(-1), respectively), mean changes in P(di) during exercise (37.1 +/- 2.4 and 38.2 +/- 2.8 cmH(2)O, respectively) and end-exercise arterial lactate (12.1 +/- 1.4 and 10.8 +/- 1.1 mmol l(-1), respectively). The difference found in diaphragmatic fatigue between the hyperoxic (at higher leg work rate) and the normoxic (at lower leg work rate) tests suggests that neither EIAH nor lactic acidosis per se are likely predominant causative factors in diaphragmatic fatigue in this population, at least at the level of S(a,O(2)) tested. Rather, this result leads us to hypothesize that blood flow competition with the legs is an important contributor to diaphragmatic fatigue in heavy exercise, assuming that higher leg work required greater leg blood flow.

Adult↗
PubMed2006

Effect of percutaneous endoscopic gastrostomy on gastro-esophageal reflux in mechanically-ventilated patients.

AIM: To investigate the effect of percutaneous endoscopic gastrostomy (PEG) on gastroesophageal reflux (GER) in mechanically-ventilated patients. METHODS: In a prospective, randomized, controlled study 36 patients with recurrent or persistent ventilator-associated pneumonia (VAP) and GER > 6% were divided into PEG group (n = 16) or non-PEG group (n = 20). Another 11 ventilated patients without reflux (GER < 3%) served as control group. Esophageal pH-metry was performed by the "pull through" method at baseline, 2 and 7 d after PEG. Patients were strictly followed up for semi-recumbent position and control of gastric nutrient residue. RESULTS: A significant decrease of median (range) reflux was observed in PEG group from 7.8 (6.2 - 15.6) at baseline to 2.7 (0 - 10.4) on d 7 post-gastrostomy (P < 0.01), while the reflux increased from 9 (6.2 - 22) to 10.8 (6.3 - 36.6) (P < 0.01) in non-PEG group. A significant correlation between GER (%) and the stay of nasogastric tube was detected (r = 0.56, P < 0.01). CONCLUSION: Gastrostomy when combined with semi-recumbent position and absence of nutrient gastric residue reduces the gastroesophageal reflux in ventilated patients.

Adult↗