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S Zakynthinos

Publications and source records attributed to S Zakynthinos.

At least 19 recordsLinked to original sources
PubMed2006

Oxygen kinetics and debt during recovery from expiratory flow-limited exercise in healthy humans.

In healthy subjects expiratory flow limitation (EFL) during exercise can lower O(2) delivery to the working muscles. We hypothesized that if this affects exercise performance it should influence O(2) kinetics at the end of exercise when the O(2) debt is repaid. We performed an incremental exercise test on six healthy males with a Starling resistor in the expiratory line limiting expiratory flow to approximately 1 l s(-1) to determine maximal EFL exercise workload (W (max)). In two more square-wave exercise runs subjects exercised with and without EFL at W (max) for 6 min, while measuring arterial O(2) saturation (% SaO(2)), end-tidal pressure of CO(2) (P (ET)CO(2)) and breath-by-breath O(2) consumption VO2 taking into account changes in O(2) stored in the lungs. Over the last minute of EFL exercise, mean P (ET)CO(2) (54.7 +/- 9.9 mmHg) was significantly higher (P < 0.05) compared to control (41.4 +/- 3.9 mmHg). At the end of EFL exercise %SaO(2) fell significantly by 4 +/- 3%. When exercise stopped, EFL was removed, and we continued to measure VO2. During recovery, there was an immediate step increase in [Formula: see text] so that repayment of EFL O(2) debt started at a higher VO2 than control. Recovery VO2 kinetics after EFL exercise was best characterized by a double-exponential function with fundamental and slow time constants of 27 +/- 11 and 1,020 +/- 305 s, compared to control values of 41 +/- 10 and 1,358 +/- 320 s, respectively. EFL O(2) debt was 52 +/- 22% greater than control (2.19 +/- 0.58 vs. 1.49 +/- 0.38 l). We conclude that EFL exercise increases the O(2) debt and leads to hypoxemia in part due to hypercapnia.

Carbon Dioxide↗
PubMed2006

Effects of rehabilitation on chest wall volume regulation during exercise in COPD patients.

In order to investigate underlying mechanisms, the present authors studied the effect of pulmonary rehabilitation on the regulation of total chest wall and compartmental (ribcage, abdominal) volumes during exercise in patients with chronic obstructive pulmonary disease. In total, 20 patients (forced expiratory volume in one second, mean +/- SEM 39 +/- 3% predicted) undertook high-intensity exercise 3 days x week(-1) for 12 weeks. Before and after rehabilitation, the changes in chest wall (cw) volumes at the end of expiration (EEV) and inspiration (EIV) were computed by optoelectronic plethysmography during incremental exercise to the limit of tolerance (W(peak)). Rehabilitation significantly improved W(peak) (57+/-7 versus 47+/-5 W). In the post-rehabilitation period and at identical work rates, significant reductions were observed in minute ventilation (35.1+/-2.7 versus 38.4+/-2.7 L x min(-1)), breathing frequency (26+/-1 versus 29+/-1 breaths x min(-1)) and EEV(cw) and EIV(cw) (by 182+/-79 and 136+/-37 mL, respectively). Inspiratory reserve volume was significantly increased (by 148+/-70 mL). Volume reductions were attributed to significant changes in abdominal EEV and EIV (by 163+/-59 and 125+/-27 mL, respectively). The improvement in W(peak) was similar in patients who progressively hyperinflated during exercise and those who did not (24 and 26%, respectively). In conclusion, pulmonary rehabilitation lowers chest wall volumes during exercise by decreasing the abdominal volumes. The improvement in exercise capacity following rehabilitation is independent of the pattern of exercise-induced dynamic hyperinflation.

Aged↗
PubMed2006

Obstructive sleep apnoea and oral breathing in patients free of nasal obstruction.

Although there is an association between nasal obstruction, oral breathing and obstructive sleep apnoea syndrome (OSAS), it remains unknown whether increased oral breathing occurs in patients with OSAS who are free of nasal obstruction. The present study evaluated the relationship between breathing route and OSAS in patients without nasal obstruction. The breathing route of 41 snorers (25 male; aged 26-77 yrs) with normal nasal resistance was examined during overnight polysomnography using a nasal cannula/pressure transducer and an oral thermistor. In total, 28 patients had OSAS (apnoeics) and 13 patients were simple snorers. Apnoeics had a higher percentage of oral and oro-nasal breathing epochs. Oral and oro-nasal breathing epochs were positively related with apnoea/hypopnoea index (AHI) and duration of apnoeas/hypopnoeas and inversely related to oxygen saturation. Additionally, oro-nasal breathing epochs correlated with body mass index (BMI). In multiple linear regression analysis, oral breathing epochs were independently related only to AHI (r2 = 0.443), and oro-nasal breathing epochs were independently related to AHI (r2 = 0.736) and BMI (r2 = 0.036). In conclusion, apnoeics spent more time breathing orally and oro-nasally than simple snorers, and the apnoea/hypopnoea index is a major determinant of the time spent breathing orally and oro-nasally.

Body Mass Index↗
PubMed2005

Patterns of dynamic hyperinflation during exercise and recovery in patients with severe chronic obstructive pulmonary disease.

BACKGROUND: Not all patients with severe chronic obstructive pulmonary disease (COPD) progressively hyperinflate during symptom limited exercise. The pattern of change in chest wall volumes (Vcw) was investigated in patients with severe COPD who progressively hyperinflate during exercise and those who do not. METHODS: Twenty patients with forced expiratory volume in 1 second (FEV(1)) 35 (2)% predicted were studied during a ramp incremental cycling test to the limit of tolerance (Wpeak). Changes in Vcw at the end of expiration (EEVcw), end of inspiration (EIVcw), and at total lung capacity (TLCVcw) were computed by optoelectronic plethysmography (OEP) during exercise and recovery. RESULTS: Two significantly different patterns of change in EEVcw were observed during exercise. Twelve patients had a progressive significant increase in EEVcw during exercise (early hyperinflators, EH) amounting to 750 (90) ml at Wpeak. In contrast, in all eight remaining patients EEVcw remained unchanged up to 66% Wpeak but increased significantly by 210 (80) ml at Wpeak (late hyperinflators, LH). Although at the limit of tolerance the increase in EEVcw was significantly greater in EH, both groups reached similar Wpeak and breathed with a tidal EIVcw that closely approached TLCVcw (EIVcw/TLCVcw 93 (1)% and 93 (3)%, respectively). EEVcw was increased by 254 (130) ml above baseline 3 minutes after exercise only in EH. CONCLUSIONS: Patients with severe COPD exhibit two patterns during exercise: early and late hyperinflation. In those who hyperinflate early, it may take several minutes before the hyperinflation is fully reversed after termination of exercise.

Exercise↗
PubMed2005

Respiratory muscle performance with stretch-shortening cycle manoeuvres: maximal inspiratory pressure-flow curves.

AIM: To test the hypothesis that the maximal inspiratory muscle (IM) performance, as assessed by the maximal IM pressure-flow relationship, is enhanced with the stretch-shortening cycle (SSC). METHODS: Maximal inspiratory flow-pressure curves were measured in 12 healthy volunteers (35 +/- 6 years) during maximal single efforts through a range of graded resistors (4-, 6-, and 8-mm diameter orifices), against an occluded airway, and with a minimal load (wide-open resistor). Maximal inspiratory efforts were initiated at a volume near residual lung volume (RV). The subjects exhaled to RV using slow (S) or fast (F) manoeuvres. With the S manoeuvre, they exhaled slowly to RV and held the breath at RV for about 4 s prior to maximal inspiration. With the F manoeuvre, they exhaled rapidly to RV and immediately inhaled maximally without a post-expiratory hold; a strategy designed to enhance inspiratory pressure via the SSC. RESULTS: The maximal inspiratory pressure-flow relationship was linear with the S and F manoeuvres (r2 = 0.88 for S and r2 = 0.88 for F manoeuvre, P < 0.0005 in all subjects). With the F manoeuvre, the pressure-flow relationship shifted to the right in a parallel fashion and the calculated maximal power increased by approximately 10% (P < 0.05) over that calculated with the S manoeuvre. CONCLUSION: The maximal inspiratory pressure-flow capacity can be enhanced with SSC manoeuvres in a manner analogous to increases in the force-velocity relationship with SSC reported for skeletal muscles.

Adult↗
PubMed2005

Does soluble triggering receptor expressed on myeloid cells-1 play any role in the pathogenesis of septic shock?

In order to define the significance of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) upon progression from sepsis or severe sepsis to septic shock a prospective study was designed with 90 enrolled patients with septic syndrome due to ventilator-associated pneumonia. Blood was sampled on seven consecutive days upon initiation of symptoms and concentrations of tumour necrosis factor-alpha (TNFalpha), interleukin-6 (IL-6), IL-8 and sTREM-1 were estimated in serum by an enzymeimmunoassay. No differences in concentrations of TNFalpha, IL-6 and IL-8 were found between patients with sepsis, severe sepsis and septic shock on the first day of presentation of symptoms. Patients presenting with septic shock had concentrations of sTREM-1 significantly higher than both patients with sepsis and severe sepsis on the first day; no difference was found between patients with sepsis and severe sepsis. A positive correlation was detected between sTREM-1 and the white blood cell count. Serum levels of sTREM-1 were significantly lower in patients where VAP resolved compared to those where VAP did not resolve; similar findings were noted between patients who eventually survived and those who died. IL-6 followed the kinetics of sTREM-1 in correlation to patients's prognosis; levels of TNFalpha and IL-8 were unrelated to prognosis. It is concluded that sTREM-1 is particularly increased upon evolution from sepsis or severe sepsis to septic shock. Its sustained increase is an indication of poor outcome. The underlined pathophysiological role of sTREM-1 for the transition from sepsis or severe sepsis to septic shock might constitute a novel target for immunomodulatory therapy.

Aged↗
PubMed2004

The immune response to resistive breathing.

Resistive breathing is an "immune challenge" for the body, initiating an inflammatory response consisting of an elevation of plasma cytokines, and the recruitment and activation of lymphocyte subpopulations. These cytokines do not originate from monocytes, but are, instead, produced within the diaphragm, secondary to the increased muscle activation. Oxidative stress is a major stimulus for the cytokine induction, secondary to resistive breathing. The production of cytokines within the diaphragm may be mediating the diaphragm muscle fibre injury that occurs with strenuous contractions, or contributing towards the expected repair process. These cytokines may also compromise diaphragmatic contractility or contribute towards the development of muscle cachexia. They may also have systemic effects, mobilising glucose from the liver and free fatty acid from the adipose tissue to the strenuously working respiratory muscles. At the same time, they stimulate the hypothalamic-pituitary-adrenal axis, leading to production of adrenocorticotropin and beta-endorphins. The adrenocorticotropin response may represent an attempt of the organism to reduce the injury occurring in the respiratory muscles via the production of glucocorticoids and the induction of the acute phase-response proteins. The beta-endorphin response would decrease the activation of the respiratory muscles and change the pattern of breathing, which becomes more rapid and shallow, possibly in an attempt to reduce and/or prevent further injury to the respiratory muscles.

Airway Resistance↗
PubMed2001

Diagnostic and prognostic significance of squamous cell carcinoma antigen in non-small cell lung cancer.

Squamous cell carcinoma antigen (SCC-Ag) is a glycoprotein secreted by non-small cell lung tumours (NSCLC). This study investigated the diagnostic and prognostic significance of SCC-Ag in NSCLC. Receiver operating characteristic (ROC) curve analysis was used to test the diagnostic performance of the SCC-Ag and determine the optimal threshold value in a group of 100 NSCLC patients undergoing surgery and 50 age matched healthy controls. This threshold was then prospectively validated in a group of 53 patients and 49 healthy controls. The prognostic significance of the preoperative SCC-Ag level and its postoperative decrease were tested using univariate and multivariate proportional hazard models. The area under the ROC curve was 0.71+/-0.04, and the best cutoff value was 1.4 ng/ml. This discriminated patients in the validation group, with a sensitivity of 0.55 and a specificity of 1.0. The hazard ratio was 0.144 (95% CI 0.074-0.281) for the postoperative decrease in the SCC Ag, and 5.823 (3.299-10.278) for the preoperative SCC Ag level. Multivariate analysis revealed that only disease stage and patients' age are strong prognostic factors for survival. In conclusion, the SCC-Ag serum level has moderate diagnostic role in NSCLC. Both the preoperative SCC-Ag level and its postoperative decrease have prognostic significance, yet inferior to the disease stage and the patient's age.

Adenocarcinoma↗
PubMed2001

The potential role of abnormal E-cadherin and alpha-, beta- and gamma-catenin immunoreactivity in the determination of the biological behaviour of keratoacanthoma.

BACKGROUND: Failure of E-cadherin and its associated proteins alpha-, beta- and gamma-catenin is believed to lead to disruption of cell-cell adhesion and to contribute to neoplasia. OBJECTIVES: To determine the pattern of E-cadherin and alpha-, beta- and gamma-catenin immunostaining in keratoacanthoma (KA) and to evaluate its potential value in routine histopathology in differentiating KA with benign from that with malignant biological behaviour. METHODS: We examined the expression of E-cadherin and alpha-, beta- and gamma-catenin in KA and correlated the histopathological features with the immunohistochemical findings. Next, we compared the immunohistochemical findings of KA with those found in malignant (squamous cell carcinoma, SCC) and benign (warts) lesions. In addition to the established histopathological criteria we used the Ki-67 index, a well-known marker of cell proliferation. Immunoperoxidase staining of E-cadherin and alpha-, beta- and gamma-catenin, and Ki-67 determination, were performed in paraffin-embedded sections of 12 KAs taken from archival material. On reviewing the histology, seven of the 12 KAs were characterized as 'classical' KA, and the rest as 'borderline' KA or KA resembling SCC. Additionally, 28 well, nine moderately and five poorly differentiated SCCs and 20 warts were examined. RESULTS: Most 'classical' KAs (79-86%) showed normal membranous immunostaining and a low Ki-67 index. The remaining 'classical' KAs showed abnormal expression, in a staining pattern resembling that of well-differentiated SCC. All 'borderline' KAs showed a high Ki-67 index (> 40%) and abnormal expression of the adhesion molecules studied, identical to that of poorly differentiated SCC. Expression of E-cadherin and alpha-, beta- and gamma-catenin was found to be more frequently abnormal in 'borderline' KA compared with that in 'classical' KA (P < 0.05). Among E-cadherin and alpha-, beta- and gamma-catenin expression and Ki-67 index, only the expression of beta-catenin was more frequently found to be abnormal in total SCC than in total KA (P < 0.05). Expression of E-cadherin and alpha-, beta- and gamma-catenin was more frequently found to be abnormal in well-differentiated SCC than in 'classical' KA (P < 0.05). In total, as well as in 'classical' or 'borderline' KA, an agreement between expression of E-cadherin and of catenins was seen. CONCLUSIONS: These findings suggest that E-cadherin and catenins may be very helpful in distinguishing between 'classical' and 'borderline' KA, as the expression of these adhesion molecules in 'classical' KA is identical to that found in normal epidermis, overlapping with well-differentiated SCC in some cases. In 'borderline' KA, expression of adhesion molecules is identical to that in poorly differentiated SCC.

Biomarkers↗
PubMed2001

Echocardiographic and ambulatory electrocardiographic findings in elite water-polo athletes.

The aim of this study was to investigate the echocardiographic and electrocardiographic findings in top water-polo athletes and test the hypothesis that their hearts exhibit dilatation associated with hypertrophy secondary to the mixed type (isotonic and isometric) of exercise they are subjected to. Eighteen athletes of the Greek national water-polo team and 15 healthy sedentary men serving as controls were studied. All underwent an echocardiogram, a standard 12-lead ECG and 24-h ECG monitoring. In athletes, as compared to healthy controls, an increase was detected in the following indices: left ventricular (LV) end-diastolic diameter index (EDDI-LV) (by 10%; P = 0.02), interventricular septal thickness (IVS) (by 32%; P<0.001), thickness of the posterior wall (PW) (by 29%; P<0.001), relative wall thickness (IVS + PW/EDD-LV) (by 12%; P < 0.001) and LV mass index (by 82%; P < 0.001). Mild asymmetric thickening of the septum (IVS/PW = 1.40 and 1.37) was measured in two athletes. LV fractional shortening was normal. Standard 12-lead ECG abnormalities (LV hypertrophy or abnormal repolarization pattern) were observed in 33% of athletes. Athletes had sinus bradycardia during day and night, respiratory arrhythmia (RA) (83% vs 40% of controls; P = 0.03) and sinus pauses (SP) (39% vs 0% of controls; P = 0.02), with occassional arrhythmias and conduction abnormalities. We conclude that top water-polo athletes have dilatation combined with substantial hypertrophy and normal systolic function of the LV In addition they present bradycardia, RA and SP, with occassional arrhythmias and conduction abnormalities.

Adaptation, Physiological↗
PubMed2000

Coagulation system and platelets are fully activated in uncomplicated sepsis.

OBJECTIVE: To test the hypothesis that the coagulation system and platelets are activated in sepsis, the uncomplicated and usually earliest stage of the septic process, and to compare the findings detected in sepsis with those found in severe sepsis and septic shock. DESIGN: Prospective study comparing patients with sepsis, severe sepsis, and septic shock, and healthy volunteers. SETTING: General intensive care unit in a tertiary university hospital. PATIENTS: Seventy-four consecutive septic patients (45 with sepsis, 15 with severe sepsis, and 14 with septic shock). Fourteen healthy volunteers served as control subjects. INTERVENTION: None. MEASUREMENTS AND MAIN RESULTS: After blood sampling, molecular activation markers of coagulation (prothrombin fragments 1 and 2, fibrinopeptide A, thrombin-antithrombin complexes, and monomers of fibrin) and of platelets (beta-thromboglobulin and platelet factor 4), several coagulation factors, global tests of coagulation (prothrombin time and activated partial thromboplastin time), and platelet count (PTL) were measured. In sepsis, prothrombin fragments 1 and 2, fibrinopeptide A, thrombin-antithrombin complexes, and monomers of fibrin were increased to 2.52+/-0.21 nmol/L, 20.88+/-2.52 ng/mL, 33.8+/-2.9 microg/L, and 69% positive, respectively, compared with control subjects (0.86+/-063 nmol/L, 1.14+/-0.15 ng/mL, 16.07+/-1.01 microg/L, and 0%, respectively). Beta-Thromboglobulin and the beta-thromboglobulin-to-platelet factor 4 ratio were also increased to 107.87+/-11.87 IU/mL and 8.86+/-1.06, compared with controls (18.36 +/-2.99 IU/mL and 2.67+/-0.52, respectively). With the exception of a decrease in factor XII and an increase in fibrinogen, coagulation factors, global coagulation tests, and PTL were not changed in sepsis. In severe sepsis and mainly in septic shock, coagulation factors were markedly decreased, global coagulation tests were prolonged, and PTL was reduced. All changes were independent of the causative infectious pathogen. CONCLUSION: Coagulation system and platelets are strongly activated in sepsis. In this stage, only factor XII is decreased. In contrast, in severe sepsis and mainly in septic shock, most of the coagulation factors are depleted, PTL is decreased, and global coagulation tests are prolonged, indicating exhaustion of hemostasis. Finally, Gram-positive, Gram-negative, and other microorganisms produce identical impairment of coagulation.

Adolescent↗
PubMed2000

Contribution of pain to inspiratory muscle dysfunction after upper abdominal surgery: A randomized controlled trial.

Upper abdominal surgery causes respiratory muscle dysfunction. Multiple factors have been implicated in the occurrence of such dysfunction; however, the role of pain remains unclear. To elucidate the role of pain, we studied 50 patients undergoing elective upper abdominal surgery in a randomized, controlled investigation. Inspiratory and expiratory muscle function were assessed through sniff mouth pressure (Psniff) and maximal expiratory pressure (MEP), respectively. Pain during the pressure maneuvers was assessed with a visual analog scale (VAS). Measurements were made before surgery (Session 1), 24 h after surgery (Session 2), and 1 h later, after intramuscular administration of pethidine (analgesia group) or placebo (placebo group) (Session 3). To evaluate the effect of pain, we used a mixed-effects model with random intercept, having either Psniff or MEP as the dependent variable and both surgical operation and the level of pain as fixed effects. Upper abdominal surgery decreased Psniff in both the analgesia and placebo groups (from 70 +/- 15 to 42 +/- 11 cm H(2)O [p < 0.05] in the analgesia group, and from 69 +/- 15 to 42 +/- 10 cm H(2)O [p < 0.05] in the placebo group). Intramuscular pethidine caused an increase in Psniff to 56 +/- 14 cm H(2)O (p < 0.05), whereas placebo had no effect. Pain increased comparably after upper abdominal surgery in both groups (from 0.3 +/- 0.6 to 4.4 +/- 1.5) [p < 0.05] in the analgesia group and from 0.4 +/- 0.5 to 4.3 +/- 1.5 [p < 0.05] in the placebo group). Intramuscular pethidine decreased pain as measured by VAS score to 2.1 +/- 1.0 (p < 0.05) in the analgesia group, whereas placebo had no effect. Psniff had a statistically significant relationship to pain (p < 0.001). Adjusting for the occurrence of surgical operation did not affect this result. MEP showed the same tendency as Psniff, but the observed changes did not reach statistical significance. We conclude that pain contributes to inspiratory muscle dysfunction after upper abdominal surgery.

Abdomen↗
PubMed1999

Weaning from mechanical ventilation.

For most mechanically ventilated patients, weaning can be accomplished quickly and easily. However, there is a smaller group of ventilated patients who fail to wean and remain ventilator-dependent. These patients account for a significant amount of health care costs and pose a great challenge for clinicians. Detailed knowledge of the etiology and pathophysiology of weaning failure is very important for the "treatment" of difficult to wean patients, and is thoroughly presented in this article. Based on this physiological background, strategies and techniques are proposed that are useful for the gradual transition to spontaneous ventilation.

Humans↗
PubMed1999

Pulmonary lactate release in patients with acute lung injury is not attributable to lung tissue hypoxia.

OBJECTIVE: To determine whether pulmonary lactate production in patients with acute lung injury is attributable to lung tissue hypoxia. DESIGN: Prospective, controlled, clinical study. SETTING: A multidisciplinary university intensive care unit in a general hospital. PATIENTS: Seventy consecutive critically ill patients requiring mechanical ventilation and invasive hemodynamic monitoring. Of these patients, 18 had no acute lung injury (no ALI); 33 had acute lung injury (ALI) (Lung Injury Score [LIS] < or =2.5); and 19 had acute respiratory distress syndrome (ARDS) (LIS >2.5). INTERVENTIONS: None. MEASUREMENTS AND MAIN RESULTS: After hemodynamic measurements, lactate and pyruvate concentrations were assessed in simultaneously drawn arterial (a) and mixed venous (v) blood samples. Pulmonary lactate release was calculated as the product of transpulmonary a-v lactate difference (L[a-v]) times the cardiac index. Two indices of anaerobic metabolism of the lung, i.e., the transpulmonary a-v difference of lactate pyruvate ratio (L/P[a-v]) and excess lactate formation across the lungs (XL), were calculated. L(a-v) and pulmonary lactate release were higher in patients with ARDS than in the other groups (p<.001), and they were also higher in patients with ALI compared with patients with no ALI (p<.001). In patients with ALI and ARDS (n = 52), pulmonary lactate release correlated significantly with LIS (r2 = .14, p<.01) and venous admixture (r2 = .13, p<.01). When all patients were lumped together (n = 70), pulmonary lactate release directly correlated with LIS (r2 = .30, p<.001), venous admixture (r2 = .26, p<.001), and P(A-a)O2 (r2 = .14, p<.01). Neither L/P(a-v) nor XL was significantly different among the three groups. CONCLUSION: The lungs of patients with ALI produce lactate that is proportional to the severity of lung injury. This lactate production does not seem to be attributable to lung tissue hypoxia.

Biomarkers↗