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  • 1
    Electronic Resource
    Electronic Resource
    Protective effects of hsp70 in inflammation (1994)
    Springer
    Cellular and molecular life sciences 50 (1994), S. 1031-1038 
    Details
    ISSN: 1420-9071
    Keywords: Heat shock proteins ; inflammation ; reactive oxygen species ; nitric oxide ; lipid peroxidation ; tumor necrosis factor α ; interleukin 1 ; adult respiratory distress syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Inflammation results from the recruitement to a given tissue or organ and the activation of leucocytes, among which the monocytes-macrophages play a major role. These phagocytic cells produce high levels of reactive oxygen species (ROS) as well as cytokines. Whereas both ROS and cytokines have the potential to regulate the expression of heat shock (HS)/stress proteins (HSP), it appears that these proteins in turn have the ability to protect cells and tissues from the deleterious effects of inflammation. The mechanisms by which such protection occurs include prevention of ROS-induced DNA strand breaks and lipid peroxidation as well as protection from mitochondrial structure and function. In vivo, HS protects organs against a number of lesions associated with the increased production of ROS and/or cytokines. In an animal model for adult respiratory distress syndrome, an acute pulmonary inflammatory condition, HS completely prevented mortality. HSP (hsp70 in particular) may also exert protective effects in the immune system by contributing to the processing and presentation of bacterial and tumoral antigens. The analysis of the expression of hsp70 may prove of diagnostic and prognostic value in inflammatory conditions and therapeutical applications are being considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01923458
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  • 2
    Electronic Resource
    Electronic Resource
    Accuracy assessment for three fiberoptic pulmonary artery catheters for $$S\bar vO_2 $$ monitoring (1994)
    Springer
    Intensive care medicine 20 (1994), S. 484-488 
    Details
    ISSN: 1432-1238
    Keywords: $$S\bar vO_2 $$ , $$S\bar vO_2 $$ monitoring ; Fiberoptic ; Pulmonary artery catheters
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To compare values of $$S\bar vO_2 $$ obtained by reflectance spectrophotometry continuous monitoring with those obtained from blood samples measurements by transmission spectrophotometry (Co-Oximetry). Design Values of $$S\bar vO_2 $$ recorded by three pulmonary artery catheters for continuous monitoring, SAT 1, SAT 2 and Oximetrix 3 (OX 3), were compared in a prospective manner to those measured on blood samples by a Co-Oximeter, using the statistical analyis of Bland and Altman. Setting Adult intensive care unit in an University Hospital. Patients 37 patients admitted for acute respiratory failure and/or shock who required hemodynamic monitoring. Main results The bias (average under- or overestimation) was small for all comparative measurements: +1.3, −0.2 and +1.0 sat% for SAT 1, SAT 2 and OX 3, respectively. However, limits of agreement were only acceptable for SAT 2 (−8.3 to +7.9 sat%) and OX 3 (−6.7 to +8.6 sat%), but not for SAT 1 (−23.3 to +25.9 sat%). No significant drift during 24 h was found with the three catheters. However, in vitro calibration was only found acceptable for SAT 2 and OX 3. The results were not influenced by the numbers of wavelengths of the device (2 for SAT 1 and SAT 2, and 3 for OX 3) nor did they correlate with any of the hemodynamic and biochemical variables tested. Conclusion For usual monitoring in the ICU, SAT 2 and OX 3, gave $$S\bar vO_2 $$ values which are in acceptable agreement with $$S\bar vO_2 $$ measured on blood samples by Co-Oximetry.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711900
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  • 3
    Electronic Resource
    Electronic Resource
    The use, and misuse, of exogenous endothelial-derived vasodilators in acute respiratory failure (1997)
    Springer
    Intensive care medicine 23 (1997), S. 1110-1118 
    Details
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050466
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  • 4
    Electronic Resource
    Electronic Resource
    Lack of efficacy of inhaled nitric oxide in ARDS (1994)
    Springer
    Intensive care medicine 20 (1994), S. 532-532 
    Details
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01711913
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  • 5
    Electronic Resource
    Electronic Resource
    Exercise increases the release of atrial natriuretic peptide in heart transplant recipients (1992)
    Springer
    European journal of clinical pharmacology 42 (1992), S. 21-24 
    Details
    ISSN: 1432-1041
    Keywords: Atrial natriuretic peptide ; Heart transplant recipients ; right-heart catheterisation ; graded submaximal exercise
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary It is known that atrial natriuretic peptide (ANP) is synthesized, stored and released from the myocytes of mammalian heart, but the role of cardiac autonomic nerves in triggering the release of ANP has not been fully assessed. We have therefore measured plasma ANP concentrations in the right atrium and the main pulmonary artery, together with pulmonary haemodynamics in 10 heart transplant (HT) recipients who underwent graded submaximal bicycle exercise during right-heart catheterisation. Pulmonary arterial blood samples and haemodynamic measurements were obtained at rest, on peak of exercise, and after ten minutes of recovery. A radioreceptor of α-human ANP was used to measure ANP levels. Exercise significantly incresed ANP levels in both the right atrium from 24 pM (resting values) to 48.5 pM, and the main pulmonary artery from 27.1 pM (resting values) to 58.4 pM. We conclude that HT recipients still retain the ability to increase ANP release in response to graded submaximal dynamic exercise, and that the mechanisms underlying ANP release depend on other factors than the integrity of cardiac innervation in man.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00314914
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  • 6
    Electronic Resource
    Electronic Resource
    Locally deposited but not inhaled frusemide reduces nasal potential difference in healthy subjects (1993)
    Springer
    European journal of clinical pharmacology 45 (1993), S. 347-351 
    Details
    ISSN: 1432-1041
    Keywords: Amiloride ; Salbutamol ; Frusemide ; ion transport ; airway epithelium ; loop diuretics ; asthma ; prostaglandins ; nasal potential difference
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Previous publications suggest that prolonged inhalation of frusemide (F) does not cause a fall in the nasal transepithelial potential difference (PD) whereas locally deposited F does. In an attempt to reconcile these observations, we have measured the effect of inhalation through the nose and local deposition of F, amiloride (A), bumetanide (B) and salbutamol (S) on nasal PD in 7 healthy male volunteers in a randomised, double blind study. Solutions of drugs ranging from 10−6 M to 10−3 M (3.10−8 M to 3.10−5 M for B) in phosphate buffered saline 0.5 ml (PBS) were sequentially deposited in both nostrils, and nasal PD was measured 5 min after each dose. In 10 further volunteers, 10−2 M solutions of A, F and S (3.10−4 M for B) 5 ml were nebulised through the nose for 15 min, when nasal PD was measured. Resting PD was similar in the left and right nostrils averaging −17.1 mV (lumen negative). Placebo, inhaled of deposited B and S, and inhaled F did not change nasal PD. Topically deposited F significantly lowered PDmax in a dose-dependent manner [10−4 M, −12% from baseline; 10−3 M, −24%] as did the more potent A [10−5 M, −19%; 10−4 M, −31%; 10−3 M, −47%]. Nebulised A (10−2 M) had the same effect on nasal PD as deposited A (10−4 M). The effects of locally deposited F and A (10−3 M) on nasal PD were additive. Our results suggest first that, aerosol administration is less effective than local application in assessing the effect of a drug on nasal PD. And second, F cannot act primarily at the cotransporter level to reduce nasal PD, as B and F share the same inhibitory effect of the basolateral Na/K/Cl cotransporter and B does not reduce nasal PD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00265953
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  • 7
    Electronic Resource
    Electronic Resource
    Inhaled and exhaled nitric oxide (1999)
    Springer
    Cellular and molecular life sciences 55 (1999), S. 1103-1112 
    Details
    ISSN: 1420-9071
    Keywords: Key words. Nitric oxide; persistent pulmonary hypertension of the newborn; acute respiratory distress syndrome; sinusitis; asthma.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Inhaled nitric oxide (NO) is used to treat various cardiopulmonary disorders associated with pulmonary hypertension. The rationale is based on the fact that NO, given by inhalation, only dilates those pulmonary vessels that perfuse well-ventilated lung units. As a result, pulmonary gas exchange is improved while pulmonary vascular resistance is reduced and pulmonary blood flow is increased. Inhaled NO has been succesfully applied to treat persistent pulmonary hypertension of the newborn, reducing the need for extracorporeal life support. Although pulmonary hypertension and altered vasoreactivity contribute to profound hypoxaemia in adult and paediatric acute respiratory distress syndrome (ARDS), the benefit of inhaled NO still remains to be established in patients with ARDS. ARDS is a complex response of the lung to direct or indirect insults, leading to pulmonary vasoconstriction and various inflammatory responses. Recent randomized trials suggest that inhaled NO only causes a transient improvement in oxygenation. Whether this effect is important in the long-term management of ARDS remains to be established. NO, measured in the exhaled breath, is an elegant and non-invasive means to monitor inflammation of the upper and lower respiratory tract. In the normal upper airways, the bulk of exhaled NO originates from the paranasal sinuses. Exhaled NO is increased in nasal allergy and decreased in cystic fibrosis, nasal polyposis and chronic sinusitis. That NO production is increased in asthmatic airways is also well established. However, several questions still need to be addressed, in particular evaluation of the sensitivity and specificity of the measurement techniques, and assessment of the bronchodilator action of endogenous NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050360
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  • 8
    Electronic Resource
    Electronic Resource
    Endothelium-derived nitric oxide and vascular physiology and pathology (1999)
    Springer
    Cellular and molecular life sciences 55 (1999), S. 1078-1087 
    Details
    ISSN: 1420-9071
    Keywords: Key words. Nitric oxide; nitric oxide synthase; endothelium; hypertension; atherosclerosis.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. In 1980, Furchgott and Zawadzki demonstrated that the relaxation of vascular smooth muscle cells in response to acetylcholine is dependent on the anatomical integrity of the endothelium. Endothelium-derived relaxing factor was identified 7 years later as the free radical gas nitric oxide (NO). In endothelium, the amino acid L-arginine is converted to L-citrulline and NO by one of the three NO synthases, the endothelial isoform (eNOS). Shear stress and cell proliferation appear to be, quantitatively, the two major regulatory factors of eNOS gene expression. However, eNOS seems to be mainly regulated by modulation of its activity. Stimulation of specific receptors to various agonists (e.g., bradykinin, serotonin, adenosine, ADP/ATP, histamine, thrombin) increases eNOS enzymatic activity at least in part through an increase in intracellular free Ca2+. However, the mechanical stimulus shear stress appears again to be the major stimulus of eNOS activity, although the precise mechanisms activating the enzyme remain to be elucidated. Phosphorylation and subcellular translocation (from plasmalemmal caveolae to the cytoskeleton or cytosol) are probably involved in these regulations. Although eNOS plays a major vasodilatory role in the control of vasomotion, it has not so far been demonstrated that a defect in endothelial NO production could be responsible for high blood pressure in humans. In contrast, a defect in endothelium-dependent vasodilation is known to be promoted by several risk factors (e.g., smoking, diabetes, hypercholesterolemia) and is also the consequence of atheroma (fatty streak infiltration of the neointima). Several mechanisms probably contribute to this decrease in NO bioavailability. Finally, a defect in NO generation contributes to the pathophysiology of pulmonary hypertension. Elucidation of the mechanisms of eNOS enzyme activity and NO bioavailability will contribute to our understanding the physiology of vasomotion and the pathophysiology of endothelial dysfunction, and could provide insights for new therapies, particularly in hypertension and atherosclerosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000180050358
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