BACKGROUND Fraction of exhaled nitric oxide (FENO) is known as a marker of inflammation in asthma, cystic fibrosis and exacerbation of COPD. However, its importance has not been established in patients using mechanical ventilation. We assessed whether FENO is elevated in patients with ventilator associated pneumonia (VAP), and physiologic or pathologic factors affecting levels of FENO in patients with mechanical ventilation. METHODS All patients (over 18-year-old) using mechanical ventilation were included, and among them, VAP patients were diagnosed on the basis of clinical pulmonary infection score (CPIS). We measured FENO in air collected during the end-expiratory pause via an off-line method. We compared the levels of FENO between patients with VAP and without, and assessed the relationship between FENO and other physiologic or pathologic characteristics; age, gender, PaO2, oxygenation index, CPIS. RESULTS A total of 43 patients (23 male, mean age 67.7 +/- 10.7) in an ICU were enrolled; 19 of them were VAP-patients (10 male, mean age 64.8 +/- 12.9). The level of FENO in the VAP-patients was substantially higher than in the non-VAP group (55.8 +/- 25.3 ppb Vs. 31.8 +/- 13.5 ppb, p < 0.001).
CPIS on day 1 and day 3, and duration of mechanical ventilation, were associated with the level of FENO, but oxygenation index, PaO2, PaO2/FiO2, and the mean PEEP were not. CONCLUSIONS FENO may be useful for the diagnosis of VAP, and is related to CPIS, as well as the duration of mechanical ventilation.
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Exhaled nitric oxide in intubated ICU patients on mechanical ventilation—a feasibility study Andreas Kofoed, Mathias Hindborg, Jeppe Hjembæk-Brandt, Christian Dalby Sørensen, Mette Kolpen, Morten H Bestle Journal of Breath Research.2023; 17(4): 046014. CrossRef
Clinical Application of Exhaled Nitric Oxide Measurements in a Korean Population Woo-Jung Song, Ji-Won Kwon, Eun-Jin Kim, Sang-Min Lee, Sae-Hoon Kim, So-Yeon Lee, Sang-Heon Kim, Heung-Woo Park, Yoon-Seok Chang, Woo Kyung Kim, Jung Yeon Shim, Ju-Hee Seo, Byoung-Ju Kim, Hyo Bin Kim, Dae Jin Song, Gwang Cheon Jang, An-Soo Jang, Jung-Won Allergy, Asthma & Immunology Research.2015; 7(1): 3. CrossRef
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Drowning is the third leading cause of unintentional accidental death globally. The most serious pathophysiologic consequence of drowning is hypoxemia from acute respiratory distress syndrome. Herein, we report a drowning victim who presented with hypothermia and cardiac arrest, followed by acute respiratory distress syndrome, rhabdomyolysis (with acute kidney injury), and disseminated intravascular coagulopathy. Aided by advanced cardiac life support and mechanical ventilation in a prone position, the patient fully recovered after two days of hospitalization. Recovery was largely attributed to early prone ventilatory positioning and use of nitric oxide gas.
BACKGROUND It is a well-known phenomenon that alveolar and peritoneal macrophages exposed to bacterial lipopolysaccharide (LPS) induce a large output of nitric oxide (NO) and an inducible nitric oxide synthase (iNOS) mRNA expression. The purpose of this study is actually how much NO production and iNOS mRAN expression are effected by anesthetics (sevoflurane and propofol) on endotoxemic rats. METHODS To examine the production of NO in peritoneal macrophages, NO concentration were measured from the rats following 2 hours exposure to LPS and 2 hours administration of sevoflurane and propofol, respectively. Culture supernatants were collected 24 hours after exposure to LPS and anesthetics and assayed by ELISA (Enzyme Linked Immunosorbent Assay) for production of NO. The iNOS mRNA expression was measured using PCR (Polymerase Chain Reaction) techniques and autoradiography. RESULTS: In the control group, the NO concentration was measured at 2 hours after infusion of LPS to rats, and showed 12 4micrometer.
After insufflations of anesthetics to experimental animals, NO concentration increased in the sevoflurane and propofol groups, 37 13 (p<0.05) and 29 12micrometer (p<0.05) respectively. The size and brightness of the iNOS mRAN bands were distinct in sevoflurane and propofol in order. CONCLUSIONS There were no different in regard of NO production and hemodynamic changes but iNOS mRNA expression between sevoflurane and propofol group in endotoxemic rats.
The mechanism is not clear, but it is related to the strong stimulating effects on the respiratory tract of inhalation anesthetics.
BACKGOUND: Bacterial endotoxin or lipopolysaccharide (LPS) is believed to mediate the tissue damage and shock observed in Gram-negative sepsis (GNS) by initiating a cascade of events, including activation of the coagulation, fibrinolytic and complement systems, and release of proinflammatory cytokines. However, the clinical pictures that result from GNS and endotoxin are quite different. The physiologic changes induced with LPS were investigated in this study. METHODS Fifty two male Sprague-Dawley rats were injected intraperitoneally with Escherichia coli LPS. Blood samples and bronchoalveolar lavage (BAL) fluid were obtained at baseline and at 2, 4, 8, 16, 24, and 48 hours after injection. Nitrate/nitrite levels were measured from plasma and BAL samples. Lipid peroxide (LPO) levels were measured from plasma. We measured also protein concentration and number of polymorphonuclear leukocytes (PMNL) and macrophages from BAL samples. RESULTS Administration of LPS caused significant increase in nitrate/nitrite concentrations of plasma and BAL fluid (p<0.01). ED50 of LPS was 1.76 mg/kg in plasma nitrate/nitrite assay. Plasma LPO levels were increased slightly after administration of LPS, but no statistical significance. Protein concentration was increased significantly (p<0.01) 4 hours after the administration of LPS. LPS induced increase of the number of PMNLs and macrophages of BAL samples significantly (p<0.05). CONCLUSIONS LPS increased NO production and alveolar permeability in rats. Also, LPS increased the number of inflammatory cells in the lung.
Bockground: Nitric oxide (NO) is an important regulator of blood flow and also works as a neuronal messenger via cyclic GMP. Recent studies regarding the therapeutic utility of nitric oxide synthase (NOS) inhibitors in reducing ischemia-induced neuronal damage are very controversial. The possible neuroprotective effect of NO or NOS inhibitors in ischemic neuronal damage could occur at the vascular and or neuronal level. This study investigated whether the NOS inhibitor, NG-nitro-L-arginine-methyl ester (L-NAME) would alter oxygen balance in ischemic cerebrocortex of isoflurane-anesthetized rats. METHODS Fifteen minutes after middle cerebral artery occlusion, L-NAME (1.5 mgxmin-1kg-1) was infused intravenously to the L-NAME group (n=14), and normal saline was given to the control group (n=14) for 45 minutes.
Regional cerebral blood flow was determined with [14C]iodoantipyrine, and arterial and venous oxygen saturations were determined by microspectrophotometry. RESULTS Regional cerebral blood flow of the ischemic cortex was significantly lower than that of the contralateral cortex in both groups. In the control group, ischemic cortex; 55+/-13, contralateral cortex; 110+/-29 mlxmin-1100 g-1, and in the L-NAME group, ischemic cortex; 35+/-13, contralateral cortex; 90+/-24 mlxmin-1100 g-1. Compared with the blood flow in the ischemic cortex of the control group, L-NAME significantly reduced ischemic blood flow by 36%.
Venous oxygen saturation was significantly increased in the ischemic cortex (41+/-1% in control, 44+/-3% in L-NAME) but decreased in the contralateral cortex (65+/-3% in control, 61+/-3% in L-NAME) by L-NAME. Ischemic cortical oxygen consumption in the L-NAME group was 39% lower than that in the corresponding control group, whereas the difference was only 11% in the contralateral sides between groups. The ratio of oxygen supply to consumption was lower in the ischemic than in the nonischemic regions in both groups. In the ischemic cortex, this ratio was significantly lower in the control group (1.7+/-0.1) than in the L-NAME group (1.9+/-0.1). In contrast, the ratio tended to be decreased by L-NAME in nonischemic regions. CONCLUSIONS These observations suggest that despite a decrease in cerebral blood flow, inhibition of nitric oxide synthesis mildly improves the oxygen supply and consumption balance in the ischemic cortex.