PubMed Health⌕ Search

Biomedical subjects

C Frostell

Publications and source records attributed to C Frostell.

At least 19 recordsLinked to original sources
PubMed2006

A retrospective survey of outpatients with long-term tracheostomy.

BACKGROUND: The Respiratory Unit (RU) at Danderyd University Hospital opened in 1982, with the expressed goal of supporting outpatients with long-term tracheostomy. The primary aim of this retrospective study in tracheostomized patients was to compare the need for hospital care in the 2-year period before and after the tracheostomy. METHODS: Data were collected from patient medical records at the RU, from the National Board of Health and Welfare, Sweden and from the Official Statistics of Sweden. The subjects were RU patients in 1982 (Group 1, n = 27) and in 1997 (Group 2, n = 106) with long-term tracheostomy surviving at least 4 years after the tracheostomy. RESULTS: Both groups had few and unchanged needs for hospital care after tracheostomy. They spent > or = 96% of their time out of hospital. In 1997, (group 2) the number of patients, diagnoses and need for home mechanical ventilation had increased. Life expectancy was assessed for patients in Group 1. Data showed that they lived as long as an age-matched and gender-adjusted control cohort. CONCLUSIONS: Long-term tracheostomy may not increase the need for hospital care and does not reduce life expectancy. These clinical observations were made in a setting where patients had regular access to a dedicated outpatient unit.

Adult↗
PubMed2003

Differential release of matrix metalloproteinase-9 and nitric oxide following infusion of endotoxin to human volunteers.

BACKGROUND: Roughly 400.000 cases of sepsis occur every year in the United States only and this is associated with a very high mortality. Bacterial lipopolysaccharide (LPS) triggers systemic inflammatory reactions in sepsis. However, down-stream cellular cascade initiated by LPS is still being elucidated. Nitric oxide (NO) and matrix metalloproteinases-2 and -9 (MMP-2 and MMP-9) are known to be induced by LPS. We have investigated the release of NO, MMP-2 and MMP-9 following infusion of LPS to volunteers. METHODS: IPS (2 ng kg-1) was infused to 10 healthy volunteers. Before the experiments were started the subjects had an intravenous catheters placed. An electrocardiogram was also placed and monitored constantly. Body temperature was measured by ear thermometer every 10 min Venous blood was collected and cell-free plasma assayed for the presence of MMP-2 and MMP-9 using zymography and NO using HPLC assay for NO metabolites, nitrite and nitrate. RESULTS: The administration of LPS resulted in increased body temperature and tachycardia. Time-dependent release of MMP-9(30 fold increase from the baseline) peaking at 2 h following infusion of LPS was observed. LPS did not significantly modify the activity of MMP-2 (P > 0.05). Infusion of LPS did not significantly change the levels of nitrite and nitrate (from 60 +/- 11 to 67 +/- 10 micro m, P > 0.05). CONCLUSION: The release of MMP-9, but not MMP-2 or NO, is a sensitive index of endotoxaemia in humans. MMP-9 release may contribute to the pathogenesis of sepsis via its pro-inflammatory effects on the vasculature.

Adult↗
PubMed2000

[Ventilation in ARDS: respirator, prone position, NO or artificial lung].

This review discusses the treatment of impaired gas exchange in acute respiratory distress syndrome (ARDS) using conventional ventilation, the open lung approach, prone position, nitric oxide (NO) inhalation and extracorporeal membrane oxygenation (ECMO). It is concluded that ventilation with high inspiratory pressures or volumes should be avoided, and that the open lung approach should be used as the first step. If this does not lead to satisfactory results, prone positioning is recommended, and if life-threatening hypoxemia persists, ECMO could be considered. NO inhalation is not recommended.

Adult↗
PubMed1999

Inhalation of nitric oxide in acute lung injury: results of a European multicentre study. The European Study Group of Inhaled Nitric Oxide.

OBJECTIVE: To determine whether inhalation of nitric oxide (INO) can increase the frequency of reversal of acute lung injury (ALI) in nitric oxide (NO) responders. DESIGN: Prospective, open, randomised, multicentre, parallel group phase III trial. SETTING: General ICUs in 43 university and regional hospitals in Europe. PATIENTS: Two hundred and sixty-eight adult patients with early ALI. INTERVENTIONS: NO responders were patients whose PaO(2) increased by more than 20 % when receiving 0, 2, 10 and 40 ppm of INO for 10 min within 96 h of study entry. Responders were randomly allocated to conventional treatment with or without INO. INO, 1-40 ppm, was given at the lowest effective dose for up to 30 days or until an end point was reached. The primary end point was reversal of ALI. Clinical outcome parameters and safety were assessed in all patients. RESULTS: Two hundred and sixty-eight patients were recruited, of which 180 were randomised NO responders. Frequency of reversal of ALI was no different in INO patients (61 %) and controls (54 %; p > 0.2). Development of severe respiratory failure was lower in the INO (2.2 % ) than controls (10.3 %; p < 0.05). The mortality at 30 days was 44 % for INO patients, 40 % for control patients (p > 0.2 vs INO) and 45 % in non-responders. CONCLUSIONS: Improvement of oxygenation by INO did not increase the frequency of reversal of ALI. Use of inhaled NO in early ALI did not alter mortality although it did reduce the frequency of severe respiratory failure in patients developing severe hypoxaemia.

Administration, Inhalation↗
PubMed1999

Inhaled nitric oxide does not influence bleeding time or platelet function in healthy volunteers.

BACKGROUND: Bleeding time has been reported to increase during gaseous nitric oxide (NO) inhalation in healthy volunteers and patients, and it has been speculated that inhaled NO inhibits platelet function. However, results have not been unanimous, and we have been unable to document any effects of inhaled NO on circulating platelets. MATERIALS AND METHODS: We performed a double-blind, placebo controlled cross-over study in which healthy volunteers (n = 15) inhaled NO (30 ppm, 30 min) or control gas. Aspirin (640 mg x 1 orally) was used as positive control on the third occasion (n = 14). Bleeding time was measured, and platelet function was determined flow cytometrically by measuring the expression of P-selectin on circulating platelets and locally activated platelets in wound blood. Skin perfusion close to the site for bleeding time incisions was assessed by laser Doppler flowmetry. RESULTS: Bleeding time was unaffected by NO, as there were slight increases during both NO and control inhalation (+20% and +14% respectively, P = 0.9). Similarly, NO inhalation had no effect on platelet P-selectin expression in either systemic or wound blood, or on skin perfusion. Aspirin pretreatment, on the other hand, prolonged bleeding time (P < 0.001) and decreased P-selectin expression of platelets in wound blood (P = 0.03). CONCLUSIONS: This first placebo-controlled study indicates that inhaled NO does not influence either bleeding time, platelet activity or skin perfusion. Thus, it is unlikely that treatment of critically ill patients with inhaled NO will aggravate haemostatic disturbances, which has previously been feared, by influencing platelet function.

Administration, Inhalation↗
PubMed1999

Neither endogenous nor inhaled nitric oxide influences the function of circulating platelets in healthy volunteers.

Experimental models have indicated prothrombotic effects of inhibition of nitric oxide (NO) production, and anti-thrombotic effects of inhaled NO, but the influence of NO on platelet function in vivo in humans is not well established. We therefore investigated the effects of systemic inhibition of NO synthesis by N(G)-monomethyl-L-arginine (L-NMMA) and of NO inhalation on platelet function in vivo. On two occasions, L-NMMA (13.5 mg/kg) or saline infusion was administered to 14 healthy volunteers in a double-blind cross-over study. After a 30 min infusion of L-NMMA or placebo, NO inhalation (30 p.p.m) was added during the remaining 30 min of infusion, on both occasions. Measurements included filtragometry ex vivo (reflecting platelet aggregability), flow-cytometric evaluation of platelets in whole blood (fibrinogen binding and P-selectin expression), plasma beta-thromboglobulin (reflecting platelet secretion), cGMP in platelets and plasma, thrombin generation markers (thrombin fragment 1+2 and thrombin-antithrombin complexes) in plasma, and bleeding time. L-NMMA increased blood pressure and decreased heart rate. NO inhalation did not influence blood pressure or heart rate, but caused a 3-fold elevation in plasma cGMP levels (P<0.001). Neither L-NMMA nor NO influenced filtragometry readings or flow-cytometric determinations of platelet fibrinogen binding and P-selectin expression. Furthermore, plasma beta-thromboglobulin, platelet cGMP and thrombin generation markers were not influenced by either treatment. Bleeding time was not influenced by L-NMMA compared with placebo, but was increased by approximately 25% during NO inhalation (P<0.01), whether NO synthesis had been inhibited or not. The prolongation of bleeding time by inhaled NO was not accompanied by any effect on the platelet variables assessed. The present results indicate that circulating platelets are not influenced by endogenous or inhaled NO, presumably due to the rapid inactivation of NO in the blood. This does not exclude possible effects of endothelial NO in the interface between the blood and the vessel wall.

Adult↗
PubMed1998

Pulmonary function in adult survivors of severe acute lung injury treated with inhaled nitric oxide.

BACKGROUND: Following an episode of acute respiratory distress syndrome (ARDS), some degree of measurable pulmonary impairment may be anticipated. ARDS is thought to be the more severe form of acute lung injury (ALI) and a recently proposed addition to conventional therapy in ALI/ARDS is inhaled nitric oxide (INO). We carried out a non-randomised follow-up study with pulmonary function tests on survivors of severe ALI/ARDS treated with INO. METHODS: Sixteen previously healthy pulmonary patients, survivors of severe ALI/ARDS, were evaluated with pulmonary function tests >8 months after the acute event. The tests included static and dynamic spirometry, diffusion capacity for carbon monoxide (DLCO), blood gas analysis and evaluation of a chest radiograph. RESULTS: The most common abnormality seen was a low DLCO in 69% of the patients. Abnormally low values were seen in forced vital capacity in 31%, in forced expiratory volume in 1 s in 13%, and in residual volume and total lung capacity in 6%. Blood gas data were within normal limits in 15/16 patients. All chest radiographs showed resolution of the interstitial and alveolar changes present during the acute event. CONCLUSION: In this non-randomised follow-up study we conclude that a degree of measurable pulmonary impairment after INO treatment in severe ALI/ARDS was common, but did not differ markedly from other published studies on pulmonary function in similar patient material. No late unexpected major abnormalities due to the inhaled nitric oxide treatment could be identified in these survivors.

Administration, Inhalation↗
PubMed1998

Individual lung blood flow during unilateral hypoxia: effects of inhaled nitric oxide.

We hypothesized that the diversion of blood away from a hypoxic lung to the opposite oxygenated lung can be enhanced by inhaling nitric oxide (NO) into the oxygenated lung. We measured individual lung blood flow when 50 ppm NO was selectively inhaled to: a hyperoxic lung during contralateral hypoxia; a normoxic lung during bilateral normoxia; and a hyperoxic lung during bilateral hyperoxia. Twenty two patients with healthy lungs were studied during intravenous anaesthesia. The lungs were separately and synchronously ventilated. The relative perfusion of each lung was assessed by the inert gas elimination technique. Unilateral hypoxic (inspiratory oxygen fraction (FI,O2) 0.05) ventilation during contralateral hyperoxia reduced the perfusion of the hypoxic lung from a mean (SD) of 47 (9)% of cardiac output (Q'), to 30 (7)% (p<0.001) of Q'. NO inhalation to the hyperoxic lung increased its blood flow from 70 (7)% to 75 (6)% (p<0.05) of Q', and reduced the blood flow to the hypoxic lung to 25 (6)% (p<0.05). Unilateral NO inhalation during bilateral normoxia or hyperoxia had no effect on pulmonary blood flow distribution. Nitric oxide inhalation to a hyperoxic lung increases the perfusion to this lung by redistribution of blood flow if the opposite lung is hypoxic.

Administration, Inhalation↗
PubMed1997

A retrospective analysis of nitric oxide inhalation in patients with severe acute lung injury in Sweden and Norway 1991-1994.

BACKGROUND: Patients with severe acute lung injury (ALI) have been treated compassionately on doctors' initiative with inhaled nitric oxide (INO) in Sweden and Norway since 1991. In 1994 the previously used technical grade nitric oxide was replaced by medical grade nitric oxide. METHODS: We have carried out a retrospective data collection on all identified adult patients treated with INO for >4 h during the period 1991-1994 focusing on safety aspects and patient outcome. We used the following exclusion criteria (1) Age <18 years, (2) Simultaneous treatment with extracorporeal removal of CO2 (3) NO inhalation period <4 h, (4) Incomplete or missing patient charts, (5) Use of INO in order to treat pulmonary hypertension following cardiac surgery, with little or no acute lung injury. RESULTS: Inclusion criteria were met by 56 out of 73 identified patients. Mean age was 48+/-19 years and the median duration of INO treatment was 102 h. PaO2/FIO2 ratio at start of treatment was 85 +/- 33 mm Hg with a lung injury score (LIS) of 3.2+/-0.8. The aetiology of the lung injury was pneumonia (n= 27), sepsis (n=12) and trauma (n=8). Survival to hospital discharge was 41% and survival after 180 d was 38%. Three serious adverse events were identified, two from technical failures of the INO delivery device and one withdrawal reaction necessitating slow weaning from INO. No methaemoglobin values >5% were reported during treatment. CONCLUSION: The overall mortality did not differ dramatically from historical controls with high mortality. Only a randomised study may determine whether INO as an adjunct to treatment alters the outcome in severe ALI. One cannot at present advocate the routine use of INO in patients with ALI outside such studies.

Administration, Inhalation↗
PubMed1997

Blockade of endogenous nitric oxide production results in moderate hypertension, reducing sympathetic activity and shortening bleeding time in healthy volunteers.

BACKGROUND: Short-term infusion of NG-monomethyl-L-arginine (L-NMMA) reversibly inhibits endogenous nitric oxide (NO) production in humans. We studied responses to more long-lasting (60 min) infusions, at doses high enough to cause effective inhibition of endogenous NO. METHODS: Eight healthy volunteers had catheters (pulmonary, arterial and venous) placed. Measurements included hemodynamics, endogenous NO levels in nasal air, bleeding time, and cyclic guanosine monophosphate (cGMP) and catecholamines in plasma. L-NMMA was infused at 0.3 mg.kg-1.min-1 during 30 min, followed by 0.15 (n = 6) or 0.3 (n = 2) mg.kg-1.min-1 during 30 min. RESULTS: L-NMMA significantly elevated mean arterial pressure by 12 +/- 3%, due to an increase in systemic vascular resistance. Cardiac output decreased by 23 +/- 3%, due to a decrease in stroke volume. Pulmonary vascular resistance (P < 0.05) increased, but mean pulmonary arterial pressure was stable. Forearm vascular resistance (P < 0.05) decreased. Bleeding time was shortened by 31 +/- 4% (P < 0.01). L-NMMA infusion reduced NO concentrations in nasal air by 64 +/- 2% (P < 0.01). Arterial pressure remained elevated and nasal NO remained depressed 90 min after the infusion, whereas most other responses were reversed at that time. Plasma cGMP showed only minor changes. Plasma norepinephrine decreased, suggesting reflexogenic inhibition of sympathetic activity, whereas epinephrine levels were low and stable throughout the experiment. CONCLUSION: Dosage of (13.5 mg.kg-1 in 60 min) L-NMMA infusion in humans was well tolerated. Pronounced and long-lasting inhibition of endogenous NO production, as evidenced by measurements in nasal air, resulted in unevenly distributed vasoconstriction, a transient decrease in cardiac output, and reflexogenic sympathetic withdrawal. Furthermore, bleeding time was shortened, suggesting platelet activation.

Adolescent↗
PubMed1997

Endogenous nitric oxide in the airways of different animal species.

BACKGROUND: High amounts of endogenous nitric oxide (NO) have been demonstrated in the human upper airway, but the role of nasal NO is still unclear. The present study aims to describe nasal NO excretion in different animal species with special living conditions or anatomy. METHODS: Domestic animals (horse, cow, pig, sheep, dog, cat) and zoo-animals (Rhesus monkey, chimpanzee, gorilla, elephant, fur seal, alpaca, yak, dolphin, camel, capybara, bear, tiger, wolf, giraffe, alligator, Harris' hawk, kangaroo) were studied awake, resting or anaesthetised. NO concentrations were measured by chemiluminescence using different analysers and techniques, including measurements on mixed exhaled air, during continuous or intermittent gas sampling, and on single breaths. RESULTS: Rhesus monkeys (number of individuals N = 5) and pigs (N = 2) were compared and displayed quite different excretion patterns. Allowing NO to accumulate in the nose during timed occlusions yielded peak concentrations in monkeys of 0.46 +/- 0.07 parts per million (ppm, mean +/- SEM), 0.59 +/- 0.08 ppm, 0.70 +/- 0.08 ppm and 1.02 +/- 0.05 ppm NO after 15, 30, 60 and 120 s of occlusion. In pigs, 0.012-0.021 ppm NO were recorded, independent of occlusion time. The chimpanzee was similar to the Rhesus monkey and the highest NO value, 2.9 ppm, was recorded after 4-5 min of occlusion. In single breaths from 3 elephants 0.031-0.082 ppm, from 1 gorilla 0.029 ppm, and from 1 chimpanzee 0.069 +/- 0.003 ppm NO (8 observations) were recorded. CONCLUSIONS: We found considerable species difference in nasal NO excretion with pronounced amounts only in primates and elephants. The physiological implications of these findings remain to be defined.

Animals↗
PubMed1997

Endogenous nitric oxide in the upper airways of premature and term infants.

Concentrations of endogenous nitric oxide (NO) were measured in premature (n = 18) and term infants (n = 7). Nasal gas was aspirated continuously and after timed occlusions, 15 s and 60 s, by a fast-response chemiluminescence analyser. The sampling flow rate was 20 ml min-1. Typical NO recordings consisted of plateaux and postocclusive peaks. In term infants peak NO concentrations (60 s occlusion) were 2.71 +/- 0.44 parts per million (ppm) within 10 min after birth, increasing (p < 0.05) to 3.81 +/- 0.25 ppm at 4-7 d postnatally. Peak NO values (15 s occlusion) averaged 1.22 +/- 0.16 ppm in premature infants (postconceptional age 25-37 weeks, body weight 623-2844 g) and the NO concentrations increased significantly with postconceptional age (p < 0.05). Nasal excretion rate, estimated from plateau NO concentrations and sampling flow rate, was 0.10 +/- 0.01 nmol min-1 kg-1 in both groups. We conclude that premature and term newborn infants excrete considerable amounts of NO in the upper airways, with hitherto not fully known functions.

Cross-Sectional Studies↗
PubMed1996

Effects of inhaled nitric oxide compared with aspirin on platelet function in vivo in healthy subjects.

1. Nitric oxide has platelet-stabilizing effects. Inhaled nitric oxide is used to treat pulmonary disorders, and may prolong bleeding times, suggesting that it has effects on haemostasis. We therefore examined if inhaled nitric oxide influences platelet function in vivo in healthy subjects. 2. Platelet aggregability (filtragometry ex vivo, which reflects aggregability in vivo), bleeding time and platelet secretion products and cGMP in plasma were studied during inhalation of two different doses of nitric oxide (30 and 80 p.p.m.; 15 min at each dose level; n = 19) and during prolonged (55 min; n = 18) inhalation of 30 p.p.m. nitric oxide. For comparison, studies were also performed before and after ingestion of 640 mg aspirin in 13 of the healthy subjects. 3. Plasma cGMP increased dose dependently during nitric oxide inhalation, suggesting guanylate cyclase activation in vivo. Platelet aggregability was, however, little affected and platelet secretion was not attenuated by nitric oxide inhalation. Bleeding time tended to increase (by 16-33%), but was significantly increased only after prolonged inhalation of nitric oxide at 30 p.p.m. 4. Aspirin (640 mg orally) caused pronounced and significant prolongations of filtragometry readings and bleeding time. Thus, the methods used were able to reveal platelet stabilization. 5. We conclude that nitric oxide inhalation causes only mild, if any, attenuation of platelet function in healthy subjects with a normal endogenous nitric oxide production. The effects may be different in disease states.

Administration, Inhalation↗
PubMed1996

Endogenous nitric oxide in the upper airways of healthy newborn infants.

The endogenous production of nitric oxide (NO) in the upper airways was studied in healthy newborn infants within the first minutes after delivery (N = 2) and at postnatal ages of 1 and 24 h (N = 13). Measurements were made in infants born vaginally or by cesarean section and at various times after the rupture of membranes. Gas was sampled from the nose and pharynx, and NO concentrations were determined by a fast response chemiluminescence analyzer. Sampling from the nose at a constant flow of 20 mL/min gave 0.27 +/- 0.01 parts per million (mean +/- SEM, ppm) of NO, independent of age and mode of delivery (vaginal delivery and cesarean section). Allowing NO to accumulate in the nose for 15-120 s yielded peak concentrations up to 4.6 ppm. A 30% increase was noted between 1 and 24 h of age. We conclude that nasal peak NO concentrations in the ppm range can be demonstrated in the healthy newborn infant within the first hour after birth. Consequently autoinhalation of endogenously produced upper airway NO may play a role in the adaptation of the respiratory system to postnatal life in the human.

Female↗
PubMed1995

Nitric oxide modulation of pulmonary blood flow distribution in lobar hypoxia.

BACKGROUND: Nitric oxide, endogenously produced or inhaled, has been shown to play an important role in the regulation of pulmonary blood flow. The inhalation of nitric oxide reduces pulmonary arterial pressure in humans, and the blockade of endogenous nitric oxide production increases the pulmonary vascular response to hypoxia. This study was performed to investigate the hypothesis that intravenous administration of an nitric oxide synthase inhibitor and regional inhalation of nitric oxide can markedly alter the distribution of pulmonary blood flow during regional hypoxia. METHODS: Hypoxia (5% O2) was induced in the left lower lobe of the pig, and the blood flow to this lobe was measured with transit-time ultrasound. Nitric oxide was administered in the gas ventilating the hypoxic lobe and the hyperoxic lung regions with and without blockade of endogenous nitric oxide production by means of N omega-nitro-L-arginine methyl ester (L-NAME). RESULTS: Hypoxia in the left lower lobe reduced blood flow to that lobe to 27 +/- 3.9% (mean +/- SEM) of baseline values (P < 0.01). L-NAME caused a further reduction in lobar blood flow in all six animals to 12 +/- 3.5% and increased arterial oxygen tension (PaO2) (P < 0.01). Without L-NAME, the inhalation of nitric oxide (40 ppm) to the hypoxic lobe increased lobar blood flow to 66 +/- 5.6% of baseline (P < 0.01) and, with L-NAME, nitric oxide delivered to the hypoxic lobe resulted in a lobar blood flow that was 88 +/- 9.3% of baseline (difference not significant). When nitric oxide was administered to the hyperoxic lung regions, after L-NAME infusion, the blood flow to the hypoxic lobe decreased to 2.5 +/- 1.6% of baseline and PaO2 was further increased (P < 0.01). CONCLUSIONS: By various combinations of nitric oxide inhalation and intravenous administration of an nitric oxide synthase inhibitor, lobar blood flow and arterial oxygenation could be markedly altered during lobar hypoxia. In particular, the combination of intravenous L-NAME and nitric oxide inhalation to the hyperoxic regions almost abolished perfusion of the hypoxic lobe and resulted in a PaO2 that equalled the prehypoxic values. This possibility of adjusting regional blood flow and thereby of improving PaO2 may be of value in the treatment of patients undergoing one-lung ventilation and of patients with acute respiratory failure.

Animals↗
PubMed1995

Clinical application of differential ventilation with selective positive end-expiratory pressure in adult respiratory distress syndrome.

Differential ventilation in the lateral position with positive end-expiratory pressure (PEEP) selectively applied to the dependent lung (DVSP) has been shown to reduce venous admixture and improve oxygenation without compromising cardiac output in short term studies of patients with acute respiratory failure. We have applied this ventilation technique as a long-term treatment in severe adult respiratory distress syndrome (ARDS) in an open clinical trial. Eleven patients with ARDS of varying aetiology were treated with DVSP for a total of 34 days. Median duration of conventional ventilatory therapy before start of DVSP was 5 days (1 to 18 days), inspiratory oxygen fraction (FIO2) was 0.61 +/- 0.16 (mean +/- s.d.), resulting in a mean arterial oxygen tension (PaO2) of 7.1 +/- 2.1 kPa (PaO2/FIO2 = 11 +/- 4 kPa). A gradual improvement in gas exchange was seen during the first 24 h of DVSP such that PaO2 increased to 8.4 +/- 1.4 with a decreased FIO2 (0.52 +/- 0.14) resulting in an increased PaO2/FIO2 (16 +/- 5 kPa). Five out of the eleven patients survived. No major complication was noted using DVSP as a method. We found a steady improvement in gas exchange over the first 24 hours in most patients. However, mortality rate was no lower than expected. Drawbacks with DVSP were increased demand on staff and difficulties with adequate endo-bronchial suctioning.

Adolescent↗
PubMed1995

Contribution from upper and lower airways to exhaled endogenous nitric oxide in humans.

Endogenous nitric oxide (NO) is thought to regulate many biological functions, including pulmonary circulation and bronchomotion, and it has been found in exhaled air. Our aim was to study the excretion of NO in different parts of the respiratory system. Exhaled concentrations of NO were measured by chemiluminescence in chronic tracheostomy outpatients (group 1), in patients admitted for minor abdominal surgery (group 2), and in patients with acute respiratory failure (ARF) during mechanical ventilation (group 3). In awake volunteers (group 4), 0.57 L/min gas was aspirated through the nasal cavity into the chemiluminescence device. In group 1 (tracheostomy, n = 5) we detected 16 +/- 2 (mean +/- s.e. mean) parts per billion (ppb) NO when exhaling through the mouth, and a lower (P < 0.05) value of 4.6 +/- 0.8 ppb NO when exhaling through the tracheostomy. Before anaesthesia, group 2 (n = 11) exhibited 18 +/- 2.4 ppb NO in orally exhaled gas, increasing considerably during exhalation through the nose. Upon endotracheal intubation exhaled NO concentration dropped to 1.3 +/- 0.2 ppb (P < 0.05). In group 3 (ARF, n = 7) tracheal NO concentrations were 0.8 +/- 0.2 ppb. In group 4 (volunteers, n = 6) 394 +/- 23 ppb NO was recorded in air from the nasal cavity. In both healthy subjects and patients with respiratory failure a significant NO excretion occurs in the lower airways and lungs. The upper airways, especially the nose, contribute the largest amount of NO (> 90%) to exhaled air. The physiological implications of an upper airway source of NO remain to be defined.

Adolescent↗