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PubMed1999

Lung injury from intratracheal and inhalation exposures to residual oil fly ash in a rat model of monocrotaline-induced pulmonary hypertension.

A rat model of monocrotaline (MCT)-induced pulmonary injury/hypertension has been recently used in particulate matter (PM) health effects studies, however, results have been equivocal. Neither the mechanism by which mortality occurs in this model nor the variation in response due to differences in PM exposure protocols (i.e., a bolus dose delivered intratracheally versus a similar cumulative dose inhaled over three days) have been fully investigated. Sprague Dawley rats (SD, 60 d old; 250-300 g) were injected with either saline (healthy) or MCT, 60 mg/kg, i.p. (to induce pulmonary injury/hypertension). Ten days later they were exposed to residual oil fly ash (ROFA), either intratracheally (IT; saline, 0.83 or 3.33 mg/kg) or by nose-only inhalation (15 mg/m3 x 6 h/d x 3 d). Lung histology, pulmonary cytokine gene expression (0 and 18 h postinhalation), and bronchoalveolar lavage fluid (BALF) markers of injury were analyzed (24 and 96 h post-IT; or 18 h post-inhalation). Data comparisons examined three primary aspects, 1) ROFA IT versus inhalation effects in healthy rats; 2) pulmonary injury caused by MCT; and 3) exacerbation of ROFA effects in MCT rats. In the first aspect, pulmonary histological lesions following ROFA inhalation in healthy rats were characterized by edema, inflammatory cell infiltration, and thickening of alveolar walls. Increases in BALF markers of lung injury and inflammation were apparent in ROFA-IT or nose-only exposed healthy rats. Increased IL-6, and MIP-2 expression were also apparent in healthy rats following ROFA inhalation. In regards to the second aspect, MCT rats exposed to saline or air showed perivascular inflammatory cell infiltrates, increased presence of large macrophages, and alveolar thickening. Consistently, BALF protein, and inflammatory markers (macrophage and neutrophil counts) were elevated indicating pulmonary injury. In regards to the third aspect, 58% of MCT rats exposed to ROFA IT died within 96 h regardless of the dose. No mortality was observed using the inhalation protocol. ROFA inhalation in MCT rats caused exacerbation of lung lesions such as increased edema, alveolar wall thickening, and inflammatory cell infiltration. This exacerbation was also evident in terms of additive or more than additive increases in BALF neutrophils, macrophages and eosinophils. IL-6 but not MIP-2 expression was more than additive in MCT rats, and persisted over 18 h following ROFA. IL-10 and cellular fibronectin expression was only increased in MCT rats exposed to ROFA. In summary, only the bolus IT ROFA caused mortality in the rat model of lung injury/hypertension. Exacerbation of histological lesions and cytokine mRNA expression were most reflective of increased ROFA susceptibility in this model.

Administration, Inhalation↗
PubMed2002

Personal sampling for inhalable aerosol exposures of carbon black manufacturing industry workers.

The study was concerned with the measurement of inhalable aerosol exposures in the carbon black production industry. The primary goal of the study was to determine the extent to which inhalable aerosol exposure, as measured by the Institute of Occupational Medicine (IOM) personal inhalable sampling head, compared to "total" aerosol exposure, as measured by traditional methodology. A secondary objective was the evaluation of another inhalable aerosol sampler for carbon black aerosol measurement. In addition, an exploratory evaluation of the applicability of the National Institute for Occupational Safety and Health (NIOSH) analytical method (Method 5040) for the determination of carbon black, measured as elemental carbon, was conducted. A field study was carried out in a number of North American carbon black production plants using three samplers: the 2 Lpm IOM sampler as a reference sampler for the inhalable fraction, the 2 Lpm closed-face 37-mm plastic cassette that has been used for many years for total aerosol, and the 3.5 Lpm GSP sampler that has recently been identified by some as a possible candidate for inhalable aerosol. No such studies have previously been reported for the carbon black industry. Further, there have been no reports of the GSP performance in direct comparison to a reference instrument like the IOM sampler. The results showed that inhalable aerosol exposures for workers in carbon black production and packing areas were higher than the corresponding total aerosol exposures by a factor of nearly three, implying the presence of significantly coarser aerosol than previously thought based simply on knowledge of the carbon black production process. The fact that the aerosols collected in portions of the process comprised high proportions of non-elemental carbon particulate was thought likely to be responsible, underlining the need to consider whether gravimetric assessment for such exposure is the most appropriate metric. In addition, and somewhat surprisingly, the GSP sampler emerged clearly as a good alternative to the IOM sampler for collecting inhalable aerosol in carbon black industry workplaces like those studied (although this conclusion cannot yet be extended to other workplaces).

Aerosols↗
PubMed2002

Long-term effects of the Eclipse cigarette substitute and the nicotine inhaler in smokers not interested in quitting.

This study investigated the long term use of Eclipse, a cigarette-like device that heats rather than burns tobacco, and the Nicorette oral inhaler, a nicotine replacement product, in a group of smokers not interested in quitting smoking. Subjects were recruited from a previous four-week controlled trial with the Eclipse and the inhaler (Fagerström, Hughes, Rasmussen, & Callas, 2000). Thirty eight subjects from the previous study were given the opportunity to continue to reduce their smoking for eight weeks and to choose Eclipse or the inhaler to aid reduction in cigarette smoking. If they did not like either of the two products they were allowed to smoke their own brand of cigarettes. A total of 39% percent chose to use the inhaler, 26% the Eclipse, and 34% neither. Number of cigarettes smoked per day decreased 86% with the Eclipse and 68% with the inhaler. Exhaled carbon monoxide increased 45% with Eclipse and decreased 47% with the inhaler. No differences were seen with craving for cigarettes between the products. Cigarette users showed stable values for cigarettes per day, exhaled carbon monoxide (CO) and nicotine/cotinine concentrations. These results replicate and extend our prior results; i.e. both Eclipse and inhaler clearly reduced smoking of traditional cigarettes and with no loss of effect over time. For Eclipse this was accompanied by maintenance of nicotine levels but increases in CO whereas for the inhaler this was accompanied by a reduction in CO intake.

Administration, Inhalation↗
PubMed2006

Enhancement of renal carcinogenicity by combined inhalation and oral exposures to chloroform in male rats.

Chloroform, ubiquitously present in indoor and outdoor air, drinking water, and some foodstuffs, enters the human body by inhalation, oral and dermal routes of exposure. In order to provide bioassay data for risk assessment of humans exposed to chloroform by multiple routes, effects of combined inhalation and oral exposures to chloroform on carcinogenicity and chronic toxicity in male F344 rats were examined. A group of 50 male rats was exposed by inhalation to 0 (clean air), 25, 50, or 100 ppm (v/v) of chloroform vapor-containing air for 6 h/d and 5 d/wk during a 104 w period, and each inhalation group was given chloroform-formulated drinking water (1000 ppm w/w) or vehicle water for 104 wk, ad libitum. Renal-cell adenomas and carcinomas and atypical renal-tubule hyperplasias were increased in the combined inhalation and oral exposure groups, but not in the oral- or inhalation-alone groups. Incidences of cytoplasmic basophilia and dilated tubular lumens in the kidney, as well as incidence of positive urinary glucose, were markedly increased by the combined exposures, compared with those after single-route exposures. It was concluded that combined inhalation and oral exposures markedly enhanced carcinogenicity and chronic toxicity in the proximal tubule of male rat kidneys, suggesting that carcinogenic and toxic effects of the combined exposures on the kidneys were greater than the ones that would be expected under an assumption that the two effects of single route exposures through inhalation and drinking were additive.

Administration, Oral↗
PubMed2003

Volatile substance and other drug abuse inhalation in Spain.

OBJECTIVE: Inhalant misuse is the intentional inhalation of volatile substances in order to obtain euphoric, disinhibiting, and exciting effects. Solvents, glues, adhesives, paints, varnishes, paint removers, dry cleaning agents, spray paints, nail polish removers, typewriter correction fluids, and aerosol propellants are common sources of volatile substance abuse. In recent years the abuse of inhalant substances, not only among those who abuse other drugs but also in teenagers and younger children, has been reported. We reviewed retrospectively the cases of inhalant misuse reported to the Spanish Poison Control Center. METHODS: Human intoxications from abuse of inhalant substances registered by our service from 1991 to 2000 were studied. Data analyzed were relative to age, gender, signs and symptoms, drug dependence antecedents, and severity of symptoms of the patients. The type of product and composition were also investigated. RESULTS: During the study period 109 cases of patients aged from 8 to 50 years were collected. A percentage of 36.6% was less or equal to 20 years old. Seventy percent corresponded to males. Of the patients, 11% presented dependence antecedents to other abuse drugs and 72.5% were symptomatic. In the symptomatic exposures clinical features affected the following systems: CNS (62.8%), gastrointestinal (8.1%), cardiovascular (8.1%), respiratory (2.9%), peripheral nervous system (1.1%), renal (1.1%), haematological (1.1%), hepatic (1.7%), and other (13.1%). The commercial products more frequently inhaled were solvents (34.9%) and glues/adhesives (22.9%). We noted the use of medicines with ethyl chloride-local anaesthetic (8.3%), three cases with aerosol bronchodilator (with fluorocarbons as propellants), and one case of xylazine inhalation. The composition most often involved was aromatic hydrocarbons (46.9%), halogenated hydrocarbons (16.5%), aliphatic hydrocarbons (11.4%), ketones (10.1%), local anaesthetic (ethyl chloride) (8.4%), ethers (2.5%), nitrous oxides (2.5%), and aliphatic nitrites (1.7%). The calls received were 59.6% from health care units and 22% from general public. Only 14% of cases were at home and 48% had moderate to severe clinical effects. Acute intoxications occurred in 82% of cases. CONCLUSIONS: Inhalation of volatile substance as abuse drugs has been detected in different age groups, including very young people. Although the principal source was industrial products, the use of drugs such as local anaesthetics and aerosol broncodilators was also detected. Based on epidemiological studies in the Spanish population (essentially adolescents and childhood) together with the ability of a Poison Center to detect sentinel-events, the community and authorities should develop strategies to prevent these exposures and the later use of other substances of abuse. In fact, recently a Law on Drug Dependences and Other Addictive Alterations has been approved in Madrid in order to take precautionary measures.

Administration, Inhalation↗
PubMed2001

Inhalation therapy of the future--how will it change the way we treat asthma?

Inhalation of drugs has made a great difference in terms of optimizing asthma therapy. The challenge for the next generation of inhalers will be to provide still greater benefits to patients in terms of efficacy, safety, and convenience. Dry powder inhalers (DPIs) are innovative new inhalation devices and comparisons with pressurized metered dose inhalers (pMDIs) show that DPIs are at least as efficient at delivering drugs, and may be a superior delivery device for some drugs. To compare different inhaler devices, drug dose comparisons that lie on the slope of the dose-response curve should be selected, and it is important to analyze the risk:benefit ratio (therapeutic ratio). Some of the new devices contain aerosols with a smaller particle size than current designs. Monodispersed aerosols with a very narrow range of particle sizes may target drug delivery to specific areas of the lung where it is most effective. However, as smaller particles are more easily absorbed into the pulmonary circulation via the alveoli, these formulations may be associated with a higher incidence of systemic side effects. The optimal particle size required to maximize the therapeutic ratio of a molecule may be different for a beta2-agonist than for an inhaled corticosteroid. A greater understanding of this relationship will be required if we are to achieve better drug targeting with future inhalers.

Administration, Inhalation↗
PubMed1999

Drug delivery from the Turbuhaler and Nebuhaler pressurized metered dose inhaler to various age groups of children with asthma.

A total of 198 children aged 3 to 15 years inhaled a single dose of 200 micrograms budesonide from a Nebuhaler pressurized metered dose inhaler (pMDI) and a Turbuhaler dry powder inhaler in a randomized crossover study. The budesonide dose delivered to a patient was assessed by measuring the amount of drug deposited on a filter inserted between the inhaler outlet and the patient's mouth. The dose of budesonide deposited on the filter and the estimated dose of particles with a mass median aerodynamic diameter (MMAD) of 5 microns or less after inhalation from the Turbuhaler were both approximately twice the values inhaled from the pMDI Nebuhaler in children less than 5 years of age (P < 0.01). The variation in the dose delivered to the patient was similar for the two inhalers in children over 5 years old. In 3- to 4-year-old children, dose delivery to the patient was higher and/or more consistent from the pMDI Nebuhaler than from the Turbuhaler. Filter dose after Turbuhaler treatment varied significantly from peak inspiratory flow rate through the Turbuhaler (PIFTbh) (P < 0.01). The percentage of children producing a PIFTbh greater than 50 L/min decreased with age (89%, 45%, and 14% in 5-, 4-, and 3-year-old children, respectively). It is concluded that drug delivery to a child with asthma varies with age and inhalation device. Further studies are needed to assess the clinical importance of this finding.

Administration, Inhalation↗
PubMed2004

Inhaled steroid delivery from small-volume holding chambers depends on age, holding chamber, and interface in children.

The relationship between the amount of inhaled steroids delivered from pressurized metered-dose inhalers used with their recommended holding chambers and age of the patients using these devices was studied in an open randomised cross-over filter study. We recruited 1-2-month-old healthy infants (n = 21), 2-3-year-old asthmatics (n = 13), 4-6-year-old asthmatics (n = 15), and 10-15-year-old asthmatics (n = 20). Each child inhaled two puffs, administered by a single investigator, of both budesonide through Nebuchamber and fluticasone propionate through Babyhaler, on two occasions. Moreover, the 4-6-year-old group inhaled via both facemask and mouthpiece. Drug, collected on a filter interposed between holding chamber and patient, was analysed by high performance liquid chromatography. Filter dose, expressed in percent of the nominal dose, was analysed in a mixed effect linear regression model with age group, holding chamber and inhalation interface (facemask or mouthpiece) as fixed effects and subject as random effect. Filter dose from both holding chambers increased significantly with age, from 3% with Babyhaler and 7% with Nebuchamber in the youngest children, to 40-41% with both holding chambers in adolescents. Nebuchamber delivered more drug than Babyhaler (p = 0.002), but variability in drug delivery (about 11%) was similar between holding chambers. Filter dose decreased from 35% to 22% with Babyhaler, and from 42% to 27% with Nebuchamber when using a mouthpiece rather than a facemask (p < 0.0001). Delivery of inhaled steroids used with their recommended holding chambers depends from age and holding chamber, but also from the inhalation interface. Lung deposition and clinical studies comparing inhalation from holding chambers with mouthpiece and facemask are urgently required.

Adolescent↗
PubMed2005

A comparison of standard inhalers for asthma with and without alcohol as the propellant on the measurement of alcohol in breath.

Because most bronchodilator inhalers contain propellant gases or a small amount of ethanol as a co-solvent, the potential for these products to generate false readings on a evidential breath alcohol instrument was evaluated in 69 volunteers with clinically stable asthma. All subjects underwent a breath test on an infrared breath alcohol analyzer (Alcotest 7110, Dräger, Lübeck, Germany) before the use of the asthma inhaler and 1 and 5 min after inhalation. The effects of antiasthmatic medications delivered by metered dose inhalers (MDIs) with alcohol as a vehicle, alcohol-free MDIs, and dry powder inhalers were assessed in homogeneous groups of four to five patients. All subjects were alcohol-free on the preliminary breath test. One minute after inhalation, negative readings were only observed in 25 (36.2%) of subjects. In 62.3% of patients, apparent alcohol results were considered interferences or unstable readings by the breath-test instrument. One subject showed a final positive breath alcohol level (0.07 mg/L). After the use of dry powder inhalers, valid results without interferences were obtained. However, 89.6% of patients in which bronchodilators were delivered by MDIs (with propellant gases in the aerosol) showed altered partial readings and labeled the final output as "invalid," but tests performed 5 min after the use of inhalers were valid and correct in all cases. MDIs with propellants as a vehicle may cause false positive breath alcohol readings in some patients. These effects are transient and may be prevented by a 5-10-min interval between the use of MDIs and breath alcohol testing.

Adult↗
PubMed1998

Inhaled prostaglandin E1 for treatment of acute lung injury in severe multiple organ failure.

UNLABELLED: Acute lung injury is characterized by hypoxemia due to pulmonary ventilation/perfusion-mismatching. I.v. administered prostaglandin E1 (PGE1), a vasodilator with a high pulmonary clearance, has been studied in acute lung injury. Inhalation of the vasodilators nitric oxide and prostacyclin improved oxygenation by selective dilation of the pulmonary vasculature in ventilated lung areas. In the present study, PGE1 inhalation was used for treatment of acute lung injury. Fifteen patients with acute lung injury defined as PaO2/fraction of inspired oxygen (FIO2) <160 mm Hg were treated with PGE1 inhalation in addition to standard intensive care. The drug was continuously delivered via a pneumatic nebulizer. Acute physiology and chronic health evaluation system II and multiple organ failure scores were (mean +/- SEM) 33 +/- 2 and 10 +/- 0.3, respectively. Inhaled PGE1 was administered for 103 +/- 17 h at a dose of 41 +/- 2 microg/h. The PaO2/FIO2 ratio increased from 105 +/- 9 to 160 +/- 17 mm Hg (P < 0.05) and to 189 +/- 25 mm Hg (P < 0.05) after 4 h and 24 h, respectively. PGE1 inhalation decreases in mean pulmonary artery pressure and central venous pressure were not statistically significant. Mean arterial pressure, pulmonary capillary wedge pressure, cardiac output, and heart rate remained unchanged. Intensive care unit mortality was 40%. The present data suggest that inhaled PGE1 is an effective therapeutic option for improving oxygenation in patients with acute lung injury. Whether inhaled PGE1 will increase survival in acute lung injury should be investigated in a controlled prospective trial. IMPLICATIONS: In patients with severe acute lung injury and multiple organ failure, inhaled prostaglandin E1 improved oxygenation and decreased venous admixture without affecting systemic hemodynamic variables. Controlled clinical trials are warranted.

APACHE↗
PubMed1977

Smoke, burns, and the natural history of inhalation injury in fire victims: a correlation of experimental and clinical data.

Mortality and morbidity in fire victims is largely a function of injury due to heat and/or smoke. While degree and area of burn together constitute a reliable numerical measure of cutaneous injury due to heat, as yet no satisfactory measure of inhalation injury has been developed. In this study, with fluid resuscitation and pulmonary infection eliminated as variables, dose-response curves were constructed as a measure of inhalation injury by exposing burned and unburned animals to smoke of constant temperature and toxicity under conditions similar to the fire situation. In these animals, the natural history of inhalation injury: 1) proved to be a relatively simple function of smoke and burn dosage; 2) appeared to simulate and therefore aid interpretation of the inhalation injury syndromes seen in human fire victims; 3) indicated that within limits [COHgb] measured immediately after injury was directly proportional to, and might prove to be a clinically valuable measure of, absorbed dose of smoke. While fluid resuscitation and pulmonary contamination with bacterial pathogens may be eliminated experimentally, such is not the case with the vast majority of fire victims admitted to burn services with associated inhalation injury. Fluid resuscitation and inhalation of a Pseudomonas aeruginosa aerosol were therefore included serially in a study of animals with inhalation injury and burns large enough to require fluid resuscitation. In these animals it was demonstrated that: 1) pulmonary edema occurred in association with too little rather than too much fluid therapy; 2) after aerosol inoculation, fatal bacterial pneumonia was difficult to produce when inhalation injury was associated with no or only small burns, but common when associated with no or only small burns, but common when associated with a burn large enough to require fluid resuscitation.

Animals↗
PubMed1995

Segmental pulmonary vascular resistance following wood smoke inhalation.

OBJECTIVES: To locate the specific site (i.e., pulmonary arteries, veins, or capillaries) of increased pulmonary vascular resistance after wood smoke inhalation and to demonstrate whether the prostanoids, thromboxane B2 or 6-keto-prostaglandin F1 alpha, play a role in these vascular resistance changes. DESIGN: Prospective, randomized, controlled trial. SETTING: Laboratory at a university medical center. SUBJECTS: Five mongrel dogs. INTERVENTIONS: The isolated canine left lower lobe preparation was used to measure changes in the pressure drop across the pulmonary arteries, veins, and capillaries. The left lower lobe was surgically isolated and perfused by a pump primed with autologous blood. The arterial and venous occlusion technique and the vascular pressure-flow relationship were used to assess changes in pulmonary vascular resistance. After baseline measurements, the left lower lobe was exposed to wood smoke for 2.5 mins and measurements were repeated. MEASUREMENTS AND MAIN RESULTS: Smoke exposure caused an immediate (5 mins post-inhalation) increase in the total pressure gradient across the lobe (baseline = 9.8 +/- 0.5 torr [1.3 +/- 0.06 kPa]); smoke inhalation = 24.3 +/- 3.9 torr [3.24 +/- 0.5 kPa]; p < .05). Total pressure drop was partitioned longitudinally into pressure drops across arteries, veins, and the middle vessels. The increase in total pressure drop was associated with a moderate increase in the pressure drop across the middle vessels (baseline = 1.1 +/- 0.2 torr [0.14 +/- 0.02 kPa]; smoke inhalation = 5.2 +/- 1.1 torr [0.69 +/- 0.14 kPa]; p < .05); a large increase in the pressure drop across the veins (baseline = 4.8 +/- 1.3 torr [0.64 +/- 0.17 kPa]; smoke inhalation = 20.7 +/- 3.4 torr [2.7 +/- 0.45 kPa]; p < .05), and no significant change in the pressure drop across the arteries (baseline = 3.7 +/- 0.4 torr [0.49 +/- 0.05 kPa]; smoke inhalation = 4.8 +/- 0.5 torr [0.64 +/- 0.06 kPa]; p = NS). Increases in the pressure drop across the middle and venous vessels were transient and no longer significantly different from baseline 15 mins after smoke inhalation. Similarly, analysis of the pulmonary artery/blood flow data demonstrated that the mean slope and pressure intercept were greater than baseline only at 5 mins postsmoke inhalation (p < .05). Thromboxane B2 did not significantly change from baseline values after smoke exposure and prostaglandin F1 alpha demonstrated a slight but significant decrease 30 mins postsmoke. Pulmonary edema was measured gravimetrically (wet/dry weight ratio) and smoke significantly increased lung water in the left lower lobe (wet/dry weight ratio = 6.55 +/- 0.4) as compared with the normal left upper lobe (wet/dry weight ratio = 4.97 +/- 0.2). CONCLUSIONS: We conclude that smoke causes an intense but transient increase in the pressure drop across the venous segment that may accelerate the formation of pulmonary edema, which is not mediated by changes in thromboxane B2 or prostaglandin F1 alpha.

Analysis of Variance↗
PubMed1996

Inhaled nitric oxide in children with severe lung disease: results of acute and prolonged therapy with two concentrations.

OBJECTIVES: To evaluate the acute effects of 11 and 60 parts per million (ppm) inhaled nitric oxide on the pulmonary vascular resistance and systemic oxygenation of children with severe lung disease, and to compare the outcome of prolonged therapy with approximately 10 and 40 ppm inhaled nitric oxide. DESIGN: Prospective, randomized study. SETTING: A 26-bed pediatric intensive care unit in a tertiary children's hospital. PATIENTS: Nineteen patients (median age 11 yrs, range 7 months to 16 yrs) with acute bilateral lung disease requiring a positive end-expiratory pressure (PEEP) of > 6 cm H2O and an FIO2 of > 0.5 for > 12 hrs were treated with inhaled nitric oxide. One patient was treated twice during the same hospitalization. INTERVENTIONS: Acute hemodynamic and blood gas effects of 11 and 60 ppm inhaled nitric oxide were studied, while delivering these concentrations in random order for intervals of 20 to 30 mins. Each interval was preceded by an interval of 20 to 30 mins without nitric oxide. Patients were then randomized and treated for a prolonged period with approximately 10 or 40 ppm inhaled nitric oxide independent of their initial acute responses to 11 and 60 ppm. Nitric oxide was discontinued when ventilatory support was decreased to a PEEP of < or = 6 cm H2O and an FIO2 of < or = 0.5. MEASUREMENTS AND MAIN RESULTS: Inhaled nitric oxide selectively decreased pulmonary vascular resistance and improved systemic oxygenation. Acute hemodynamic and blood gas effects of 11 and 60 ppm nitric oxide were similar. Systemic oxygenation improved to a greater extent in patients with radiographic evidence of residual aerated lung regions than in patients with diffuse bilateral lung disease. Maximum methemoglobin concentrations were greater in patients treated for a prolonged period with 40 ppm nitric oxide. The mortality and duration of therapy were similar for patients treated with 10 and 40 ppm inhaled nitric oxide. CONCLUSIONS: Pulmonary vascular resistance and systemic oxygenation are acutely improved to a similar extent by 11 and 60 ppm inhaled nitric oxide, and concentrations in excess of 10 ppm are probably not needed for prolonged therapy of children with severe lung disease.

Administration, Inhalation↗
PubMed1998

Inhaled nitric oxide: technical aspects of administration and monitoring.

OBJECTIVES: Clinical applications of inhaled nitric oxide (NO) therapy resulted in the development of delivery systems and monitoring devices applicable to routine clinical care. This article presents the various components necessary for an adequate clinical use of inhaled NO, and discusses the NO gas mixture cylinders, inhaled NO delivery techniques and specifications, monitoring devices, and ending with an exhaustive description of the scavengers of nitrogen oxides (NOx). DATA SOURCES: Computerized search (CURRENT CONTENTS, MEDLINE) of published original research and review articles (approximately 200), conference abstracts and compendiums up to May 1997 (approximately 50), personal files, and contact with expert informants. STUDY SELECTION: Technical, experimental, and clinical reports were selected from the recent English, French, German, and Spanish literature, if pertinent to the administration or monitoring of inhaled NO. DATA EXTRACTION: The authors extracted all applicable data. DATA SYNTHESIS: The production of NO gas mixture cylinders must be certified with respect to gas purity, stability, and concentration (limits between 100 and 1000 ppm), guaranteed calibration, and specific color. An ideal inhaled NO delivery device requires a synchronized delivery, a minimal production of nitrogen dioxide (NO2), and should be simple to use (verification, calibration, convenient flushing, cylinder change possible while in use and a simple alarm setting) with full information (high and low alarms and available precision monitoring of NO, NO2, and O2). Emergency and transport systems must be readily available. The choice of the monitoring device (chemiluminescence or electrochemistry) should be made based on the knowledge of their strength and weakness for a particular clinical application. Finally, scavengers of NOx should be used with caution until specific filters are proven safe and effective. CONCLUSIONS: The great expectancies generated by inhaled NO action have led researchers to design personal inhaled NO delivery systems, but only with mitigated results. At present, medical companies are finding a financial interest in designing a delivery system which will suit the needs of clinicians and this, along with official governmental approval, will only then permit the use of inhaled NO safely and on a larger scale.

Administration, Inhalation↗
PubMed2002

Inhaled prostacyclin for the treatment of pulmonary hypertension after cardiac surgery.

OBJECTIVE: To describe the effects of inhaled prostacyclin administered after cardiopulmonary bypass (CPB) to a patient with severe pulmonary hypertension. DESIGN: Case report and literature review. SETTING: Cardiac surgical operating rooms and postoperative recovery unit. PATIENTS: A 63-yr-old female who had undergone mitral and aortic valve replacement for rheumatic heart disease. INTERVENTIONS: Administration of inhaled prostacyclin to decrease pulmonary artery pressures and to permit discontinuation of CPB. MEASUREMENTS AND MAIN RESULTS: The patient was unable to be removed from CPB because of severe pulmonary hypertension precipitating acute right heart failure, despite administration of milrinone, norepinephrine, and nitroglycerin infusions. Inhaled prostacyclin was started at a dosage of 50 ng/kg/min, and the patient was able to be weaned from CPB. The inhaled prostacyclin was continued for 4 days postoperatively, with no signs of tolerance or systemic effects. CONCLUSION: Inhaled prostacyclin is an effective and selective pulmonary vasodilator at the dosage given in this report. Prolonged use is not associated with tolerance or systemic effects. The apparatus required for the delivery of inhaled prostacyclin is simple, inexpensive, and readily available in most hospitals. A review of the literature suggests that inhaled prostacyclin is effective in a number of clinical settings and displays comparable efficacy and hemodynamic effects to inhaled nitric oxide.

Administration, Inhalation↗
PubMed2003

Combination of intravenously infused methylene blue and inhaled nitric oxide ameliorates endotoxin-induced lung injury in awake sheep.

OBJECTIVE: To evaluate the effects of a combination of methylene blue, an inhibitor of the nitric oxide pathway, and inhaled nitric oxide on endotoxin-induced acute lung injury in awake sheep. DESIGN: Prospective, randomized, controlled experimental study. SETTING: University animal laboratory. SUBJECTS: Twenty-four yearling, awake sheep. INTERVENTIONS: The sheep were anesthetized and instrumented with vascular catheters. After 1 wk of recovery, the animals underwent tracheotomy and were subjected to intravenous infusions of endotoxin 10 ng x kg-1 x min-1 and isotonic saline 3 mL x kg-1 x hr-1 for 8 hrs. The sheep were randomly assigned to three groups of eight animals each: a) the control group received endotoxin and saline; b) the INO group received endotoxin, saline, and inhaled nitric oxide 40 ppm for 5 hrs; and c) the MB/INO group received endotoxin, saline, and methylene blue 3 mg/kg as an intravenous bolus injection followed by a continuous infusion of 3 mg x kg-1 x min-1 for 6 hrs in combination with inhaled nitric oxide 40 ppm for 5 hrs. MEASUREMENTS AND MAIN RESULTS: Hemodynamic variables and blood gases were determined hourly. In the early phase of endotoxemia (0-2 hrs), methylene blue/inhaled nitric oxide reduced the increments in pulmonary arterial pressure, pulmonary microvascular pressure, and pulmonary vascular resistance index by 60% compared with the controls and to a greater extent than did inhaled nitric oxide alone. During the late phase, all the preceding variables returned closely to baseline following inhaled nitric oxide or methylene blue/inhaled nitric oxide but remained remarkably elevated in the control group. Inhaled nitric oxide and methylene blue/inhaled nitric oxide reduced the increase in extravascular lung water by 40% and 80%, respectively. Inhaled nitric oxide transiently attenuated the increase in venous admixture and did not prevent a decrease in arterial oxygenation. In the methylene blue/inhaled nitric oxide group, blood gases remained unchanged from baseline. CONCLUSIONS: In sheep, methylene blue/inhaled nitric oxide protects more efficiently against acute lung injury than inhaled nitric oxide alone, as indicated by a milder pulmonary hypertension, less extravascular lung water accumulation, and maintained gas exchange.

Administration, Inhalation↗
PubMedDate not supplied

High frequency percussive ventilation in pediatric patients with inhalation injury.

The objective of this study was to present data that showed high frequency percussive ventilation (HFPV) was superior to traditional mechanical ventilation for the treatment of children with inhalation injuries. Inhalation injuries continue to be the number one cause of death of patients with thermal injuries in the United States. Therapy for this condition has consisted of conservative pulmonary toilet and mechanical ventilation. Despite improvements in the management of burn injury, patients with inhalation injury develop pneumonia and pneumothorax, leading to adult respiratory distress syndrome. Unfortunately, inhalation injury that is complicated by pneumonia has been shown to increase mortality by 60% in these patients. Cioffi has shown that prophylactic use of HFPV in adult patients with inhalation injury has been a successful method of reducing the incidence of pneumonia and mortality. The effects of HFPV on the incidence of pneumonia, peak inspiratory pressures, and arterial partial pressure of oxygen/fraction of inspired concentration of oxygen (P/F) ratios were retrospectively studied in 13 children with inhalation injuries and compared with historic controls treated with conventional mechanical ventilation. All patients were treated with our standard inhalation injury protocol and extubated when they met standard extubation criteria. Patients ranged in age from 6 to 9 years, and most had burns covering greater than 50% of their total body surface areas. No deaths occurred in either group, but the patients who were treated with HFPV had no cases of pneumonia (P < .05), better P/F ratios (P < .05), lower peak inspiratory pressures, and less work of breathing (P < .05) as compared with our control group. On the basis of our clinical experience and data, the use of HFPV seems to be an effective treatment for the reduction of pulmonary morbidity in pediatric patients with inhalation injuries.

Case-Control Studies↗
PubMed1983

Effect of inhalation injury on lung water accumulation.

Fourteen thermally injured patients with severe inhalation injury were sequentially studied with the thermal-green dye double indicator dilution technique of extravascular lung water (EVLW) measurement. Eight females and six males (average age, 49 years, and average thermal burn, 37% body surface) were studied for 2-31 days postinjury. All were burned in a closed space, had facial burns, soot in their sputum, and a mean carboxyhemoglobin level of 30%. Nine patients died, six of sepsis, one each of acute renal failure, hepatorenal syndrome, and anoxic brain damage. Mean EVLW on admission was 7.0 +/- 2.9 ml/kg and remained normal in the five survivors and in the patients dying of acute renal failure and anoxic brain damage. Six patients had increases in EVLW, caused by altered pulmonary capillary permeability in five and by elevation of hydrostatic pressures in one patient (hepatorenal death). Of the five patients with permeability edema, one appeared to result from a direct early effect of inhalation injury resulting in an EVLW of 13.3 ml/kg on admission. The other four patients had EVLW increases after the onset of sepsis, resulting in a mean EVLW of 23.2 +/0- 7.2 ml/kg at death (p less than 0.01). Seventy-one per cent of all patients developed pneumonia, which appears to have caused an EVLW increase in one patient; the other EVLW increases were caused by systemic sepsis. In our present study of 14 patients with definite severe inhalation injury only one had an early increase in EVLW directly related to the inhalation injury, an early effect on capillary permeability presumably caused by direct chemical toxicity of inhaled gases. The remaining four cases of permeability edema occurred 4-24 days postinjury and resulted from burn wound or pulmonary sepsis. We thus conclude that increases in EVLW after thermal and inhalational injury are primarily caused by systemic or pulmonary sepsis, and have a delayed onset. Early increases in EVLW may be a result of the chemical toxicity of inhaled gases but are very uncommon, moderate in degree, and are seen only with the severest cases of inhalation injury.

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