Decrease In Tidal Volume Research Articles

Lung volume quantified by MRI reflects extracellular-matrix deposition and altered pulmonary function in bleomycin models of fibrosis: effects of SOM230.

Idiopathic pulmonary fibrosis is a progressive and lethal disease, characterized by loss of lung elasticity and alveolar surface area, secondary to alveolar epithelial cell injury, reactive inflammation, proliferation of fibroblasts, and deposition of extracellular matrix. The effects of oropharyngeal aspiration of bleomycin in Sprague-Dawley rats and C57BL/6 mice, as well as of intratracheal administration of ovalbumin to actively sensitized Brown Norway rats on total lung volume as assessed noninvasively by magnetic resonance imaging (MRI) were investigated here. Lung injury and volume were quantified by using nongated or respiratory-gated MRI acquisitions [ultrashort echo time (UTE) or gradient-echo techniques]. Lung function of bleomycin-challenged rats was examined additionally using a flexiVent system. Postmortem analyses included histology of collagen and hydroxyproline assays. Bleomycin induced an increase of MRI-assessed total lung volume, lung dry and wet weights, and hydroxyproline content as well as collagen amount. In bleomycin-treated rats, gated MRI showed an increased volume of the lung in the inspiratory and expiratory phases of the respiratory cycle and a temporary decrease of tidal volume. Decreased dynamic lung compliance was found in bleomycin-challenged rats. Bleomycin-induced increase of MRI-detected lung volume was consistent with tissue deposition during fibrotic processes resulting in decreased lung elasticity, whereas influences by edema or emphysema could be excluded. In ovalbumin-challenged rats, total lung volume quantified by MRI remained unchanged. The somatostatin analog, SOM230, was shown to have therapeutic effects on established bleomycin-induced fibrosis in rats. This work suggests MRI-detected total lung volume as readout for tissue-deposition in small rodent bleomycin models of pulmonary fibrosis.

Role of central and peripheral opiate receptors in the effects of fentanyl on analgesia, ventilation and arterial blood-gas chemistry in conscious rats

This study determined the effects of the peripherally restricted μ-opiate receptor (μ-OR) antagonist, naloxone methiodide (NLXmi) on fentanyl (25μg/kg, i.v.)-induced changes in (1) analgesia, (2) arterial blood gas chemistry (ABG) and alveolar-arterial gradient (A-a gradient), and (3) ventilatory parameters, in conscious rats. The fentanyl-induced increase in analgesia was minimally affected by a 1.5mg/kg of NLXmi but was attenuated by a 5.0mg/kg dose. Fentanyl decreased arterial blood pH, pO2 and sO2 and increased pCO2 and A-a gradient. These responses were markedly diminished in NLXmi (1.5mg/kg)-pretreated rats. Fentanyl caused ventilatory depression (e.g., decreases in tidal volume and peak inspiratory flow). Pretreatment with NLXmi (1.5mg/kg, i.v.) antagonized the fentanyl decrease in tidal volume but minimally affected the other responses. These findings suggest that (1) the analgesia and ventilatory depression caused by fentanyl involve peripheral μ-ORs and (2) NLXmi prevents the fentanyl effects on ABG by blocking the negative actions of the opioid on tidal volume and A-a gradient.

Evolution of Mortality over Time in Patients Receiving Mechanical Ventilation

Baseline characteristics and management have changed over time in patients requiring mechanical ventilation; however, the impact of these changes on patient outcomes is unclear. To estimate whether mortality in mechanically ventilated patients has changed over time. Prospective cohort studies conducted in 1998, 2004, and 2010, including patients receiving mechanical ventilation for more than 12 hours in a 1-month period, from 927 units in 40 countries. To examine effects over time on mortality in intensive care units, we performed generalized estimating equation models. We included 18,302 patients. The reasons for initiating mechanical ventilation varied significantly among cohorts. Ventilatory management changed over time (P < 0.001), with increased use of noninvasive positive-pressure ventilation (5% in 1998 to 14% in 2010), a decrease in tidal volume (mean 8.8 ml/kg actual body weight [SD = 2.1] in 1998 to 6.9 ml/kg [SD = 1.9] in 2010), and an increase in applied positive end-expiratory pressure (mean 4.2 cm H2O [SD = 3.8] in 1998 to 7.0 cm of H2O [SD = 3.0] in 2010). Crude mortality in the intensive care unit decreased in 2010 compared with 1998 (28 versus 31%; odds ratio, 0.87; 95% confidence interval, 0.80-0.94), despite a similar complication rate. Hospital mortality decreased similarly. After adjusting for baseline and management variables, this difference remained significant (odds ratio, 0.78; 95% confidence interval, 0.67-0.92). Patient characteristics and ventilation practices have changed over time, and outcomes of mechanically ventilated patients have improved. Clinical trials registered with www.clinicaltrials.gov (NCT01093482).

Co-activation of μ- and δ-opioid receptors elicits tolerance to morphine-induced ventilatory depression via generation of peroxynitrite

We determined whether pretreatment with (1) the μ-/δ-opioid receptor (μ-/δ-OR) antagonist, naloxone, (2) the δ1,2-OR antagonist, naltrindole, or (3) the peroxynitrite scavenger, d-penicillamine, affects the development of tolerance to the ventilatory depressant effects of morphine in rats. The injection of morphine in vehicle-pretreated rats decreased minute ventilation predominantly via decreases in tidal volume. Pretreatment with naloxone blunted the responses to morphine whereas pretreatment with naltrindole or d-penicillamine did not. A second injection of morphine, given one day later, elicited markedly smaller responses in vehicle rats whereas it elicited pronounced ventilatory depression in rats that were pretreated with naloxone, naltrindole or d-penicillamine (prior to morphine) the day before. Moreover, the ventilatory responses elicited by subsequent exposure to a hypoxic–hypercapnic challenge were markedly depressed in naloxone- or d-penicillamine-pretreated rats compared to vehicle-pretreated rats. These findings suggest that activation of μ- and δ-ORs causes tolerance to the ventilatory depressant effects of morphine at least partly via the generation of peroxynitrite.

Mechanisms of nasal high flow on ventilation during wakefulness and sleep

Nasal high flow (NHF) has been shown to increase expiratory pressure and reduce respiratory rate but the mechanisms involved remain unclear. Ten healthy participants [age, 22 ± 2 yr; body mass index (BMI), 24 ± 2 kg/m(2)] were recruited to determine ventilatory responses to NHF of air at 37°C and fully saturated with water. We conducted a randomized, controlled, cross-over study consisting of four separate ∼60-min visits, each 1 wk apart, to determine the effect of NHF on ventilation during wakefulness (NHF at 0, 15, 30, and 45 liters/min) and sleep (NHF at 0, 15, and 30 liters/min). In addition, a nasal cavity model was used to compare pressure/air-flow relationships of NHF and continuous positive airway pressure (CPAP) throughout simulated breathing. During wakefulness, NHF led to an increase in tidal volume from 0.7 ± 0.1 liter to 0.8 ± 0.2, 1.0 ± 0.2, and 1.3 ± 0.2 liters, and a reduction in respiratory rate (fR) from 16 ± 2 to 13 ± 3, 10 ± 3, and 8 ± 3 breaths/min (baseline to 15, 30, and 45 liters/min NHF, respectively; P < 0.01). In contrast, during sleep, NHF led to a ∼20% fall in minute ventilation due to a decrease in tidal volume and no change in fR. In the nasal cavity model, NHF increased expiratory but decreased inspiratory resistance depending on both the cannula size and the expiratory flow rate. The mechanisms of action for NHF differ from those of CPAP and are sleep/wake-state dependent. NHF may be utilized to increase tidal breathing during wakefulness and to relieve respiratory loads during sleep.

A study of respiratory rate, tidal volume, inspiratory capacity and inspiratory reserve volume in different trimesters of pregnancy

Background: The anatomical, physiological and biochemical adaptations in pregnancy are profound. Many of these changes begin soon after fertilization and continue throughout the gestation and changes in the respiratory system are part of the same process. However there is insufficient information regarding the changes in respiratory parameters in different trimesters of pregnancy. Aims: The aim of the study was designed to evaluate the pulmonary function tests in 1 st , 2 nd and 3 rd trimesters of pregnancy and compare them with non-pregnant control group. Materials and Methods: A cross-sectional study was carried in 200 healthy women in the age range of 19-35 years. The subjects were distributed in four groups, as control (non-pregnant) group and 1 st , 2 nd and 3 rd trimester pregnant groups. Number of subjects in each group was 50. Respiratory parameters in control and study groups were recorded. Statistical Analysis: By ' Z ' test. Results: There was gradual significant increase in respiratory rate in all trimesters of pregnancy. There was a gradual decrease in tidal volume in 1 st , 2 nd and 3 rd trimesters of pregnancy when compared to non pregnant women. There was significant decrease in Inspiratory Reserve Volume and Inspiratory Capacity. Conclusion: The changes in pulmonary function are attributed to major adaptations in the maternal respiratory system and are influenced by the mechanical pressure of enlarging gravid uterus, elevating the diaphragm and restricting the movements of lungs thus hampering the forceful expiration and also might be due to decline in alveolar Pco 2 caused by hyperventilation which acts as bronchoconstrictor; in addition to sensitization of respiratory center due to progesterone

Low-dose morphine elicits ventilatory excitant and depressant responses in conscious rats: Role of peripheral μ-opioid receptors.

The systemic administration of morphine affects ventilation via a mixture of central and peripheral actions. The aims of this study were to characterize the ventilatory responses elicited by a low dose of morphine in conscious rats; to determine whether tolerance develops to these responses; and to determine the potential roles of peripheral μ-opioid receptors (μ-ORs) in these responses. Ventilatory parameters were monitored via unrestrained whole-body plethysmography. Conscious male Sprague-Dawley rats received an intravenous injection of vehicle or the peripherally-restricted μ-OR antagonist, naloxone methiodide (NLXmi), and then three successive injections of morphine (1 mg/kg) given 30 min apart. The first injection of morphine in vehicle-treated rats elicited an array of ventilatory excitant (i.e., increases in frequency of breathing, minute volume, respiratory drive, peak inspiratory and expiratory flows, accompanied by decreases in inspiratory time and end inspiratory pause) and inhibitory (i.e., a decrease in tidal volume and an increase in expiratory time) responses. Subsequent injections of morphine elicited progressively and substantially smaller responses. The pattern of ventilatory responses elicited by the first injection of morphine was substantially affected by pretreatment with NLXmi whereas NLXmi minimally affected the development of tolerance to these responses. Low-dose morphine elicits an array of ventilatory excitant and depressant effects in conscious rats that are subject to the development of tolerance. Many of these initial actions of morphine appear to involve activation of peripheral μ-ORs whereas the development of tolerance to these responses does not.

Morphine has latent deleterious effects on the ventilatory responses to a hypoxic challenge*

The aim of this study was to determine whether morphine depresses the ventilatory responses elicited by a hypoxic challenge (10% O2, 90% N2) in conscious rats at a time when the effects of morphine on arterial blood gas (ABG) chemistry, Alveolar-arterial (A-a) gradient and minute ventilation (VM) had completely subsided. In vehicle-treated rats, each episode of hypoxia stimulated ventilatory function and the responses generally subsided during each normoxic period. Morphine (5 mg/kg, i.v.) induced an array of depressant effects on ABG chemistry, A-a gradient and VM (via decreases in tidal volume). Despite resolution of these morphine-induced effects, the first episode of hypoxia elicited substantially smaller increases in VM than in vehicle-treated rats, due mainly to smaller increases in frequency of breathing. The pattern of ventilatory responses during subsequent episodes of hypoxia and normoxia changed substantially in morphine-treated rats. It is evident that morphine has latent deleterious effects on ventilatory responses elicited by hypoxic challenge.

Occurrence bilateral bronchospasm consequently after unilateral bronchospasm

Occurrence bilateral bronchospasm consequently after unilateral bronchospasm

Effects of fresh and aged traffic-related particles on breathing pattern, cellular responses, and oxidative stress

Air pollution is comprised of a complex mixture of gaseous and particulate pollutants emitted from multiple sources. During transport in the atmosphere, emissions undergo photochemical reactions, which may change their toxicity. Toxicological and epidemiological studies have linked vehicular emissions to respiratory and cardiovascular health effects. The aim of this study was to investigate the toxicity of primary and secondary traffic particles. Male Sprague–Dawley rats were exposed to either filtered air (control group) or one of three types of atmospheres: fresh primary particles from a major traffic tunnel plenum (P); secondary organic aerosol formed from photochemical oxidation of primary tunnel gases after filtration of primary particles (SOA); or photochemically aged primary particles plus secondary organic aerosols (P + SOA). In each exposure, 80–90 % of pollutant gases were removed using a non-selective denuder. Animals were exposed for 5 h per day, with varying number of days of exposure. Outcomes included: breathing pattern, broncho-alveolar lavage (BAL), complete blood count, and in vivo chemiluminescence (IVCL). Consistent mass concentration (approximately 50 μg/m3) was achieved for all exposures. Respiratory data showed many changes with each exposure type. All exposures produced decreases in tidal volume, minute volume, inspiratory and expiratory flows. There were mild inflammatory changes in BAL, with increased neutrophils for the SOA and P + SOA exposures and lymphocytes for the P and P + SOA exposure, with no changes in any test exposure for total protein, β-NAG or IVCL. All exposures produced changes compared to filtered air. Exposures containing particles (P and P + SOA) had stronger effects than SOA.

Effects of 28 days silicon dioxide aerosol exposure on respiratory parameters, blood biochemical variables and lung histopathology in rats

Inhalation toxicity of silicon dioxide aerosol (150, 300mg/m3) daily over a period of 28 days was carried out in rats. The changes in respiratory variables during the period of exposure were monitored using a computer programme that recognizes the modifications of the breathing pattern. Exposure to the aerosol caused a time dependent decrease in tidal volume, with an increase in respiratory frequency compared to the control. Biochemical variables and histopathological observation were noted at 28th day following the start of exposure. Biochemical markers of silica induced lung injury like plasma alkaline phosphatase, lactate dehydrogenase and angiotensine converting enzyme activities increased in a concentration dependent manner compared to control. Increase in the plasma enzymatic activities indicates endothelial lung damage, increased lung membrane permeability. Histopathological observation of the lungs confirmed concentration dependent granulomatous inflammation, fibrosis and proteinacious degeneration. Aggregates of mononuclear cells with entrapped silica particles circumscribed by fibroblast were observed in 300mg/m3 silica aerosol exposed group at higher magnification. Decrease in tidal volume and increase in respiratory frequency might be due to the thickening of the alveolar wall leading to a decreased alveolar volume and lowered elasticity of the lung tissue. The trends in histological and biochemical data are in conformity with the respiratory data in the present study. This study reports for the first time, the changes in respiratory variables during silica aerosol exposure over a period of 28 days.

Obstructive Sleep Apnea and Respiratory Complications Associated with Vagus Nerve Stimulators

Intermittent vagus nerve stimulation can reduce the frequency of seizures in patients with refractory epilepsy. Stimulation of vagus nerve afferent fibers can also cause vocal cord dysfunction, laryngeal spasm, cough, dyspnea, nausea, and vomiting. Vagus nerve stimulation causes an increase in respiratory rate, decrease in respiratory amplitude, decrease in tidal volume, and decrease in oxygen saturation during periods of device activation. It usually does not cause an arousal, or a change in heart rate or blood pressure. Most patients have an increase in their apnea-hypopnea index (AHI). Patients with VNS can have central apneas, obstructive hypopneas, and obstructive apneas. These respiratory events can be reduced with changes in the vagus nerve stimulator operational parameters or with the use of CPAP. In summary, there are complex relationships between epilepsy and obstructive sleep apneas. In particular, patients with refractory epilepsy need assessment for undiagnosed and untreated obstructive sleep apnea before implantation of vagus nerve stimulator devices. Patients with vagus nerve stimulators often have an increase in apneic events after implantation, and these patients need screening for sleep apnea both before and after implantation.

Do Unexpected Panic Attacks Occur Spontaneously?

Spontaneous or unexpected panic attacks, per definition, occur "out of the blue," in the absence of cues or triggers. Accordingly, physiological arousal or instability should occur at the onset of, or during, the attack, but not preceding it. To test this hypothesis, we examined if points of significant autonomic changes preceded the onset of spontaneous panic attacks. Forty-three panic disorder patients underwent repeated 24-hour ambulatory monitoring. Thirteen natural panic attacks were recorded during 1960 hours of monitoring. Minute-by-minute epochs beginning 60 minutes before and continuing to 10 minutes after the onset of individual attacks were examined for respiration, heart rate, and skin conductance level. Measures were controlled for physical activity and vocalization and compared with time matched control periods within the same person. Significant patterns of instability across a number of autonomic and respiratory variables were detected as early as 47 minutes before panic onset. The final minutes before onset were dominated by respiratory changes, with significant decreases in tidal volume followed by abrupt carbon dioxide partial pressure increases. Panic attack onset was characterized by heart rate and tidal volume increases and a drop in carbon dioxide partial pressure. Symptom report was consistent with these changes. Skin conductance levels were generally elevated in the hour before, and during, the attacks. Changes in the matched control periods were largely absent. Significant autonomic irregularities preceded the onset of attacks that were reported as abrupt and unexpected. The findings invite reconsideration of the current diagnostic distinction between uncued and cued panic attacks.

In vitro performance comparison of the Sensormedics 3100A and B high-frequency oscillatory ventilators

The Sensormedics 3100A and 3100B are widely used to provide high-frequency oscillatory ventilation in clinical practice. Infants and children <35 kg are typically oscillated with the 3100A and >35 kg with the 3100B. This study compares the effect of ventilator and patient parameters on delivered tidal volume during high-frequency oscillatory ventilation of a test lung with these devices. Laboratory-based study. Test lung and Sensormedics 3100A and 3100B high-frequency oscillators. A previously validated hot-wire flowmeter (Florian) was placed in series with either a 3100A (n = 3) or 3100B (n = 3) ventilator and a Michigan test lung. Tidal volumes were measured over a range of mean airway pressure, inspiratory:expiratory ratio, frequency, pressure amplitude, and endotracheal tube internal diameter. The 3100A and 3100B delivered similar tidal volumes across a range of ventilator parameters for an inspiratory:expiratory ratio of 1:1, differing by <10%. However, at an inspiratory:expiratory ratio of 1:2, there was a statistically significant decrease in tidal volume for the 3100B compared with the 3100A at lower frequencies, which was partially mitigated by increasing pressure amplitude. The difference in the generated pressure and flow waveforms may account for the observed tidal volume differences between the high-frequency oscillatory ventilation models. Delivered tidal volume was highly dependent on endotracheal tube size. Multiple variables contribute to the delivered tidal volume during high-frequency oscillatory ventilation, including ventilator model selection and endotracheal tube size. It is possible that real-time, clinical monitoring of delivered tidal volume during high-frequency oscillatory ventilation would allow better titration and maximize performance of these ventilators in caring for critically ill patients.

Detection of Hypoventilation by Capnography and Its Association With Hypoxia in Children Undergoing Sedation With Ketamine

Hypopneic hypoventilation, a decrease in tidal volume without a change in respiratory rate, is not easily detected by standard monitoring practices during sedation but can be detected by capnography. Our goal was to determine the frequency of hypopneic hypoventilation and its association with hypoxia in children undergoing sedation with ketamine. Children who received intravenous ketamine with or without midazolam for sedation in a pediatric emergency department were prospectively enrolled. Heart rate, respiratory rate, pulse oximetry, and end-tidal carbon dioxide (ET(CO2)) levels were recorded every 30 seconds. Fifty-eight subjects were included in this study. Fifty percent of subjects had recorded ET(CO2) values less than 30 mm Hg without a rise in respiratory rate. Twenty-eight percent of subjects experienced a decrease in pulse oximetry less than 95%. Patients who experienced a persistent decrease in ET(CO2) at least 30 seconds in length were much more likely to have a persistent decrease in pulse oximetry than those with normal or transient decreases in ET(CO2) (relative risk, 6.6; 95% confidence interval, 1.4-30.5). Decreases in ET(CO2) occurred on an average of 3.7 minutes before decreases in pulse oximetry. Hypopneic hypoventilation as detected by capnography is common in children undergoing sedation with ketamine with or without midazolam. Hypoxia is frequently preceded by low ET(CO2) levels. Further studies are needed to determine if the addition of routine monitoring with capnography can reduce the frequency of hypoxia in children undergoing sedation.

An evaluation of bag-valve-mask ventilation using an ergonomically designed facemask among novice users: A simulation-based pilot study

Purpose We sought to compare the ability of novice operators to provide artificial ventilation using a standard facemask and a new ergonomically designed facemask. Whether or not proper technique was used was also assessed. Methods Thirty-two allied-health students used both masks in random crossover fashion to ventilate an airway trainer. Breaths were delivered by a mechanical ventilator and exhaled tidal volume was recorded for each of 12 breaths for each participant for each mask. The effect of each mask during ventilation over time was assessed using repeated-measures ANOVA. Assessment of mask technique among participants and association between mask type and hand repositioning were analyzed using the Wilcoxon-Rank Sum Test and McNemar's paired proportions test, respectively. Results The tidal volume achieved when participants used the ergonomic mask was higher than when participants used the standard mask by the fourth breath (361 ± 104 mL vs. 264 ± 163 mL; Bonferroni adjusted p-value = 0.040) and increased over time. The repeated-measures ANOVA showed that the ergonomic mask consistently resulted in higher tidal volumes than the standard mask regardless of rescuer's gender. Over time the standard mask resulted in a linear decrease in tidal volume of −10 mL/breath (estimated difference in decay of 10 mL/breath versus the ergonomic mask; p < 0.001). Conclusion Novice airway operators were better able to provide facemask ventilation using an ergonomically designed mask than with a traditional facemask. We conclude that better hand position facilitating improved mask seal and less operator fatigue account for our findings.

NPY Y 1 receptors are involved in cardio-respiratory responses to intravenous injection of neuropeptide Y in anaesthetized rats

The respiratory effects evoked by systemic injection of neuropeptide Y (NPY) were studied in anaesthetized, spontaneously breathing rats that were (i) neurally intact; (ii) subjected to bilateral midcervical vagotomy (MC vagi cut); (iii) midcervically vagotomized and treated by supranodosal denervation (NG vagi cut); (iv) neurally intact, before and after pharmacological blockade of the NPY Y 1 and NPY Y 2 receptors. An intravenous (iv) bolus of NPY (100 μg/kg) induced slowing down of the respiratory rate, decreased tidal volume and heart rate, and increased mean arterial blood pressure. After section of midcervical vagi, NPY still evoked the cardio-respiratory changes. Supranodose vagotomy abolished the fall in respiratory rate and reduced significantly the decreases in tidal volume and minute ventilation. This level of vagotomy did not affect vasopressor and bradycardic effects of NPY. Blockade of NPY Y 1 receptors with an intravenous dose of 5 mg/kg of BMS 193885, reduced significantly the cardio-respiratory effects of NPY injection. Pre-treatment with BIIE 0246, NPY 2 receptor antagonist at a dose of 1–2.5 mg/kg was not effective in blocking the response to NPY. The results of this study indicate that NPY-evoked activation of NPY Y 1 receptors decreases both components of the breathing pattern, and this response is primarily mediated central to the cervical vagi. Bradycardia and hypertensive effect of NPY are attributed to the excitation of peripheral and central NPY Y 1 receptors and occur outside of the vagal pathways.

The effect of bilateral vagal blockade on respiration

Although respiratory regulation has been extensively studied so far, the relation between the vagal nerves and respiratory reflex in man is still open to controversy. This paper describes the effect of bilateral vagal blockade on respiration. 1) Dyspnea due to unilateral bronchial occlusion. This type of dyspnea is caused by extreme depression of the intrabronchial pressure on the occluded side and is accompanied by a rapid increase in respiratory rate and a rapid decrease in tidal volume. This type of dyspnea is relieved by blockade of the ipsilateral cervical vagal nerve. 2) Animal experiments on bilateral lung transplantation, heart-lung transplantation and bilateral cervical vagal blockade. The respiratory changes induced by CO2 inhalation, low O2 inhalation, respiratory stimulant. Loss of blood or fever stimulation in the manipulated dogs were compared with those in normal controls. CO2 inhalation alone produced differences in the respiratory rates and tidal volumes between the two groups. The tidal volume increase under CO2 inhalation was suppressed by the inflation reflex but other afferent vagal nerves seemed to be closely associated with the increased respiratory rate. 3) Vagal nerve reflex in humans. Blockade of the bilateral cervical vagal nerves in an awake state resulted in irregular PETCO2 in cases that had been stable and sometimes produced a pattern of Cheyne-Stokes respiration. Inhalation of 5% CO2 restored the regular rhythm of respiration and enhanced the response to CO2. When subjected to bilateral vagal blockade in an awake state, the patient expressed an unbearbly uneasy dyspneic sensation as if he were pulled into a bottomless abyss. This was demonstrated by the unstable FRC level.

Use of a Helium-Oxygen Mixture to Facilitate Ventilation During Bronchoscopy Through a Laryngeal Mask Airway

Flexible fiberoptic bronchoscopy may be performed in infants and children for various diagnostic and therapeutic purposes. In infants and children, general anesthesia may be used to facilitate the procedure. When general anesthesia is used, a laryngeal mask may be used to control the airway. However, as the passage of the bronchoscope decreases the cross-sectional airway inside the laryngeal mask airway (LMA) for gas exchange, increases in respiratory resistance may occur. We present our experience with the use of a helium-oxygen mixture to facilitate bronchoscopy through an LMA during general anesthesia in infants and children. We retrospectively reviewed changes in tidal volume, respiratory rate, and transcutaneous carbon dioxide (TC-CO(2)) during 3 phases of general anesthetic care. Phase 1 was pressure support breathing of an air-oxygen mixture through an LMA during sevoflurane anesthesia prior to the start of bronchoscopy, phase 2 was with the bronchoscope inserted through the LMA during pressure support ventilation of sevoflurane in an air-oxygen mixture, and phase 3 was with the bronchoscope inserted through the LMA during pressure support breathing of sevoflurane in a helium-oxygen mixture. The study cohort included 6 patients, ranging in age from 14 to 49 months. There was a statistically significant increase in respiratory rate, increase in TC-CO(2), and decrease in tidal volume with the insertion of the bronchoscope through the LMA when compared to baseline values (phase 2 vs phase 1). These values returned to values that were comparable to the baseline values when a helium-oxygen mixture was administered (phase 1 vs phase 3). A helium-oxygen mixture decreases resistance to gas flow during bronchoscopy through an LMA in infants and children receiving general anesthesia with sevoflurane and pressure support ventilation.

Amelioration of pulmonary dysfunction and neutrophilic inflammation by PPARγ agonist in LPS-exposed guinea pigs

Airway dysfunction and pulmonary neutrophilic inflammation are the major characteristics of inflammatory conditions of lungs like chronic obstructive pulmonary disease (COPD). Lipopolysaccharide (LPS), a constituent of cigarette smoke, has been identified as the most important risk factor for COPD development. Inhalation exposure to LPS or cigarette smoke elicits an inflammatory response accompanied by airway hyperresponsiveness, elevated proinflammatory mediators and inflammatory cells similar to COPD. In the present study, we have evaluated the effects of pioglitazone, a peroxisome proliferator-activated receptor gamma (PPARγ) agonist, in LPS-induced pulmonary dysfunction, inflammatory changes and oxidative stress in guinea pigs. Inhalation exposure to nebulised LPS (30 μg ml −1) resulted in significant increase in the breathing frequency and bronchoconstriction accompanied with a significant decrease in tidal volume. Our results demonstrated that the LPS-induced pulmonary dysfunction was temporally associated with neutrophil infiltration as evident from heavy neutrophilia, increased TNFα in bronchoalveolar lavage fluid (BAL), elevated myeloperoxidase (MPO) level and histology of the lung tissue. Exposure to LPS also produced significant increase in tissue malondialdehyde (MDA) level indicating underlying oxidative stress. The results also reveal that pioglitazone (3, 10 and 30 mg kg −1, p.o.) is effective in abrogating the pulmonary dysfunction by attenuating neutrophilia, TNFα release and oxidative stress in LPS-induced model of acute lung inflammation. Results from the present study have added to the emergent body of evidence that PPARγ agonists are effective in the therapy of inflammatory disease of the lungs.