BACKGROUND: Nitric oxide (NO) is a selective pulmonary vasodilator, and inhaled NO has bronchodilatory action due to their relaxation effect on conducting airway smooth muscle. The aim of this study was to evaluate the effects of inhaled NO on respiratory system mechanics in cats. METHODS: Nineteen cats were divided into 3 groups according to the doses of NO administered; group C (control, n=7), group 20 (20 ppm of NO, n=7), and group 40 (40 ppm of NO, n=5). After measuring the baseline value, methacholine chloride 25 microgram/kg/min was infused to induce bronchoconstriction. Inhalation of NO was started for each group 15 minutes after methacholine infusion. Pressure, volume, and flow rate were monitored with Bicore CP100 pulmonary monitor and the data were transferred to a personal computer and analyzed by a processing software. Respiratory system, airway and tissue viscoelastic resistances, and dynamic and static compliances were calculated. RESULTS: Methacholine infusion increased both airway and tissue resistances. Fifteen minutes after inhaling NO, airway resistances for NO 20 ppm and 40 ppm decreased to 65.8+/-8.5% and 62.2+/-8.9% of the control value (p<0.05). The values of tissue resistances for NO 20 ppm and 40 ppm decreased to 72.4+/-10.8% and 78.2+/-10.5% of the control value respectively (p<0.05). And thirty minutes after inhaling NO, there were also decreases of airway and tissue viscoelastic resistances in both groups but had no differences compared with fifteen minutes' values. There were no significant differences between the NO 20 ppm and 40 ppm in the values of airway and tissue viscoelastic resistances. CONCLUSION: Inhaled NO of 20 ppm and 40 ppm decreased both airway and tissue viscoelastic resistances and airway resistance was decreased more markedly than tissue resistance. There were no significant differences between 20 ppm and 40 ppm of NO in respiratory system mechanics in cats.
Airway Resistance ; Animals ; Bronchoconstriction* ; Cats* ; Inhalation ; Mechanics* ; Methacholine Chloride ; Microcomputers ; Muscle, Smooth ; Nitric Oxide* ; Relaxation ; Respiratory System*

BACKGROUND: The aim of this study was to compare the effects of isoflurane and enflurane on respiratory resistance using flow-interruption technique. METHODS: Twenty one cats were divided into 3 groups according to the agents administered; Control(control), Isoflurane(1 MAC of isoflurane) and Enflurane(1 MAC of enflurane) groups. Tracheal pressure was measured at 2 cm beyond the distal end of the tube. After measuring the baseline value, methacholine chloride(25 microgram/kg/min) was infused to induce bronchoconstriction which was continued throughout the experiment. Anesthetics were administered for each group 15 minutes after methacholine infusion (control value) via low pressure inlet of the ventilator. Measurements were made every 15 minutes. Intermittent mandatory ventilation was applied with Servo 900C ventilator. Inspiratory flow rate and tidal volume were fixed throughout the experiment for each subject. Pressure, volume and flow were monitored with Bicore CP100 pulmonary monitor. The data were transferred to a personal computer and analyzed by a processing software. Respiratory system, airway and tissue resistances, and dynamic and static compliances were calculated. RESULTS: Methacholine infusion increased both airway and tissue resistances. Fifteen minutes after administering inhalation anesthetics(M30), airway resistances for isoflurane and enflurane decreased to 50.8+/-4.7% and 62.5+/-4.9% of the control value(p<0.05). And the values of tissue resistances for isoflurane and enflurane decreased to 54.7+/-6.2% and 68.0+/-4.4% of the control value respectively (p<0.05). There were significant differences between the isoflurane and enflurane in the values of airway and tissue resistances at M30(p<0.05). But there were no significant differences between the two agents in the values of airway and tissue resistances at M45. CONCLUSION: For isoflurane and enflurane, both airway and tissue resistances are reduced. Isoflurane is more potent than enflurane in reversing methacholine-induced bronchoconstriction in this animal model.
Airway Resistance ; Anesthetics ; Animals ; Bays ; Bronchoconstriction* ; Cats* ; Enflurane* ; Inhalation ; Isoflurane* ; Methacholine Chloride ; Microcomputers ; Models, Animal ; Respiratory Mechanics* ; Respiratory System ; Tidal Volume ; Ventilation ; Ventilators, Mechanical

BACKGROUND: The aim of this study was to evaluate the influence of oral clonidine premedication on respiratory mechanics by tracheal intubation in smokers. METHODS: Thirty male smoker patients were randomly divided into 3 groups. For group 1 (n = 10), l microgram/kg of clonidine was premedicated. For group 2 (n = 10), 2 microgram/kg of clonidine was premedicated. Group 3 (n = 10, control group) was the no premedication group. After anesthetic induction, CMV was applied with a Siemens Servo 900C ventilator, and anesthetic gases were supplied via the low pressure inlet of the ventilator. Tidal volume (10 ml/kg) was fixed during measurements for each patient. End-inspiratory occlusion was applied for at least 3 seconds and tracheal pressure was measured at the distal end of the endotracheal tube. Pressure, flow and volume were monitored and recorded with a Bicore CP-100 pulmonary monitor. Data were measured after 2 (100% O2) and 5 (1.5 vol% enflurane with 50% N2O) minutes of tracheal intubation. Data were transferred to PC and analyzed by processing software (ANADAT). Total respiratory (Rrs), airway (Raw) and tissue (Rve) resistances, along with static (Cstat), dynamic (Cdyn) compliances were calculated. RESULTS: There were no significant differences for Rrs, Raw, Rve, Cstat and Cdyn in the three groups. CONCLUSIONS: Oral clonidine premedication in dosages up to 2 microgram/kg do not affect the changes of respiratory mechanics caused by tracheal intubation in smokers.
Anesthetics, Inhalation ; Bays ; Clonidine* ; Enflurane ; Humans ; Intubation* ; Male ; Mechanics* ; Premedication* ; Respiratory Mechanics ; Respiratory System* ; Tidal Volume ; Ventilators, Mechanical

BACKGROUND: The aim of this study was to evaluate the influence of oral clonidine premedication on respiratory mechanics by tracheal intubation in smokers. METHODS: Thirty male smoker patients were randomly divided into 3 groups. For group 1 (n = 10), l microgram/kg of clonidine was premedicated. For group 2 (n = 10), 2 microgram/kg of clonidine was premedicated. Group 3 (n = 10, control group) was the no premedication group. After anesthetic induction, CMV was applied with a Siemens Servo 900C ventilator, and anesthetic gases were supplied via the low pressure inlet of the ventilator. Tidal volume (10 ml/kg) was fixed during measurements for each patient. End-inspiratory occlusion was applied for at least 3 seconds and tracheal pressure was measured at the distal end of the endotracheal tube. Pressure, flow and volume were monitored and recorded with a Bicore CP-100 pulmonary monitor. Data were measured after 2 (100% O2) and 5 (1.5 vol% enflurane with 50% N2O) minutes of tracheal intubation. Data were transferred to PC and analyzed by processing software (ANADAT). Total respiratory (Rrs), airway (Raw) and tissue (Rve) resistances, along with static (Cstat), dynamic (Cdyn) compliances were calculated. RESULTS: There were no significant differences for Rrs, Raw, Rve, Cstat and Cdyn in the three groups. CONCLUSIONS: Oral clonidine premedication in dosages up to 2 microgram/kg do not affect the changes of respiratory mechanics caused by tracheal intubation in smokers.
Anesthetics, Inhalation ; Bays ; Clonidine* ; Enflurane ; Humans ; Intubation* ; Male ; Mechanics* ; Premedication* ; Respiratory Mechanics ; Respiratory System* ; Tidal Volume ; Ventilators, Mechanical

No abstract available.
Laparoscopy ; Respiratory Mechanics

No abstract available.
Respiration, Artificial* ; Respiratory Mechanics*

BACKGROUND: Reduced lung compliance and increased lung resistance are the primary lung mechanical abnomalities in acute respiratory distress syndrome (ARDS). Although there is little information regarding the mecha nisms responsible for the increases in the respiratory resistance of ARDS, bronchodilators have been frequently administered in mechanically ventilated ARDS patient. To determine the effect of a bronchodilator on the respiratory mechanics depending on the level of applied positive end-expiratory pressure (PEEP), the change in the respiratory mechanics by salbutamol ingalation was measured under the variable PEEP level in patients with ARDS. METHODS: Fifteen mechanically ventilated paralyzed ARDS patientss (14 of male, mean age 57 years) were enrolled in this study. The respiratory system compiance, and the maximum and minimun inspiratory occlusion method during constant flow inflaction using the CP-100 pulmonary monitor (Bicore, Irvine, CA, USA). The measurements were performed at randomly applied 8, 10 and 12 cm H2O PEEP before and 30 mins after administrating salbutamol using a meter-dose-inhaler (100 micro gram X 6). RESULTS: 1) The maximum inspiratory resistance of the lung was higher than the reported normol values due to an increase in the minimal inspiratory resistance and additional resistance. 2) The maximum inspiratory resistance and peak airway pressure were significantly higher at 12 cm H2O of PEEP compared with those at 10cm H2O of PEEP. 3) Salbutamol induced a significant decrease in the maximum and the minimum inspiratory resistance but no significant change in the additional resistance only was observed at 12 cm H2O of PEEP (from 15.66+/-1.99 to 13.54+/-2.41, from 10.24+/-2.98 to 8.04+/-2.34, and from 5.42+/-3.41 to 5.50+/-3.58 cm H2O/l/sec, respectively). 4) The lung compliance did not change at the applied PEEP and salbutamol inhalation levels. CONCLUSIONS: The bronchodiator response would be different depending on the level of applied PEEP despite the increased respiratory resistance in patients with ARDS.
Albuterol ; Bronchodilator Agents ; Humans ; Inhalation* ; Lung ; Lung Compliance ; Male ; Positive-Pressure Respiration ; Respiratory Distress Syndrome, Adult* ; Respiratory Mechanics* ; Respiratory System

BACKGROUND: Although there are improvements of clinical symtoms after bronchodilator inhalation in COPD patients, it has been noted that there was no increase of FEV1 in some cases. FEV1 did not reflect precisely the improvement of ventilatory mechanics after bronchodilator inhalation in these COPD patients. The main pathophysiology of COPD is obstruction of airway in expiratory phase but in result, the load of respiratory system is increased in inspiratory phase. Therefore the improvement of clinical symptoms after bronchodilator inhalation may be due to the decrease of inspiratory load. So we performed the study which investigated the effect of bronchodilator on inspiratory response of vetilatory mechanics in COPD patients. METHODS: In 17 stable COPD patients, inspiratory and expiratory forced flow-volume curves were measured respectively before bronchodilator inhalation. l0mg of salbutamol solution was inhaled via jet nebulizer for 4 minutes. Forced expiratory and inspiratory flow-volume curves were measured again 15 minutes after bronchodilator inhalation. RESULTS: FEV1, FVC and FEV1/FVC% were 0.92 +/-0.34L(38.3+/- 14.9% predicted), 2.5+/-0.81L (71.1 +/-21.0% predicted) and 43.1+/-14.5% respectively before bronchodilator inhalation. The values of increase of FEV1, FVC and PIF(Peak Inspiratory Flow) were 0.15 +/-0.13L(relative increase: 17.0%), 0.58+/-0.38 L(29.0%) and 1.0+/-0.56L/sec(37.5%) respectively after bronchodilator inhalation. The increase of PIF was twice more than FEV1 in average(p<0.001). The increase of PIF in these patients whose FEV1 was not increased after bronchodilator inhalation were 35.0%, 44.0% and 55.5% respectively. CONCLUSION: The inspiratory parameter reflected improvement of ventilatory mechanics by inhaled bronchodilater better than expiratory parameters in COPD patients.
Albuterol ; Humans ; Inhalation ; Mechanics ; Nebulizers and Vaporizers ; Pulmonary Disease, Chronic Obstructive* ; Respiratory System

No abstract available.
Humans ; Prone Position* ; Respiratory Mechanics*

No abstract available.
Humans ; Prone Position* ; Respiratory Mechanics*