Effect of age on lung mechanics and airway reactivity in lambs

1986 ◽  
Vol 61 (6) ◽  
pp. 2074-2080 ◽  
Author(s):  
R. A. Sauder ◽  
K. J. McNicol ◽  
A. A. Stecenko
Keyword(s):  
Citric Acid ◽  
Dynamic Compliance ◽  
Lung Mechanics ◽  
Base Line ◽  
Airway Reactivity ◽  
Airway Opening ◽  
Residual Capacity ◽  
Nasotracheal Tube ◽  
Males And Females ◽  
Significant Change

We studied airway reactivity (AR) to aerosolized histamine, carbachol, and citric acid in lambs 1 mo of age to adulthood. Awake lambs were intubated and studied in a plethysmograph that measured dynamic compliance (Cdyn), resistance of the lung (RL), and functional residual capacity (FRC). Pleural pressure was measured using a Silastic balloon in the pleural space, and airway opening pressure (Pao) was measured using a catheter placed 1–2 cm distal to the nasotracheal tube. At the ages of 1, 3, 5, and 7 mo and adulthood, measurements of Cdyn, RL, and FRC were obtained in 46 sheep (22 males, 24 females). AR to carbachol, histamine, and citric acid was measured in each sheep in randomized order on three separate days by giving increasing concentrations of the drug in a noncumulative fashion. The dose that would have caused a 35% reduction in Cdyn (ED65Cdyn), a doubling of RL (ED200RL), or a 50% increase in FRC (ED150FRC) was calculated. In both males and females, base-line Cdyn increased (r = 0.81, P less than 0.01) with age, as did FRC (r = 0.87, P less than 0.01). There was no significant change in RL in either sex with age or in the group as a whole. There was a significant increase in AR to both histamine and carbachol with increasing age as measured by a decrease in ED65Cdyn (P less than 0.01 and P less than 0.05, respectively) with age. There was no significant change in AR with age as measured by RL or FRC for any of the three bronchoconstrictors tested.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of endotoxin on airway responsiveness to aerosol histamine in sheep

1983 ◽  
Vol 54 (6) ◽  
pp. 1463-1468 ◽  
Author(s):  
A. A. Hutchison ◽  
J. M. Hinson ◽  
K. L. Brigham ◽  
J. R. Snapper
Keyword(s):  
Dynamic Compliance ◽  
Airway Responsiveness ◽  
Lymph Flow ◽  
Lung Mechanics ◽  
Whole Body ◽  
Base Line ◽  
Residual Capacity ◽  
Induced Changes ◽  
Lung Lymph ◽  
Lung Lymph Flow

This study tested the hypothesis that in the awake sheep, airway responsiveness to aerosol histamine would be increased acutely by endotoxemia. Eleven sheep were chronically instrumented to allow for measurements of lung lymph flow, vascular pressures, and lung mechanics. Awake sheep were studied in a whole-body plethysmograph designed to measure dynamic compliance (Cdyn), resistance of the lung (RL), and functional residual capacity (FRC). Pulmonary responsiveness to aerosol histamine was assessed by giving five breaths of increasing concentrations of histamine (0.1–50 mg/ml) until Cdyn decreased to 65% (of control) or until 50 mg/ml of histamine had been given. Escherichia coli endotoxin (0.2–0.5 microgram/kg) was then infused, and at 5 h after endotoxemia pulmonary responsiveness to aerosol histamine was remeasured. After endotoxin, 9 of the 11 sheep exhibited decreased Cdyn at a lower concentration of histamine compared with the preendotoxin level (P less than 0.05). The mean of the log dose of histamine necessary to reduce Cdyn to 65% of control was 1.00 +/- 0.16 (SE) before endotoxin and 0.027 +/- 0.29 5 h after endotoxin; i.e., histamine responsiveness was increased. In the last 3 sheep studied, atropine (0.1 mg/kg iv) was given after the second aerosol histamine challenge, and a third dose-response curve was performed. Atropine did not return the endotoxin-induced increase in histamine responsiveness to base line. There was no correlation between the change in histamine responsiveness and the endotoxin-induced changes in Cdyn, FRC, RL, alveolar-arterial O2 difference, pulmonary arterial pressure, or lung lymph flow.

Lung mechanics and airway reactivity in sheep during development of oxygen toxicity

1990 ◽  
Vol 69 (5) ◽  
pp. 1779-1785 ◽  
Author(s):  
M. Fukushima ◽  
L. S. King ◽  
K. H. Kang ◽  
M. Banerjee ◽  
J. H. Newman
Keyword(s):  
Static Pressure ◽  
Positive Airway Pressure ◽  
Oxygen Toxicity ◽  
Dynamic Compliance ◽  
Lung Mechanics ◽  
Lung Edema ◽  
Airway Reactivity ◽  
Residual Capacity ◽  
Lung Lymph ◽  
Airway Abnormalities

The causes of respiratory distress in O2 toxicity are not well understood. The purpose of this study was to better define the airway abnormalities caused by breathing 100% O2. Sheep were instrumented for measurements of dynamic compliance (Cdyn), functional residual capacity by body plethysmography (FRC), hemodynamics, and lung lymph flow. Each day Cdyn and FRC were measured before, during, and after the application of 45 min continuous positive airway pressure (CPAP) at 15 cmH2O. The amount of aerosol histamine necessary to reduce Cdyn 35% from baseline (ED35) was measured each day as was the response to aerosol metaproterenol. Cdyn decreased progressively from 0.083 +/- 0.005 (SE) 1/cmH2O at baseline to 0.032 +/- 0.004 l/cm H2O at 96 h of O2. Surprisingly, FRC did not decrease (1,397 +/- 153 ml at baseline vs. 1,523 +/- 139 ml at 96 h). The ED35 to histamine did not vary among days or from air controls. Metaproterenol produced a variable inconsistent increase in Cdyn. We also measured changes in Cdyn during changes in respiratory rate and static pressure-volume relationships in five other sheep. We found a small but significant frequency dependence of compliance and an increase in lung stiffness with O2 toxicity. We conclude that in adult sheep O2 toxicity reduces Cdyn but does not increase airway reactivity. The large reduction in Cdyn in O2 toxicity results from processes other than increased airway reactivity or reduced lung volume, and Cdyn decreases before the development of lung edema.

Evaluation of the mechanism of decreased airway responsiveness in lambs

1989 ◽  
Vol 66 (2) ◽  
pp. 727-731 ◽  
Author(s):  
A. Stecenko ◽  
K. McNicol ◽  
S. Polk
Keyword(s):  
Dynamic Compliance ◽  
Open Lung Biopsy ◽  
Airway Responsiveness ◽  
Lung Mechanics ◽  
Saline Control ◽  
Aerosol Delivery ◽  
Adult Sheep ◽  
Adrenergic Activity ◽  
Residual Capacity

In this study we investigated three possible mechanisms for the decreased airway responsiveness (AR) found in young lambs. To evaluate aerosol delivery, 6 adult sheep (9 mo-3 yr old) and 12 lambs (4–8 wk old) were challenged with aerosol (aH) and intravenous histamine (ivH). Awake animals were intubated and studied in a plethysmograph, which measured dynamic compliance (Cdyn), resistance of the lung, and functional residual capacity. AR to histamine was measured by administration of increasing concentrations of histamine until a significant change in lung mechanics occurred or until the maximum dose of histamine was given. In all six adult sheep, the response to both aH and iVH was a decrease in Cdyn. In two lambs Cdyn was decreased with both aH and ivH, in five lambs with neither, in three lambs with aH only, and in two lambs with ivH only. To examine the role of beta-adrenergic activity in determining AR, six adult sheep and six lambs received ivH and on a separate day ivH with propranolol pretreatment (p + ivH). The median effective dose of histamine that caused a reduction in Cdyn to 65% of normal saline control (ED65Cdyn) for the adult sheep given ivH was 3.60 (range 0.23–4.85) and 0.70 (range 0.49–8.0) micrograms.kg-1.min-1 for p + ivH (P = NS). The median ED65Cdyn for the six lambs was 8.0 micrograms.kg-1.min-1 for both ivH alone and p + ivH. To evaluate the role of airway smooth muscle (SM), AR to aH was quantitated in six adult sheep and six lambs, and then an open-lung biopsy was performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Differences in airway reactivity in normal and allergic sheep after exposure to sulfur dioxide

1981 ◽  
Vol 51 (6) ◽  
pp. 1651-1656 ◽  
Author(s):  
W. M. Abraham ◽  
W. Oliver ◽  
M. J. Welker ◽  
M. M. King ◽  
A. Wanner ◽  
...  
Keyword(s):  
Sulfur Dioxide ◽  
Flow Resistance ◽  
Ascaris Suum ◽  
Dynamic Compliance ◽  
Airway Reactivity ◽  
Pulmonary Flow ◽  
Significant Change ◽  
Conscious Sheep

The effect of breathing 5 ppm sulfur dioxide (SO2) on airway reactivity was studied in both normal and allergic conscious sheep. Allergic sheep were defined as animals in which inhalation of Ascaris suum extract resulted in bronchospasm as evidenced by an increase in mean pulmonary flow resistance (RL), hyperinflation, and a fall in dynamic compliance. Airway reactivity was assessed by measuring the increase of RL after 18 breaths of 0.25% carbachol (c), from an initial RL value obtained after 18 breaths of buffered saline (s) [RL(c-s)]. RL and RL(c-s) were determined prior to, immediately after, and 24 h after exposure to 5 ppm SO4 for 4 h. In both groups RL remained unchanged after SO2 exposure. Prior to exposure, RL(c-s) was not significantly different in seven normal (0.3 +/- 0.1) and seven allergic sheep [0.4 +/- 0.2 (SD) cmH2O X l–1 X s], and there was no significant change in RL (c-s) immediately after SO2 exposure in either group. Twenty-four h later, RL(c-s) RL(c-s) increased to 0.7 +/- 0.8 (P less than 0.2) in normal and to 1.8 +/- 0.9 cmH2O X l-1 X s (P less than 0.01) in allergic sheep. Because the increase in RL(c-s) after 24 h was greater (P less than 0.01) in allergic than in normal sheep, we conclude that SO2 exposure increased airway reactivity more in the former than in the latter.

Effect of granulocyte depletion on altered lung mechanics after endotoxemia in sheep

1983 ◽  
Vol 55 (1) ◽  
pp. 92-99 ◽  
Author(s):  
J. M. Hinson ◽  
A. A. Hutchison ◽  
M. L. Ogletree ◽  
K. L. Brigham ◽  
J. R. Snapper
Keyword(s):  
Dynamic Compliance ◽  
Lung Mechanics ◽  
Arterial Oxygen ◽  
Base Line ◽  
Mean Pulmonary Arterial Pressure ◽  
Before And After ◽  
Airway Response ◽  
Pulmonary Arterial ◽  
Line P

To examine the role of circulating granulocytes in the airway changes caused by endotoxemia, we measured the response of chronically instrumented unanesthetized sheep to endotoxemia before and after granulocyte depletion with hydroxyurea. Granulocyte depletion did not affect the increases in mean pulmonary arterial pressure caused by endotoxin [peak pressure 59 +/- 8 cmH2O +/- (SE) control, 51 +/- 8 cmH2O granulocyte depleted]. However, the early (30-60 min after endotoxin) airway response to endotoxemia was markedly attenuated. Without granulocyte depletion, endotoxin caused dynamic compliance (Cdyn) to decrease to 41 +/- 10% of the base-line value and total lung resistance (RL) to increase to 283 +/- 61% of base line. When animals were granulocyte depleted, endotoxin decreased Cdyn to 69 +/- 6% (P less than 0.05) of base line and increased RL to 141 +/- 20% of base line (P less than 0.05). Granulocyte depletion also attenuated the effect of endotoxin on arterial oxygenation. During the maximum airway response to endotoxin, the alveolar-to-arterial oxygen gradient was 47 +/- 5 Torr in control studies and 32 +/- 2 Torr in granulocyte depleted studies (P less than 0.05). We conclude that interaction of granulocytes with the lung contributes to the changes in lung mechanics observed following endotoxemia and that the early pulmonary hypertension and the early alterations in lung mechanics caused by endotoxemia are caused by separate processes.

Effects of nitroprusside on lung mechanics and hemodynamics after endotoxemia in awake sheep

1988 ◽  
Vol 64 (5) ◽  
pp. 2026-2032 ◽  
Author(s):  
P. Wright ◽  
Y. Ishihara ◽  
G. R. Bernard
Keyword(s):  
Pulmonary Arterial Pressure ◽  
Dynamic Compliance ◽  
Blood Oxygenation ◽  
Lung Mechanics ◽  
Base Line ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
Dose Dependent ◽  
Intravenous Sodium

We examined the effects of intravenous sodium nitroprusside (NP) infusion on pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), dynamic compliance (Cdyn), resistance to airflow across the lungs (RL), and alveolar-arterial O2 pressure gradient (PAO2-PaO2) (room air) after endotoxemia in awake sheep. NP infused 2.5 h after endotoxin administration immediately reduced mean Ppa from 30 +/- 3 to 17 +/- 3 (SE) cmH2O, PVR from 6.3 +/- 0.7 to 4.8 +/- 0.5 cmH2O.l-1.min, and RL from 340 +/- 48 of base line to 205 +/- 73% and increased Cdyn from 54 +/- 5 of base line to 80 +/- 14% without affecting PAO2--PaO2. Ppa and lung mechanics returned immediately to preinfusion levels when NP was stopped. In vitro experiments with NP showed a dose-dependent relaxation of preconstricted pulmonary artery and vein, carbachol-preconstricted sheep tracheal strips, and bronchial rings. We conclude that NP reverses pulmonary hypertension and lung mechanics abnormalities after endotoxin and that this is due to effects of NP on airway and vascular smooth muscle. The return of these abnormalities after NP cessation suggests the continued presence of vascular and airway-constricting factors late after endotoxin. The lack of effect of NP on blood oxygenation suggests that deleterious effects on hypoxic vasoconstriction are offset by improved lung mechanics.

Effects of hypoxia on lung mechanics in the newborn cat

1987 ◽  
Vol 65 (6) ◽  
pp. 1234-1238 ◽  
Author(s):  
John T. Fisher ◽  
Mark A. Waldron ◽  
Craig J. Armstrong
Keyword(s):  
Ventilatory Response ◽  
Transpulmonary Pressure ◽  
Dynamic Compliance ◽  
Lung Mechanics ◽  
Experimental Protocol ◽  
Maximal Increase ◽  
Inspiratory Resistance ◽  
Residual Capacity ◽  
Bilateral Vagotomy ◽  
Ventilatory Response To Hypoxia

The present study was designed to investigate the effects of hypoxia on lung mechanics in the newborn cat and to determine if vagal efferent innervation to the airways is involved in the response. We studied 11 animals, aged 2–7 days, anesthetized with a mixture of chloralose–urethane administered intraperitoneally. A tracheal cannula was inserted just below the larynx and following paralysis (pancuronium bromide), mechanical ventilation was initiated. A pneumothorax was created by a midline thoracotomy and an end-expiratory load was applied to maintain functional residual capacity. Animals were placed in a flow plethysmograph from which measurements of transpulmonary pressure, flow, and volume, mean inspiratory resistance, and dynamic compliance of the lung were calculated. The experimental protocol consisted of a series of 8-min trials, each preceded by a controlled volume history. The hypoxia challenge was composed of 1 min of ventilation with 40% O2, followed by 5 min exposure to 10% O2 and 2 min of recovery. In the majority of animals (7 out of 11), hypoxia had no effect on lung mechanics compared with control trials. Four animals responded to hypoxia with an increase in resistance and a decrease in compliance. Resistance remained elevated throughout the hypoxia with an average maximal increase of 47.2 ± 22.2% (SD). Dynamic compliance was significantly decreased at the 2nd, 3rd, and 4th min only of hypoxia. Bilateral vagotomy abolished the response in the four animals and hypoxia had no effect on mechanics postvagotomy. Our data suggest that in most cases changes in lung mechanics do not play a causal role in the biphasic ventilatory response to hypoxia seen in the newborn.

Effect of aerosol histamine on lung lymph in awake sheep

1984 ◽  
Vol 56 (4) ◽  
pp. 1090-1098 ◽  
Author(s):  
A. A. Hutchison ◽  
G. R. Bernard ◽  
J. R. Snapper ◽  
K. L. Brigham
Keyword(s):  
Vascular Permeability ◽  
Foley Catheter ◽  
Dynamic Compliance ◽  
Lung Mechanics ◽  
Base Line ◽  
Plasma Protein Concentration ◽  
Pulmonary Vascular Permeability ◽  
The Mean ◽  
Lung Lymph ◽  
Sustained Increase

This study examined the effect of aerosol histamine on lung lymph in the awake sheep. Eleven sheep were chronically instrumented for measurement of lung lymph, lung mechanics, and vascular pressures. Aerosol histamine was given by use of a Collison nebulizer and delivered via a tracheostomy tube. Five breaths of a 30 mg/ml histamine solution caused lung lymph flow (QL) to increase from a base line of 5.5 +/- 0.5 (SE) ml/h to 14.3 +/- 1.5 (P less than 0.05) and the lymph-to-plasma protein concentration ratio (L/P) to increase from 0.63 +/- 0.02 to 0.72 +/- 0.02 (P less than 0.05). The concentration of aerosol histamine required to change QL by 30% (ED130QL) was determined by giving increasing concentrations of aerosol histamine every 15 min. The mean ED130QL was 22.2 mg/ml. The dose of histamine required to increase QL by 30% did not correlate (r = 0.04, n = 7) with the dose required to decrease dynamic compliance by 35%. The increase in QL lasted 100 +/- 19 min. Hourly exposure to five breaths of 30 mg/ml for 5 h caused a sustained increase in QL in two sheep and a waning effect in two sheep. The combination of aerosol histamine and elevated microvascular pressure (achieved by inflating a Foley catheter situated in the left atrium) caused changes in QL and L/P not totally consistent with the hypothesis that histamine increased pulmonary vascular permeability. Increased vascular permeability in the bronchial circulation was considered a likely explanation of the data.

Airway reactivity in infants: a positive response to methacholine and metaproterenol

1987 ◽  
Vol 62 (3) ◽  
pp. 1155-1159 ◽  
Author(s):  
R. S. Tepper
Keyword(s):  
Challenge Test ◽  
Threshold Concentration ◽  
Base Line ◽  
Tidal Breathing ◽  
Airway Reactivity ◽  
Bronchial Smooth Muscle ◽  
Bronchial Challenge ◽  
Control Value ◽  
Residual Capacity ◽  
The Mean

Because the presence of bronchial smooth muscle reactivity in infants remains controversial, airway reactivity was assessed in 10 normal, asymptomatic male infants less than 15 mo of age by measuring the changes that occurred in the maximal expiratory flows at functional residual capacity (VmaxFRC) during a methacholine bronchial challenge test. Sleeping infants inhaled doubling concentrations of methacholine by 2 min of tidal breathing, starting with a concentration of 0.075 mg/ml, and the bronchial challenge was stopped when VmaxFRC decreased by at least 40%. The threshold concentration of methacholine required to produce a decrease in VmaxFRC by 2 SD's of the control value was 0.43 mg/ml (0.11–0.90). By a methacholine concentration of 1.2 mg/ml, all infants decreased VmaxFRC by at least 40% (range 40–75%), and the mean dose required to produce a 40% decrease was 0.72 mg/ml. The airway reactivity was not related to base-line flows. During the methacholine challenge, no infant developed wheezing, but the percent oxygen saturation for the group decreased significantly (P less than 0.05) from 94 to 92%. Following the methacholine, the infants inhaled the bronchodilator metaproterenol, and 10 min later, VmaxFRC returned to base line. This study demonstrates that infants exhibit airway reactivity as evidenced by bronchoconstriction with methacholine and the subsequent bronchodilation with metaproterenol.

Effects of arachidonic acid, PGF2 alpha, and a PGH2 analogue on airway diameters in dogs

1982 ◽  
Vol 53 (4) ◽  
pp. 1005-1014 ◽  
Author(s):  
S. F. Quan ◽  
M. A. Moon ◽  
R. J. Lemen
Keyword(s):  
Arachidonic Acid ◽  
Smooth Muscle ◽  
Dynamic Compliance ◽  
Dienoic Acid ◽  
Lung Mechanics ◽  
Base Line ◽  
Direct Effects ◽  
Prostaglandin F2 Alpha ◽  
Lung Resistance ◽  
Anesthetized Dogs

The effects of intravenous arachidonic acid, a prostaglandin H2 analogue [(15S)-hydroxyl-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid (PGH2-A)], and prostaglandin F2 alpha (PGF2 alpha) on lung mechanics and airway diameters were compared using tantalum bronchography in 20 paralyzed, artificially ventilated, pentobarbital-anesthetized dogs. These agents produced dose-related increases in lung resistance (RL) and decreases in dynamic compliance (Cdyn). Both RL and Cdyn changed maximally within 25 s after injection. RL, however, returned to base line within 2 min, whereas the decrease in Cdyn persisted much longer. Changes in the diameter of airways less than 2 mm produced small changes in RL and Cdyn. Larger changes in RL corresponded with changes in airways as large as 4 mm. Vagal reflexes or pulmonary edema were not important contributors to these effects. These data suggest that the changes in RL and Cdyn produced by intravascular injections of arachidonic acid, PGH2-A, and PGF2 alpha result from their direct effects on smooth muscle in airways as large as 4 mm.

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