Vascular and airway effects of endogenous cyclooxygenase products during lung inflation

1985 ◽  
Vol 59 (3) ◽  
pp. 884-889 ◽  
Author(s):  
H. Baier ◽  
L. Yerger ◽  
R. Moas ◽  
A. Wanner
Keyword(s):  
Transpulmonary Pressure ◽  
Mean Value ◽  
Base Line ◽  
Pulmonary Resistance ◽  
Flow Probe ◽  
Lung Inflation ◽  
Mechanically Ventilated ◽  
Before And After ◽  
Electromagnetic Flow Probe ◽  
Induced Changes

The influence of lung inflation on lung elasticity and pulmonary resistance (RL) and on pulmonary and bronchial hemodynamics was examined in five anesthetized, mechanically ventilated adult sheep before and after treatment with the cyclooxygenase inhibitor indomethacin (2 mg/kg). Lung inflation was accomplished by increasing levels of positive end-expiratory pressure (PEEP). Measurements of pulmonary vascular resistance (PVR), bronchial blood flow (Qbr), and RL were obtained with a Swan-Ganz catheter, with an electromagnetic flow probe placed around the carinal artery, and by relating airflow to transpulmonary pressure (Ptp), respectively. Before indomethacin, increasing PEEP from 5 to 15 cmH2O increased mean lung volume (VL) to 135% (P less than 0.01), Ptp to 165% (P less than 0.005), and PVR to 132% (P less than 0.05) of base line and decreased mean Qbr (normalized for cardiac output) to 53% (P less than 0.05) of base line. Mean RL showed a tendency to decrease with a mean value of 67% of base line at 15 cmH2O PEEP. After indomethacin the corresponding values were 121% for VL, 155% for Ptp, 124% for PVR, 35% for Qbr, and 31% for RL. The PEEP-dependent changes were not different before and after indomethacin except for mean VL, which increased less (P less than 0.05) after indomethacin. The failure of indomethacin to modify PEEP-induced changes in RL, PVR, and Qbr was also present when these parameters were expressed as a function of Ptp. These findings suggest that the cyclooxygenase products elaborated during lung inflation reduce lung elasticity but fail to influence airflow resistance and pulmonary and bronchial hemodynamics.

Changes in regional lung impedance after intravenous histamine bolus in dogs: effects of lung volume

1995 ◽  
Vol 78 (3) ◽  
pp. 875-880 ◽  
Author(s):  
Z. Balassy ◽  
M. Mishima ◽  
J. H. Bates
Keyword(s):  
Lung Volume ◽  
Time Course ◽  
Lung Inflation ◽  
Lung Elastance ◽  
Airway Narrowing ◽  
Tracheal Pressure ◽  
Lung Resistance ◽  
Regional Lung ◽  
Before And After ◽  
Induced Changes

We measured the effect of lung volume on the time course of regional lung input impedance (ZA) after bolus intravenous administration of 2 mg of histamine in seven open-chest dogs using alveolar capsule oscillators. ZA (24–200 Hz) was obtained during apnea at constant lung volume every 2 s for 80 s at lung inflation pressures of 0.1, 0.2, 0.3, 0.5, 0.7, and 1.0 kPa. Local airway resistance (RA) and elastance of the local lung region were calculated by fitting a four-parameter model to the measured ZA. Total lung resistance and lung elastance were also calculated from tracheal pressure and flow measured during mechanical ventilation (0.3 Hz) just before and after each set of ZA measurements. We found the histamine-induced changes in both lung resistance and lung elastance to decrease with increasing lung volume. RA also showed a large negative dependency on lung volume, and the variation between different RA measurements became markedly increased as lung volume decreased. In contrast, local airway elastance was essentially unaffected by lung volume. These results support the idea that parenchymal tethering of the very distal airways impedes their narrowing during bronchoconstriction. They also indicate that reduced parenchymal tethering causes airway narrowing to become markedly more inhomogeneous.

Effects of ozone on cyclooxygenase metabolites in the baboon tracheobronchial tree

1990 ◽  
Vol 69 (1) ◽  
pp. 245-250 ◽  
Author(s):  
J. M. Fouke ◽  
R. A. DeLemos ◽  
M. J. Dunn ◽  
E. R. McFadden
Keyword(s):  
Arachidonic Acid ◽  
Hydrolysis Product ◽  
Tracheobronchial Tree ◽  
Ozone Exposure ◽  
Base Line ◽  
Respiratory Resistance ◽  
Pulmonary Resistance ◽  
Short Term ◽  
Short Term Exposure ◽  
Before And After

Short-term exposure to 0.5 parts per million (ppm) ozone has been shown to cause an increase in respiratory resistance in primates that can be diminished by 50% with pretreatment with cromolyn sodium. Because of the known membrane-stabilizing effects of cromolyn and the resultant inhibition of mediator production, we hypothesized a role for the products of arachidonic acid (AA) metabolism in these events. We exposed five adult male baboons to 0.5 ppm ozone on two occasions, once with cromolyn pretreatment and once without. Pulmonary resistance (RL) was monitored and bronchoalveolar lavage (BAL) was performed before and after each exposure. The BAL was analyzed for a stable hydrolysis product of prostacyclin, 6-keto-prostaglandin (PG) F1 alpha, PGE2, a stable hydrolysis product of thromboxane (Tx) A2, TxB2, and PGF2 alpha. RL increased after ozone exposure (1.62 +/- 0.23 to 3.77 +/- 0.51 cmH2O.l-1.s, difference 2.15; P less than 0.02), and this effect was partially blocked by cromolyn (1.93 +/- 0.09 to 3.18 +/- 0.40 cmH2O.l-1.s, difference 1.25; P less than 0.02). The base-line levels of the metabolites of AA in the BAL were as follows (in pg/ml): 6-keto-PGF1 alpha 72.78 +/- 12.6, PGE2 145.92 +/- 30.52, TxB2 52.52 +/- 9.56, and PGF2 alpha 22.28 +/- 5.42. Ozone exposure had no effect on the level of any of these prostanoids (P = NS). These studies quantify the magnitude of cyclooxygenase products of AA metabolism in BAL from baboon lungs and demonstrate that changes in the levels of these mediators in BAL are not prerequisites for ozone-induced increases in respiratory resistance.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals High-resolution spatial measurements of ventilation-perfusion heterogeneity in rats

2010 ◽  
Vol 108 (5) ◽  
pp. 1395-1401 ◽  
Author(s):  
H. Thomas Robertson ◽  
Melissa A. Krueger ◽  
Wayne J. E. Lamm ◽  
Robb W. Glenny
Keyword(s):  
High Resolution ◽  
Regional Blood Flow ◽  
Laboratory Animals ◽  
Fluorescence Signal ◽  
Method Error ◽  
Mechanically Ventilated ◽  
Before And After ◽  
The Mean ◽  
Induced Changes ◽  
High Resolution Method

This study was designed to validate a high-resolution method to measure regional ventilation (V̇a) in small laboratory animals, and to compare regional V̇a and perfusion (Q̇) before and after methacholine-induced bronchoconstriction. A mixture of two different colors of 0.04-μm fluorescent microspheres (FMS) was aerosolized and administered to five anesthetized, mechanically ventilated rats. Those rats also received an intravenous injection of a mixture of two different colors of 15-μm FMS to measure regional blood flow (Q̇). Five additional rats were labeled with aerosol and intravenous FMS, injected with intravenous methacholine, and then relabeled with a second pair of aerosol and intravenous FMS colors. After death, the lungs were reinflated, frozen, and sequentially sliced in 16-μm intervals on an imaging cryomicrotome set to acquire signal for each of the FMS colors. The reconstructed lung images were sampled using randomly placed 3-mm radius spheres. V̇a within each sphere was estimated from the aerosol fluorescence signal, and Q̇ was estimated from the number of 15-μm FMS within each sphere. Method error ranged from 6 to 8% for Q̇ and 0.5 to 4.0% for V̇a. The mean coefficient of variation for Q̇ was 17%, and for V̇a was 34%. The administration of methacholine altered the distribution of both V̇a and Q̇ within lung regions, with a change in V̇a distribution nearly twice as large as that seen for Q̇. The methacholine-induced changes in V̇a were not associated with compensatory shifts in Q̇. Cryomicrotome images of FMS markers provide a high-resolution, anatomically specific means of measuring regional V̇a/Q̇ responses in the rat.

Prostaglandins: renal vascular responses to bradykinin, histamine, and nitroglycerine

1978 ◽  
Vol 234 (4) ◽  
pp. H496-H502 ◽  
Author(s):  
L. P. Feigen ◽  
B. M. Chapnick ◽  
J. E. Flemming ◽  
P. J. Kadowitz
Keyword(s):  
Blood Flow ◽  
Arachidonic Acid ◽  
Cyclooxygenase Inhibitors ◽  
Flow Probe ◽  
Vascular Responses ◽  
Vasodilator Activity ◽  
Before And After ◽  
Anesthetized Dogs ◽  
Electromagnetic Flow Probe ◽  
Renal Vascular

A study was undertaken to evaluate the effects of inhibitors of prostaglandin (PG) synthesis on renal vascular responses to several renal vasodilators in anesthetized dogs. Indomethacin (IND) and meclofenamate (MEC), two dissimilar cyclooxygenase inhibitors were used. An electromagnetic flow probe was placed on the renal artery and a needle was inserted proximal to the probe. Injections of bradykinin, histamine, nitroglycerine, and arachidonic acid (AA) were given before and after administration of IND or MEC, 2.5 mg/kg body wt. In each experiment, inhibition of PG synthesis was estimated by reduction of vasodilator activity following AA injection. Although renal vascular resistance increased slightly after IND or MEC, elevations of renal blood flow in response to injections of bradykinin and nitroglycerine were not affected by PG synthesis inhibitors, whereas percent responses to histamine were enhanced by IND but not MEC. In addition, the action of 5 mg/kg IND on responses to injections and infusions of bradykinin was evaluated. No decrease in vasodilator activity following the kinin was detected in these studies. These results demonstrate that renal vascular responses to bradykinin, histamine, and nitroglycerine were not dependent on endogenously produced products of cyclooxygenase (e.g., prostaglandins) in the kidney of the anesthetized dog.

Neutral endopeptidase inhibitor potentiates allergic bronchoconstriction in guinea pigs in vivo

1993 ◽  
Vol 75 (1) ◽  
pp. 185-190 ◽  
Author(s):  
O. Kawano ◽  
H. Kohrogi ◽  
T. Yamaguchi ◽  
S. Araki ◽  
M. Ando
Keyword(s):  
Guinea Pig ◽  
Guinea Pigs ◽  
Transpulmonary Pressure ◽  
Neutral Endopeptidase ◽  
Allergic Response ◽  
Pulmonary Resistance ◽  
Parasympathetic Nerve ◽  
Mechanically Ventilated ◽  
Airway Response

To determine whether endogenous tachykinins are released in allergic airway response to contribute to bronchoconstriction and whether neutral endopeptidase (NEP), which effectively cleaves tachykinins, modulates that bronchoconstriction, we studied the effects of the NEP inhibitor phosphoramidon on bronchoconstriction induced by allergic response in anesthetized guinea pigs. We mechanically ventilated the guinea pigs sensitized with ovalbumin (OVA) in a bodyplethysmograph and measured the pulmonary resistance (RL). We exposed the sensitized guinea pigs to doubling concentrations of OVA aerosols from 2(-5)% (wt/vol) until the transpulmonary pressure increased more than twofold from the baseline. After the final exposure, we exposed them to phosphoramidon (10(-4) M) or its vehicle. Phosphoramidon significantly potentiated the increased RL induced by OVA challenge. Phosphoramidon also significantly potentiated the increased RL in the guinea pigs treated with atropine, but the potentiation was significantly reduced. In contrast, phosphoramidon failed to potentiate the increased RL induced by OVA in guinea pigs pretreated with capsaicin. These results suggest that 1) endogenous tachykinin-like substances are released in allergic airway response and that 2) when endogenous NEP is inhibited in the guinea pig airways in vivo, the substances contribute to bronchoconstriction by partly activating the parasympathetic nerve.

Regulation of bronchomotor tone by lung inflation in asthmatic and nonasthmatic subjects

1981 ◽  
Vol 50 (5) ◽  
pp. 1079-1086 ◽  
Author(s):  
J. E. Fish ◽  
M. G. Ankin ◽  
J. F. Kelly ◽  
V. I. Peterman
Keyword(s):  
Airway Obstruction ◽  
Total Lung Capacity ◽  
Base Line ◽  
Deep Inspiration ◽  
Lung Inflation ◽  
Lung Capacity ◽  
Impaired Ability ◽  
Before And After ◽  
Airway Conductance ◽  
Bronchomotor Tone

We examined the effects of lung inflation on induced airway obstruction in 14 atopic asthmatic and 14 atopic nonasthmatic subjects. Subjects were challenged with aerosols of methacholine (MCh) and pollen antigen (Ag), and the effects of inflation were assessed with partial ad full flow-volume curves and by comparing airway conductance measurements before and after deep inspiration to total lung capacity (TLC). Whereas bronchoconstriction was transiently abolished or reduced with inspiration in nonasthmatics, these effects were absent or diminished in asthmatic subjects. Dissimilarities could not be explained by differences in base-line lung function or degree of obstruction produced. Deep inspiration had a greater effect in reducing airway obstruction produced with MCh than with Ag in nonasthmatics. In addition, atropine pretreatment had no effect on inspiration responses in asthmatics given Ag, suggesting that vagal reflexes were not the cause of an impaired ability to reduce bronchomotor tone by lung inflation. Our findings reveal the existence of an intrinsic means of regulating bronchomotor toe by active changes in lung volume and that such a mechanism is impaired in asthma. We suggest that airway hyperactivity in asthma is perhaps less a reflection of enhanced end-organ responsiveness than a reflection of this impaired capacity.

Effect of lung volume on collateral ventilation in the dog

1980 ◽  
Vol 49 (1) ◽  
pp. 9-15 ◽  
Author(s):  
J. Kaplan ◽  
R. C. Koehler ◽  
P. B. Terry ◽  
H. A. Menkes ◽  
R. J. Traystman
Keyword(s):  
Lung Volume ◽  
Transpulmonary Pressure ◽  
Relative Increase ◽  
Small Airways ◽  
Lung Inflation ◽  
Before And After ◽  
Collateral Pathways ◽  
Flow Through ◽  
Collateral Ventilation

We studied the effect of lung volume on resistance through collateral pathways (Rcoll) and small airways (Rsaw) before and after the injection of methacholine into obstructed segments of intact dogs. Before methacholine, Rcoll decreased 15.0 ± 4.9 (SE)% per cmH2O increase in transpulmonary pressure (Ptp) and Rsaw decreased 5.1 ± 7.0 (SE)% per cmH2O increase in Ptp. Following methacholine, lung inflation resulted in similar decreases in Rcoll and Rsaw. The fall in Rcoll was significantly greater than the fall in Rsaw. When pressure in an obstructed segment (Ps) was increased with constant Ptp (nonhomogeneous inflation), Rcoll fell approximately half as much for each cmH2O increase in pressure compared to when Ptp was increased (homogeneous inflation). We conclude 1) that increases in lung volume have small effects on Rsaw so that there is a relative increase in flow through collateral channels serving obstructed poritons of lung and 2) that Rcoll is a function of the size of the obstructed segment that increases more under homogeneous than nonhomogeneous conditions.

Respiratory mechanics in men following a deep air dive

1986 ◽  
Vol 61 (2) ◽  
pp. 734-740 ◽  
Author(s):  
P. W. Catron ◽  
J. Bertoncini ◽  
R. P. Layton ◽  
M. E. Bradley ◽  
E. T. Flynn
Keyword(s):  
Lung Function ◽  
Vital Capacity ◽  
Respiratory Mechanics ◽  
Decompression Sickness ◽  
Lung Compliance ◽  
Lung Mechanics ◽  
Base Line ◽  
Pulmonary Resistance ◽  
Doppler Signals ◽  
Before And After

The mechanical properties of the lungs were measured in 10 men before and after a simulated air dive to 285 ft of seawater (87 m). The objective was to determine whether a dive likely to produce pulmonary bubble emboli would alter lung mechanics. Lung function was measured predive and at 1, 2, 3, 6, 7, and 23 h postdive. Measurements of lung function were also made at identical times on a control day when no dive was made. Each set of measurements included precordial Doppler signals, pulmonary resistance, quasistatic lung compliance, forced vital capacity (FVC), forced expired volume after 1.0 s (FEV 1.0), the ratio of FEV 1.0 to FVC (FEV 1.0/FVC%), and maximal airflow after 50 and 75% of the vital capacity had been expired (Vmax50 and Vmax75, respectively). Base-line measurements of pulmonary resistance and quasistatic compliance were normal in all subjects. FVC and FEV 1.0 were greater than predicted for most subjects and were increased proportionately so that the FEV 1.0/FVC% was normal. Following the dive, bubble signals were heard in four subjects, and two subjects had mild symptoms of decompression sickness. No subject demonstrated any alteration in lung function that could be attributed to the dive. We concluded that stressful decompressions capable of producing “silent” pulmonary bubble emboli do not alter lung mechanics.

Expiratory bulbospinal neurons of dogs. II. Laterality of responses to spatial and temporal pulmonary vagal inputs

1992 ◽  
Vol 262 (6) ◽  
pp. R1087-R1095 ◽  
Author(s):  
M. Tonkovic-Capin ◽  
E. J. Zuperku ◽  
J. Bajic ◽  
F. A. Hopp
Keyword(s):  
Neuronal Response ◽  
Stimulus Frequency ◽  
Transpulmonary Pressure ◽  
Vagus Nerves ◽  
Afferent Pathways ◽  
Lung Inflation ◽  
Type D ◽  
Before And After ◽  
Thiopental Sodium ◽  
Synaptic Mechanisms

Pulmonary mechanoreceptors with vagal fibers produce a combination of excitation and inhibition in the majority of the expiratory bulbospinal (EBS) neurons of dogs. Both aspects of this transpulmonary pressure-dependent neuronal response appear to be slowly adapting and activated at low pressure levels, suggesting the involvement of the slowly adapting pulmonary stretch receptors (PSRs). The purpose of the present study was to determine the contribution of different afferent pathways to each of the response components and to characterize the spatial and temporal processing of ipsi-, contra-, and bilateral vagal afferent inputs by two types of EBS neurons. For this purpose low-intensity electrical stimulation of the intact, desheathed, vagus nerves was used in thiopental sodium-anesthetized paralyzed dogs. The phrenic neurogram was used to synchronize both ventilation and stimulation. During test respiratory cycles, pulse trains (4-5 s duration) were applied during the neural expiratory phase to each and both vagus nerves. The mean discharge frequency (Fn) during the stimulus period was obtained from cycle-triggered histogram data. Plots of Fn vs. stimulus strength and Fn vs. stimulus frequency suggest that inhibition of both type D and type A EBS neurons is mediated mainly by the ipsilateral vagus nerve, and that the excitation of type D neurons is mediated bilaterally. These conclusions are also supported by inflation responses obtained before and after unilateral vagotomies. Differences in latencies and spatial and temporal summation characteristics suggest the possible involvement of different 1) types of PSRs, 2) central pathways, and/or 3) synaptic mechanisms in the biphasic response of the caudal ventral EBS neurons to lung inflation.

Effects of deep inhalation in asthma: relative airway and parenchymal hysteresis

1985 ◽  
Vol 59 (5) ◽  
pp. 1590-1596 ◽  
Author(s):  
C. B. Burns ◽  
W. R. Taylor ◽  
R. H. Ingram
Keyword(s):  
Transpulmonary Pressure ◽  
Large Degree ◽  
Base Line ◽  
Flow Volume ◽  
High Group ◽  
Before And After ◽  
Complete Study ◽  
Anatomical Dead Space ◽  
Residual Capacity ◽  
Expiratory Flow

Asthmatic subjects were screened for the effects or volume history on the degree of induced airway obstruction with methacholine by comparing isovolumic maximal expiratory flows (Vmax) from partial expiratory flow-volume curves (P) begun near functional residual capacity (FRC) followed by maximal expiratory flow-volume (M) maneuvers begun from total lung capacity (TLC). The isovolumic Vmax values from M and P maneuvers defined two groups: one had a high M/P ratio (high group), indicating a large degree of reversal with deep inhalation, another had a low M/P ratio (low group), indicating minimal reversal. No differences were found between groups. A more complete study was later performed in which we measured specific airway conductance (sGaw) and anatomical dead space (VD) as indices of airway size and hysteresis before and after deep inhalation. The area of quasi-static transpulmonary pressure (Ptp) volume (V) curves from FRC to TLC and back to FRC was measured as an index of parenchymal hysteresis. At base line both groups showed a decrease in both sGaw and VD after a deep inhalation (DI). After constriction neither group changed VD after DI, whereas sGaw increased significantly in the high group after DI. This suggests that dilation of airways with DI occurred peripheral to those contributing to VD in the high group. The areas of the Ptp-V curves were equal at base line; yet the increase in areas with constriction in the low group was much greater.

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