Effects of pulmonary congestion on airway reactivity to histamine aerosol in dogs

1984 ◽  
Vol 57 (6) ◽  
pp. 1640-1647 ◽  
Author(s):  
R. Kikuchi ◽  
K. Sekizawa ◽  
H. Sasaki ◽  
Y. Hirose ◽  
N. Matsumoto ◽  
...  

We examined the effect of acute pulmonary vascular congestion on bronchial reactivity in dogs in a standard challenge protocol. Airway responsiveness to histamine whose concentration was varied in a stepwise incremental fashion was assessed from changes in pulmonary resistance (RL) and dynamic compliance (Cdyn) in 10 anesthetized dogs. Brief acute pulmonary congestion was created by inflating a balloon placed in the left atrium to raise left atrial pressure to 20-30 cmH2O for 1 min. Pulmonary congestion did not change RL in the control condition. However, after histamine inhalation, RL was further increased by pulmonary congestion, making the two effects synergistic. This phenomenon could not be observed with vagi cut. Pulmonary congestion decreased Cdyn in all dogs regardless of histamine concentration, with or without vagotomy. We conclude that pulmonary vascular congestion makes the bronchi hyperreactive through vagal reflexes. The reduction in Cdyn caused by pulmonary congestion appears to stem mainly from the narrowing of peripheral airways by adjacent vascular engorgement.

1980 ◽  
Vol 49 (4) ◽  
pp. 620-626 ◽  
Author(s):  
T. C. Lloyd

Two types of experiments were performed in anesthetized dogs on cardiopulmonary bypass to see if pulmonary vascular congestion and left heart distension would induce reflex bronchoconstriction. First we distended the isolated left heart and lung vessels with blood while ventilating the lungs and measuring airflow, tidal volume, and transpulmonary pressures. Congestion reduced dynamic compliance and increased inspiratory resistance. Vagotomy increased compliance and decreased resistance but did not alter the effects of congestion. Then we measured changes in tracheal wall tension while we separately distended the pulmonary vessels and left heart. Left heart distension increased tracheal tension, whereas pulmonary congestion increased tension in some dogs but decreased it in others. All effects were eliminated by vagotomy. We concluded that although left heart distension and pulmonary vascular congestion may reflexly increase airway tone, pulmonary congestion may at some times reflexly reduce tone. None of these reflex changes, however, appear to be important in the modest (approximately 20%) changes in airflow dynamics observed during combined left heart and pulmonary vascular distension.


1977 ◽  
Vol 43 (4) ◽  
pp. 643-647 ◽  
Author(s):  
M. K. Benson ◽  
P. D. Graf

The interaction between the effects of vagal stimulation and inhaled histamine on the bronchi was studied in anesthetized dogs. Reactivity was assessed by measuring changes in bronchial caliber visualized with tantalum bronchograms. In seven vagotomized dogs the bronchoconstrictor response to a combination of electrical stimulation of the vagus nerves and inhaled histamine solution produced a mean reduction in airway diameter (Daw) of 2.21 mm which was significantly greater than the additive results of the two stimuli applied separately (mean decrease in Daw 0.29 +/- 0.91 mm). In three dogs the effect of vagal stimulation was to produce a shift in the dose-response curve to inhaled histamine. These results indicate that the effect of the base-line bronchomotor tone must be considered in the evaluation of the effect of vagal blockade on airway reactivity. An increase in the resting degree of bronchomotor tone may contribute to the hyperreactivity observed in patients with asthma.


1982 ◽  
Vol 52 (5) ◽  
pp. 1363-1367 ◽  
Author(s):  
A. R. Leff ◽  
N. M. Munoz ◽  
B. Alderman

Because isometric systems differ substantially from methods of measuring airway smooth muscle tone that depend on airway diameter, we determined the sensitivity and significance of data derived from these different methods in 20 anesthetized dogs. The airway contractile response was measured directly from an isometric tracheal segment in situ and simultaneously as pulmonary resistance (RL) and dynamic compliance (Cdyn). The contractile response to intravenous (iv) methacholine (MC) (2.6 X 10(-11) to 2.6 X 10(-6) mol/kg) and norepinephrine (NE) (1.2 X 10(-11) to 1.2 X 10(-6) mol/kg) was measured in dose-response studies of beta-blocked and ganglion-blocked animals. A statistically significant change in isometric tracheal tension was first observed at 2.6 X 10(-10) mol/kg iv MC and 1.2 X 10(-9) mol/kg iv NE. Statistically significant changes in Cdyn and RL did not occur at doses less than 10(-8) mol/kg for either agonist. Substantial increase in isometric tracheal tension (greater than 10 g force/cm) occurred before any change in RL or Cdyn. These finding indicate that change in isometric tension reflects parallel changes in RL and Cdyn. For NE and MC, tracheal tension is a more sensitive and selective measurement of airway contraction than RL or Cdyn.


1989 ◽  
Vol 66 (5) ◽  
pp. 2061-2070 ◽  
Author(s):  
Y. Ploysongsang ◽  
R. P. Michel ◽  
A. Rossi ◽  
L. Zocchi ◽  
J. Milic-Emili ◽  
...  

Five mongrel dogs (2 interstitial and 3 alveolar edema) were studied. Lung mechanics were measured by recording the flow, volume, and esophageal pressure according to the standard technique. Edema was produced by infusion of Ringer lactate solution. Lung sounds were recorded on tape from the dependent part of the chest wall. Lung sound signals were high-pass filtered at 100 Hz and subjected to fast Fourier transform. Samples of lung sounds were analyzed before (control) and at 5, 10, 20, 30, and 40 min after the infusion. The mean, median, and mode frequencies of sound power spectra at the control time were, respectively, 169.6 +/- 29.19, 129.6 +/- 29.81, and 136.0 +/- 29.87 (SD) Hz. These values increased significantly at 5 min after infusion to 194.0 +/- 26.08 (P less than 0.0037), 150.2 +/- 23.48 (P less than 0.0085), and 164.6 +/- 28.74 Hz (P less than 0.02), respectively. These values stayed significantly elevated at 10, 20, 30, and 40 min. The pulmonary wedge pressure, lung dynamic compliance, and pulmonary resistance were measured also at the same times. The mean, median, and mode frequencies correlated with pulmonary wedge pressure (P less than 0.00001, P less than 0.0001, P less than 0.0001), lung dynamic compliance (P less than 0.001, P less than 0.0001, P less than 0.0001), and pulmonary resistance (P less than 0.00001, P less than 0.00001, P less than 0.0001), respectively. There were no significant adventitious sounds up to 40 and 50 min after infusion. We concluded that pulmonary congestion and early edema alter the frequency characteristics of lung sounds early, before the occurrence of adventitious sounds. These altered lung sounds may be used as an index of pulmonary congestion and impending edema.


1979 ◽  
Vol 47 (1) ◽  
pp. 161-168 ◽  
Author(s):  
P. V. Bhansali ◽  
C. G. Irvin ◽  
J. A. Dempsey ◽  
R. Bush ◽  
J. G. Webster

We have investigated a new technique that could be specific for detecting small airway diseases. We measured resistance in nine subjects, evaluating the effect of breathing 80% He-20%O2, air, and 80% SF6–20% O2 at different flow rates (0.25--1.01 l/s) and frequencies (4--12 Hz). To test the sensitivity and specificity of this new technique, we used intravenous histamine infusion to cause peripheral constriction. During histamine infusion six of nine subjects showed the following changes: 1) dynamic compliance decreased; 2) subjects developed frequency dependence of compliance, and 3) there was no significant change in pulmonary resistance or Rrs (respiratory resistance) at 4 Hz. These data suggested a time-constant discrepancy in the periphery due to histamine infusion. These six subjects also developed frequency dependence of resistance (delta Rrs from 4 to 12 Hz), which was significant when breathing air (-22 +/- 6%) and maximal when we used He-O2 (-32 +/- 3%). We conclude that He-O2 can improve the specificity of frequency dependence of Rrs for detecting events occurring in the peripheral airways.


1978 ◽  
Vol 45 (3) ◽  
pp. 385-391 ◽  
Author(s):  
T. C. Lloyd

Prior experiments showed that pulmonary congestion may initiate tachypnea from lung receptors and that left atrial distention has no significant effect on breathing, but in those experiments secondary reflexes could have determined the results. In this study we separately distended the entire pulmonary vascular bed, the arterial compartment, and the left atrium in dogs perfused and oxygenated by an external system while ventilating and while not ventilating the lungs. Distending pressures ranged from 20 to 70 Torr, and as output variables we measured the initial rate of inspiration, peak inspiratory magnitude, inspiratory duration, expiratory duration, and breathing frequency from the diaphragmatic electromyogram. Total vascular congestion caused prolongation of expiration and lowering of frequency without effect on inspiratory duration, its rate or magnitude. A smaller depression was induced from the arterial compartment. Left atrial distention, which failed to occur sufficiently often to be attributable to dogs in general, had much less effect. However, when a related change in breathing did occur, it was limited to a shortening of inspiratory duration.


1988 ◽  
Vol 65 (6) ◽  
pp. 2720-2725 ◽  
Author(s):  
R. V. Broadstone ◽  
J. S. Scott ◽  
F. J. Derksen ◽  
N. E. Robinson

The effects of atropine on lung function and airway reactivity in two groups of ponies were measured. Principal ponies had a history of recurrent airway obstruction when housed in a barn and fed hay; control ponies had no history of airway obstruction. Principal and control ponies were paired, and measurements were made when principal ponies were in clinical remission (period A) and during an acute attack of airway obstruction (period B). Atropine did not alter pulmonary resistance (RL), dynamic compliance (Cdyn), or airway responsiveness in either group of ponies at period A or in the controls at period B. In principal ponies at period B, atropine did not alter Cdyn or the concentration of aerosol histamine required to decrease Cdyn to 65% of base line (ED65Cdyn) but reduced RL and the change in RL induced by 0.1 mg/ml histamine (delta RL0.1). It is likely that the latter observation was due to geometric changes in the airways, because the change in RL and in delta RL0.1 were significantly correlated. The results of this study show little resting bronchomotor tone in normal ponies, but a major portion of the increase in RL in principals at period B is mediated via muscarinic receptors. Little evidence exists for muscarinic receptor involvement in the response to aerosol histamine in either principal or control ponies.


1994 ◽  
Vol 77 (6) ◽  
pp. 2633-2640 ◽  
Author(s):  
K. Ravi ◽  
C. T. Kappagoda ◽  
A. C. Bonham

We examined the effects of low-nicotine cigarette smoke, pulmonary venous congestion, and their combination on the activity of rapidly (RAR) and slowly adapting receptors (SAR) in anesthetized rabbits. Pulmonary venous congestion was achieved by inflating a balloon in the left atrium to increase left atrial pressure. We examined smoke effects on RARs (averaged over 15 breaths) at baseline left atrial pressure and at subthreshold and suprathreshold increases in left atrial pressure. At baseline, smoke significantly increased RAR activity from 12.1 +/- 4.2 to 16.2 +/- 4.2 impulses/breath (P < 0.05). At subthreshold increases in left atrial pressure (2.9 +/- 0.6 mmHg), smoke produced larger increases in RAR activity (12.3 +/- 3.3 to 22.5 +/- 4.1 impulses/breath; P < 0.05). Suprathreshold increases in left atrial pressure (9.2 +/- 1.1 mmHg) alone increased RAR activity from 10.9 +/- 3.2 to 19.8 +/- 5.9 impulses/breath (P < 0.05). Smoke had no additional effect (22.3 +/- 4.8 impulses/breath; P > 0.05). There was, however, a transient increase in RAR activity (1st 3 breaths of smoke) under all three conditions. Of nine SARs examined, only two were stimulated by smoke. We conclude that in the rabbit smoke-induced stimulation of RARs is augmented by mild pulmonary venous congestion. of RARs is augmented by mild pulmonary venous congestion.


2019 ◽  
Vol 16 (3(Suppl.)) ◽  
pp. 0719
Author(s):  
Hadeel Kamil Khaleel

            The present study aimed to investigate the histological changes of heart, lung, liver and kidney which caused by different concentrations (10, 20 and 40 mg/kg) of Ivabradine. Results of the study revealed some histological changes represented by aggregation of the lymphocytes around respiratory bronchioles of the lung. In the liver, the drug caused hepatocyte necrosis and infiltration of the lymphocytes. In Kidney, there are no histopathological modifications in the tissue after the animals treated with 10 mg\kg of Ivabradine. When the animals treated with Ivabradine drug at 20mg/kg of bw, dose showed vascular congestion between myocardial fibers of heart. Emphysematous changes of the alveoli and infiltration of lymphocytes around respiratory bronchioles of lung. In the liver there were dilated blood sinusoids. Also, there are vascular congestion and congestion of capillaries in the glomerular of kidney. Male mice treated with Ivabradine drug at 40 mg/kg of bw cause increase spaces between myocardial fibers, cardiac atrophy and myocardial degeneration in the heart. In addition, there are infiltration of lymphocytes around respiratory bronchioles, pulmonary congestion and emphysematous changes of the alveoli in lung. In the liver, the drug cause amyloid deposition and degeneration of hepatocytes. Furthermore, the drug caused vascular congestion in the kidney. Conclusion: From the current study, we conclude that the different concentrations of Ivabradine caused tissue changes in the heart, lung, liver and kidneys. The study should continue using different drugs and concentrations.


1981 ◽  
Vol 51 (6) ◽  
pp. 1651-1656 ◽  
Author(s):  
W. M. Abraham ◽  
W. Oliver ◽  
M. J. Welker ◽  
M. M. King ◽  
A. Wanner ◽  
...  

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.


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