Reflex effects of left heart and pulmonary vascular distension on airways of dogs

1980 ◽  
Vol 49 (4) ◽  
pp. 620-626 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Dynamic Compliance ◽  
Pulmonary Congestion ◽  
Wall Tension ◽  
Left Heart ◽  
Pulmonary Vessels ◽  
Vascular Congestion ◽  
Inspiratory Resistance ◽  
Anesthetized Dogs ◽  
Lung Vessels ◽  
Airway Tone

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.

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 ◽  
...  
Keyword(s):  
Left Atrial ◽  
Dynamic Compliance ◽  
Pulmonary Congestion ◽  
Bronchial Reactivity ◽  
Pulmonary Resistance ◽  
Airway Reactivity ◽  
Histamine Concentration ◽  
Peripheral Airways ◽  
Vascular Congestion ◽  
Anesthetized Dogs

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.

Breathing response to lung congestion with and without left heart distension

1988 ◽  
Vol 65 (1) ◽  
pp. 131-136 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Main Pulmonary Artery ◽  
Vagal Afferents ◽  
Left Heart ◽  
Anesthetized Dogs ◽  
Group 3 ◽  
Group 2 ◽  
Lung Vessels ◽  
Depressor Reflex ◽  
Depressor Effect

This study compared the effect of lung congestion with and without left heart (LH) distension on breathing frequency (fr) and discriminated among responses mediated by myelinated and nonmyelinated vagal afferents. Cardiopulmonary bypass perfusion of anesthetized dogs was used to isolate reflexes. The following three groups were prepared: 1) lung vessels pressurized by pumping into the main pulmonary artery (MPA); 2) lungs and fibrillating LH pressurized by pumping into MPA while draining from LH; 3) lungs congested by occluding several pulmonary veins while holding cardiac output constant. Congestion of lungs alone in groups 1 and 3 depressed fr. Congestion of lungs and distension of LH (group 2) caused transient depression of fr but a steady-state excitation. Cooling cervical vagi to 8 degrees C prevented depression of fr by congestion in all groups. In groups 1 and 2, in which MPA pressure was higher than in group 3, congestion during vagal cooling stimulated breathing. I conclude that lung congestion may stimulate fr via C-fiber afferents, but this may be overcome by a depressor effect via myelinated afferents. Simultaneous LH distension may reflexly stimulate breathing and overcome the lung depressor reflex.

Control of breathing in anesthetized dogs by a left-heart baroreflex

1986 ◽  
Vol 61 (6) ◽  
pp. 2095-2101 ◽  
Author(s):  
T. C. Lloyd
Keyword(s):  
Pulmonary Veins ◽  
Vagal Afferents ◽  
Low Flow ◽  
Base Line ◽  
Left Heart ◽  
Breathing Frequency ◽  
Autonomic Ganglion ◽  
Anesthetized Dogs ◽  
The Right ◽  
Vagal Cooling

Anesthetized open-chest dogs on cardiopulmonary bypass were used to test the hypothesis that breathing reflexly responds to distension of the left-heart chambers. Bypass perfusion withdrew systemic flow from the right atrium and returned it to the aorta after gas exchange. Ventricles were fibrillated. The left heart was isolated by tying all pulmonary veins, and it was perfused separately at low flow admitted through one pulmonary vein and withdrawn from the ventricle. Left-heart pressure was intermittently raised abruptly from a nominal base line of 0 by partial occlusion of outflow. Pressures from approximately 10 to 50 cmH2O caused proportional increases in breathing frequency and decreases in expiratory and inspiratory times. Changes occurred immediately, reached a plateau within approximately 20 s, and were sustained for periods of observation as long as 3 min. Recovery to base line followed stimulus removal. Vagal cooling to 8 degrees C prevented responses, but autonomic ganglion blockade with hexamethonium had no effect. I conclude that breathing may be stimulated by left-heart distension and that this is mediated by large myelinated vagal afferents.

Effect of small doses of 5-hydroxytryptamine (serotonin) on pulmonary circulation in the closed-chest dog

1959 ◽  
Vol 197 (5) ◽  
pp. 963-967 ◽  
Author(s):  
John T. Shepherd ◽  
David E. Donald ◽  
Erland Linder ◽  
H. J. C. Swan
Keyword(s):  
Pulmonary Artery ◽  
Pulmonary Blood Flow ◽  
Pulmonary Veins ◽  
Pulmonary Vessels ◽  
Isolated Perfused Lung ◽  
Small Doses ◽  
Perfused Lung ◽  
Anesthetized Dogs ◽  
Flow Through ◽  
The Difference

5-Hydroxytryptamine (serotonin) was infused into anesthetized dogs at a rate of 20 µg/kg/min. In nine sets of observations on three dogs the increase in the difference of pressure between the pulmonary artery and the left atrium, which averaged 55%, consistently exceeded the increase in pulmonary blood flow, which averaged 16%. 5-HT therefore is a potent constrictor of pulmonary vessels, even in small concentrations. No changes in the pulmonary-artery wedge and pulmonary-vein pressures were detected during the infusions of 5-HT, nor was there any change in the volume of blood between the pulmonary artery and the root of the aorta. With this dose of 5-HT the principal site of the increased resistance to flow through the lungs appeared to be in the precapillary vessels. In the isolated perfused lung, moderate constriction of pulmonary veins also was produced by large doses of 5-HT.

scholarly journals Investigating the Histological Changes in Heart, Lung, Liver and Kidney of Male Albino Mice Treated with Ivabradine

2019 ◽  
Vol 16 (3(Suppl.)) ◽  
pp. 0719
Author(s):  
Hadeel Kamil Khaleel
Keyword(s):  
Pulmonary Congestion ◽  
Male Mice ◽  
Histological Changes ◽  
Cardiac Atrophy ◽  
Vascular Congestion ◽  
Myocardial Degeneration ◽  
Liver And Kidney ◽  
Tissue Changes ◽  
Myocardial Fibers ◽  
Hepatocyte Necrosis

            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.

Abstract 18446: Identification of a Novel Cellular Actor Participating in Vascular Remodeling During Pulmonary Arterial Hypertension : the PW1+ Progenitor Cells

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
France Dierick
Keyword(s):  
Bone Marrow ◽  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Vascular Remodeling ◽  
Bone Marrow Cells ◽  
Mouse Lung ◽  
Pulmonary Vessels ◽  
Pulmonary Arterial ◽  
Lung Vessels

AIM: PW1+ progenitors were identified in various adult tissues and can differentiate in smooth muscle cells (SMC) in vitro. Our hypothesis is that PW1+ progenitors are recruited to participate in the vascular remodeling during pulmonary arterial hypertension (PAH). METHODS: PW1IRESnLacZ+/- mice express the β-galactosidase as a reporter gene for PW1 expression allowing to follow the lineage of PW1+ cells during a few days. These mice were exposed to chronic hypoxia (CH) to induce PAH, lung vessels neomuscularisation and SMC proliferation. PW1+ and β-Gal+ cells were studied by FACS and by immunofluorescence. RESULTS: PW1+ cells are localized in the lung parenchyma and in the perivascular zone in rodent and human lung. Two PW1+ populations were identified by flow cytometry in the mouse lung 1/ a Sca-1high/CD34high/PDGFR-α+ population which differentiates into calponin+ or α-SMA+ SMC and into vWF+ endothelial cell and 2/ a CD34-/CD146+ population expressing pericyte markers. After 2-4 days of CH, the number of lung PW1+ cells is increased (x3.5, p<0.01) and, in small pulmonary vessels media, the proportion of β-Gal+ SMC derived from PW1+ cells is increased (64±6% vs 35±3%, p<0.05) suggesting a recruitment and differentiation of PW1+ cells into lung vascular SMC. Moreover WT mice irradiated and engrafted with GFP+/β-Gal+ bone marrow cells do not show any increase in GFP+ SMC in lung vessels and do not show any β-Gal+ cells in the lung indicating that the lung PW1+ progenitors are not derived from bone marrow . Moreover, in the human PAH lung, PW1+ cells were observed in remodeled vascular structures: in the media of remodeled vessel and in plexiform lesions. CONCLUSION: These results suggest that lung resident PW1+ progenitors are recruited to participate in the vascular remodeling of small pulmonary vessels in experimental and human PAH. These progenitors show characteristics of pericytes and of vascular progenitors.

MECHANICS OF RESPIRATION IN BRONCHIOLITIS

PEDIATRICS ◽  
1964 ◽  
Vol 33 (1) ◽  
pp. 45-54
Author(s):  
Ingeborg Krieger
Keyword(s):  
Disease Process ◽  
Dynamic Compliance ◽  
Minute Volume ◽  
Normal Lung ◽  
Elastic Recoil ◽  
Pulmonary Hyperinflation ◽  
Inspiratory Resistance ◽  
Measured Flow ◽  
The Mean ◽  
High Level

Data on the pressure-flow-volume relationships in bronchiolitis were obtained by recording simultaneously tidal volumes and esophageal pressures per unit of time in 24 infants with bronchiolitis. All infants had acute pulmonary hyperinflation. The values for dynamic compliance were markedly decreased. The decrease is presumably caused by unequal ventilation at high respiratory frequencies and by the increased retractive force active in a previously normal lung at a high level of inflation. The mean tidal volume/m2 was lower and the mean minute volume/m2 higher than normal. Expiratory flow was rapid and expiration shorter than inspiration in most cases. The mean expiratory resistance was lower than the mean inspiratory resistance and below normal when compared with the values of 24 normal infants. The mean combined resistance was in the normal range. Judging from known anatomical changes in bronchiolitis, an elevated combined resistance had been expected. The finding of low values for resistance can be explained by Otis' theory of the "equality of time constants," i.e., when flow is rapid in a system of unequally obstructed airways, the measured resistance will approximate that in the larger airways. It thus appears that the measurement of resistance in the common pathway does in certain conditions not represent the true resistance in the peripherie, particularly not the resistance of the more severely affected branches. It is suggested that the finding of a short expiratory phase is caused by the increased elastic recoil, which distends the airways at high lung volumes and consequently facilitates flow in those bronchioles which are only minimally involved by the disease process. Flow in the more severely obstructed bronchioles will decrease when a given pressure is greater than that necessary for maximal flow. It appears that the measured flow in the present cases with bronchiolitic pulmonary hyperinflation is not representative of over-all effective flow as indicated by the findings of paradoxically low values for resistance.

Pulmonary response to antigen infusion in the sensitized guinea pig: modification by atropine

1975 ◽  
Vol 39 (6) ◽  
pp. 916-919 ◽  
Author(s):  
J. M. Drazen ◽  
K. F. Austen
Keyword(s):  
Pressure Pulse ◽  
Weight Ratio ◽  
Dry Weight ◽  
Dynamic Compliance ◽  
Minute Volume ◽  
Pulmonary Response ◽  
Peripheral Airway ◽  
Atropine Treatment ◽  
Airway Tone ◽  
Central Airway

Alterations in pulmonary conductance, dynamic compliance, respiratory frequency, minute volume, mean arterial pressure, pulse rate, relaxation volume-to-dry weight ratio, and wet-to-dry weight ratio resulting from antigen infusion in sensitized guinea pigs was examined with and without atropine treatment. In untreated animals 3 min after antigen infusion there were significant decreases in dynamic compliance and pulmonary conductance with an increase in relaxation volume-to-dry weight ratio while other parameters were not altered. In atropine-treated animals antigen infusion resulted in a decreased dynamic compliance and an increased relaxation volume-to-dry weight ratio but no significant change in pulmonary conductance. This suggests that the alterations in large and central airway tone resulting from antigen infusion are mediated predominantly by secondary cholinergic mechanisms while peripheral airway effects are mainly noncholinergic.

Pulmonary mechanics during induced pulmonary edema in anesthetized dogs

1959 ◽  
Vol 14 (2) ◽  
pp. 177-186 ◽  
Author(s):  
C. D. Cook ◽  
J. Mead ◽  
G. L. Schreiner ◽  
N. R. Frank ◽  
J. M. Craig
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Tidal Range ◽  
Pulmonary Mechanics ◽  
Vascular Congestion ◽  
Anesthetized Dogs ◽  
Trapped Gas ◽  
Aortic Obstruction ◽  
Gas Volume ◽  
Normal Lungs

In order to study the mechanisms underlying the changes in the mechanical properties of the lungs during pulmonary edema, pulmonary vascular congestion was produced in spontaneously breathing, anesthetized dogs by partial aortic obstruction and intravenous infusion. Brief periods of congestion were associated with small changes in the lung compliance compared with the progressive and striking compliance reduction (-78%) noted with more prolonged congestion. Lung volume at end-expiration showed little change if edema fluid and trapped gas as well as the ventilated gas volume were taken into account. When edematous lungs were forcibly inflated beyond the tidal range, it was found that the overall compliance at a distending pressure of 30 cm H2O was not much less (-6%) than that of normal lungs. Furthermore, edematous lungs manifested marked ‘static’ hysteresis during such maneuvers. These findings suggested that surface phenomena were responsible for the mechanical behavior of edematous lungs rather than vascular congestion, per se, or intrinsic tissue changes. This was borne out by experiments on excised lungs which showed that the elastic properties of edematous lungs were not significantly different from normal lungs when surface forces were minimized. Submitted on August 25, 1958

Nonadrenergic inhibitory innervation to the airways of the newborn cat

1989 ◽  
Vol 66 (4) ◽  
pp. 1995-2000 ◽  
Author(s):  
M. A. Waldron ◽  
B. J. Connelly ◽  
J. T. Fisher
Keyword(s):  
Smooth Muscle ◽  
Stimulus Frequency ◽  
Dynamic Compliance ◽  
Cholinergic Innervation ◽  
Vagus Nerves ◽  
Inhibitory System ◽  
Mechanically Ventilated ◽  
Inspiratory Resistance ◽  
Stimulating Electrodes ◽  
Slow Onset

Vagal, nonadrenergic inhibitory system (NAIS) innervation to airway smooth muscle has been demonstrated in adults of several species, including humans. However, the functional status of this system in newborns is not known. The NAIS of intestinal smooth muscle has been demonstrated in newborns and develops in parallel with cholinergic innervation (14). Since the lung is derived embryologically from the foregut and cholinergic innervation is operative at birth, we tested the hypothesis that NAIS innervation to the airways is functional in newborn cats. Nineteen cats (2–11 days of age) were anesthetized with chloralose-urethan, and a tracheal cannula was inserted. The chest was opened and the animals were mechanically ventilated. The cervical vagus nerves were separated from the sympathetics, cut, and placed on stimulating electrodes. Mean inspiratory resistance (RL, I) and dynamic compliance (Cdyn, L) were measured on a breath-by-breath basis. Atropine and propranolol were administered (2 mg/kg iv) to block cholinergic and adrenergic pathways, respectively. Subsequently, serotonin infusion was used to increase RL, I approximately 150%. Stimulation (10 s) at frequencies ranging from 2 to 20/s caused a slow-onset (30 s to peak) long-lasting decrease in RL, I and a much smaller increase in Cdyn, L. The magnitude and duration of the bronchodilation increased with stimulus frequency to a plateau at approximately 15/s. At a stimulus frequency of 2/s, RL, I decreased 11 +/- 1.9 vs 36 +/- 4.8% (SE) at 20/s, whereas Cdyn, L increased 2 +/- 1.1 vs. 6 +/- 1.7%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

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