Pulmonary arterial distension and activity in phrenic nerve of anesthetized dogs

1979 ◽  
Vol 46 (4) ◽  
pp. 625-631 ◽  
Author(s):  
W. O. Kan ◽  
J. R. Ledsome ◽  
C. P. Bolter

In chloralose-anesthetized dogs a constant-flow, right atrium-to-left pulmonary artery, right-heart bypass was created. The right lung root was completely occluded and an isolated pouch of the main pulmonary arteries was perfused with venous blood at controlled nonpulsatile pressures between 10 and 90 Torr. An increase in pulmonary arterial pouch pressure caused an increase in systemic arterial pressure and in respiratory drive. In animals with afferent nerves intact, the increase in respiratory drive was indicated by an increase in the amplitude of the integrated phrenic electroneurogram. In animals with the left vagus nerve cut immediately above the left lung root, the increase in respiratory drive was evident by a shortening of the time of expiration. All responses were abolished by bilateral section of the cervical vagosympathetic trunks. It is concluded that in the preparation described pulmonary arterial distension causes a reflex increase in systemic vascular resistance and in respiratory drive, the afferent path of the reflex being in the vagus nerves.

1962 ◽  
Vol 203 (5) ◽  
pp. 947-950 ◽  
Author(s):  
Koichiro Takasaki

In open-chested, anesthetized dogs the pulmonary venous outflow of the left lung was diverted into an external bypass so that the flow rate could be measured and blood prevented from returning immediately to the general circulation. Pulmonary arterial pressure was recorded in the left pulmonary artery; systemic arterial pressure and heart rate were also recorded. Injection of nicotine, veratrine, or Veriloid into this limited lung circulation produced a systemic depressor response and bradycardia. Both effects were abolished by vagotomy. It is concluded that these systemic cardiovascular effects are mediated through vagal chemoreceptors. There is no reason to implicate a mechanical pulmonary depressor reflex since these drugs produce no change in the pulmonary arterial pressure.


1995 ◽  
Vol 269 (4) ◽  
pp. R943-R947
Author(s):  
Y. Kikuchi ◽  
H. Nakazawa ◽  
D. L. Traber

We developed a chronic lung fistula that drains only the left lung, allowing for evaluation of injury in a single lung. To remove lymph drainage from the right lung into the caudal mediastinal lymph node, the right lower pulmonary ligament was severed. Pneumatic occluders were placed on the left pulmonary arteries and veins. To ensure that lymph drained from only the left lung, we increased the right pulmonary arterial pressure (RPAP) from 21.2 +/- 0.5 to 36.5 +/- 0.6 mmHg. The left pulmonary arterial pressure (LPAP) was kept at wedge pressure level for 1 h by inflating pneumatic occluders. Lymph flow from the left lung fistula was stable during this occlusion. Six hours after recovery was increased the LPAP from a baseline level of 19.1 +/- 1.0 to 36.4 +/- 0.9 mmHg and the RPAP from 21.2 +/- 0.5 to 38.0 +/- 0.8 mmHg for 2 h by inflating the pneumatic occluders on the left and right pulmonary veins. Lymph flow increased from 5.3 +/- 1.0 to 28.0 +/- 2.9 ml/h. Reflection coefficient was calculated at 0.80 +/- 0.02.


2000 ◽  
Vol 10 (4) ◽  
pp. 419-422 ◽  
Author(s):  
Astolfo Serra ◽  
Francisco Chamie ◽  
R.M. Freedom

AbstractMajor abnormalities of pulmonary circulation are uncommon in the patient with pulmonary atresia and intact ventricular septum. Non-confluent pulmonary arteries have only rarely been described in this setting. In this case report, we describe a patient in whom the pulmonary arteries are non-confluent, with the right pulmonary artery supplied through a right-sided arterial duct, and the left pulmonary artery most likely through a fifth aortic arch, thus providing a systemic-to-pulmonary arterial connection. We discuss the various forms of non-confluent pulmonary arteries in the setting of pulmonary atresia and intact ventricular septum.


2018 ◽  
Vol 28 (8) ◽  
pp. 1074-1076 ◽  
Author(s):  
Juan D. Cano Sierra ◽  
Camilo F. Mestra ◽  
Miguel A. Ronderos Dumit

AbstractMowat–Wilson syndrome is a genetic condition due to a mutation in the ZEB2 gene; it affects many systems including the cardiovascular system. The pulmonary arterial sling originates from a failure of development of the proximal portion of the left sixth aortic arch, resulting in an anomalous left pulmonary artery origin from the posterior wall of the right pulmonary artery and the left pulmonary artery crossing to the left lung between the trachea and the oesophagus. We present a 4-month-old infant with Mowat–Wilson syndrome and left pulmonary arterial sling, and discuss the association of these two rare conditions. Pulmonary arterial sling is significantly more frequent in patients with Mowat–Wilson syndrome than in the general population.


1976 ◽  
Vol 40 (6) ◽  
pp. 883-888 ◽  
Author(s):  
J. C. Newell ◽  
M. G. Levitzky ◽  
J. A. Krasney ◽  
R. E. Dutton

In 16 dogs ventilated with 100% O2, control blood flow to the left lung was 35 +/- 2% of aortic flow. When left lung atelectasis was induced, left pulmonary artery flow fell to 19 +/- 2% of aortic flow. A large retrograde component of flow developed in this pulmonary artery, suggesting that blood flows into the pulmonary arteries of both lungs during systole, but flows back out of the collapsed lung and into the uncollapsed lung during diastole. Systemic PaO2 remained above 78 mmHg. Subsequently, when the ventilation of the right lung was changed from oxygen to room air, systemic PaO2 fell to 64 +/- 3 mmHg and atelectatic left lung flow rose from 19 +/- 2% to 28 +/- 2% f aortic flow. This was associated with a reduction in reflux from the atelectatic lung. These results suggest that the attenuation of flow to an atelectatic lung is more pronounced if systemic normoxemia is maintained by adequate oxygenation of the normal lung.


2014 ◽  
Vol 117 (5) ◽  
pp. 535-543 ◽  
Author(s):  
Justin A. R. Lang ◽  
James T. Pearson ◽  
Arjan B. te Pas ◽  
Megan J. Wallace ◽  
Melissa L. Siew ◽  
...  

At birth, the transition to newborn life is triggered by lung aeration, which stimulates a large increase in pulmonary blood flow (PBF). Current theories predict that the increase in PBF is spatially related to ventilated lung regions as they aerate after birth. Using simultaneous phase-contrast X-ray imaging and angiography we investigated the spatial relationships between lung aeration and the increase in PBF after birth. Six near-term (30-day gestation) rabbits were delivered by caesarean section, intubated and an intravenous catheter inserted, before they were positioned for X-ray imaging. During imaging, iodine was injected before ventilation onset, after ventilation of the right lung only, and after ventilation of both lungs. Unilateral ventilation increased iodine levels entering both left and right pulmonary arteries (PAs) and significantly increased heart rate, iodine ejection per beat, diameters of both left and right PAs, and number of visible vessels in both lungs. Within the 6th intercostal space, the mean gray level (relative measure of iodine level) increased from 68.3 ± 11.6 and 70.3 ± 7.5%·s to 136.3 ± 22.6 and 136.3 ± 23.7%·s in the left and right PAs, respectively. No differences were observed between vessels in the left and right lungs, despite the left lung not initially being ventilated. The increase in PBF at birth is not spatially related to lung aeration allowing a large ventilation/perfusion mismatch, or pulmonary shunting, to occur in the partially aerated lung at birth.


Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Atsuko Kato ◽  
Christian Drolet ◽  
Shi-Joon Yoo ◽  
Andrew Redington ◽  
Lars Grosse-Wortmann

Introduction: The left pulmonary artery (LPA) contributes more than the right (RPA) to total pulmonary regurgitation (PR) in patients after tetralogy of Fallot (TOF) repair, but the mechanism of this difference is not well known. We hypothesized that unilaterally increased pulmonary vascular resistance (PVR), resulting from lung compression by the enlarged and levorotated heart leads to greater PR in the LPA. This study aimed to analyze the interplay between heart and lung size, mediastinal geometry, and differential PR. Methods: This is a single-center retrospective analysis of 50 magnetic resonance studies in patients after TOF repair. Patients with more than mild discrete branch pulmonary artery stenosis were excluded. Blood flow was measured by phase-contrast velocity encoding within the branch pulmonary arteries. On the axial image with the largest total cardiac surface area, cardiac angle (α) between the thoracic anterior-posterior line and the interventricular septum, right and left lung areas as well as right and left hemithorax areas were measured (Figure). Results: There was no difference in LPA and RPA diameters. The LPA showed significantly less total forward flow (p=0.04), smaller net forward flow (p=<0.001), and greater RF (p=0.001) than the RPA. Left lung area was smaller than the right (p<0.001). RVEDVi correlated with LPA RF (R=0.48, p<0.001), but not with RPA RF. Larger RVEDVi correlated with a larger α angle (R=0.46, p<0.001), i.e. a more leftward cardiac axis and with smaller left lung area (R=-0.58, p<0.001). LPA RF, but not RPA RF, correlated inversely with left lung area indexed to the left hemithorax area (R=-0.34, p=0.02). Conclusions: An enlarged and levorotated heart - as a result of PR - is associated with smaller left lung size, and augments diastolic flow reversal in the LPA, presumably via increased left PVR. By imposing a further volume load on the RV, LPA regurgitation may thus close a positive feed-back loop of PR and RV dilatation.


1981 ◽  
Vol 50 (1) ◽  
pp. 102-106 ◽  
Author(s):  
P. S. Barie ◽  
T. S. Hakim ◽  
A. B. Malik

We determined the effect of pulmonary hypoperfusion on extravascular water accumulation in anesthetized dogs by occluding the left pulmonary artery for 3 h and then reperfusing it for 24 h. The lung was reperfused either at normal left atrial pressure (Pla) or during increased Pla induced by a left atrial balloon. In each case the extravascular water content-to-bloodless dry weight ratio (W/D) of the left lung was compared with that of the right lung. The W/D of the left lung of 3.26 +/- 0.49 ml/g was not significantly different from the value of 2.87 +/- 0.37 for the right lung after the reperfusion at normal Pla. However, the W/D of the left lung of 5.10 +/- 0.38 ml/g was greater (P less than 0.05) than the value of 4.42 +/- 0.34 for the right lung after reperfusion at Pla of 25 Torr. This difference could not be prevented by pretreatment with heparin, suggesting that the increase in lung water content was not due to activation of intravascular coagulation secondary to stasis occurring during the occlusion. Because the left lung was more edematous than the right one, even though both lungs had been subjected to the same increase in Pla, the results suggest that a period of pulmonary hypoperfusion causes an increase in the interstitial protein concentration.


1995 ◽  
Vol 117 (2) ◽  
pp. 237-241
Author(s):  
H. Katayama ◽  
G. W. Henry ◽  
C. L. Lucas ◽  
B. Ha ◽  
J. I. Ferreiro ◽  
...  

We studied the detailed profiles of blood flow in the right and left pulmonary arteries using 20 MHz pulsed Doppler ultrasound equipment in a lamb model. Fourteen lambs aged four to six weeks were selected. In six lambs, monocrotaline pyrrole was injected parenterally to create pulmonary hypertension (PH group). Eight other lambs served as unaltered controls (control group). The blood flow velocities were sampled in 1mm increments along the anterior—posterior axis of the branch arteries. The maximum velocity of the forward flow in the left pulmonary artery was higher than that in the right pulmonary artery in the control group (71.7 ± 15.9cm/s vs 60.2 ± 13.5; p < 0.05). The fastest backward flow was located at the posterior position of the vessel in the right pulmonary artery in the control group. No significant bias in location was shown in the left pulmonary artery. Using indices of P90, acceleration time, P90*AcT, the velocity waveforms in the PH group were compared with those in the control group. In the left pulmonary artery, every index in the control group showed a significantly greater value that in the PH group. On the other hand, no significant differences were found between either group in the right pulmonary artery.


1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.


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