Local control of pulmonary resistance and lung compliance in the canine lung

1975 ◽  
Vol 39 (4) ◽  
pp. 580-589 ◽  
Author(s):  
R. L. Coon ◽  
C. C. Rattenborg ◽  
J. P. Kampine
Keyword(s):  
Pulmonary Artery ◽  
Local Control ◽  
Vagal Stimulation ◽  
Lower Lobe ◽  
Lung Compliance ◽  
Artery Occlusion ◽  
Pulmonary Resistance ◽  
Acid Infusion ◽  
Acid Base Status

Local control of pulmonary resistance and lung compliance was studied in the in situ left lower lobe of the canine lung. Recirculation of blood through the lobe while the Pco2 of the ventilatory gas was varied resulted in an increase in resistance and a decrease in compliance only when the pulmonary venous pH was greater than 7.42. Alternating sodium bicarbonate and lactic acid infusion while alveolar Pco2 was maintained below 5 mmHg demonstrated the dependence of the hypocapnic response on the acid-base status of the blood perfusing the respiratory airways. The increase in resistance and decrease in compliance observed at a pulmonary venous pH of 7.64 was comparable to that observed after lobar pulmonary artery occlusion. Varying degrees of hypoxia did not significantly affect bronchomotor tone, nor was the bronchoconstriction following lobar pulmonary artery occlusion affected by the hypoxia. Vagal stimulation superimposed on a stepwise increase in pulmonary venous pH from 7.32 to 7.62 resulted in an increase in resistance which paralleled the increase in resistance when pulmonary venous pH alone was increased. Compliance was not significantly affected by vagal stimulation at any level of pulmonary venous pH.

scholarly journals Pneumonectomy is necessary following delayed detection of pulmonary artery compromise

2019 ◽  
Vol 30 (1) ◽  
pp. 154-155
Author(s):  
Ambria S Moten ◽  
Abbas E Abbas
Keyword(s):  
Pulmonary Artery ◽  
Blood Supply ◽  
Lung Tissue ◽  
Collateral Circulation ◽  
Lower Lobe ◽  
Left Lower Lobe ◽  
Completion Pneumonectomy

Abstract It has been previously suggested that lung tissue remains viable without blood supply from the pulmonary artery (PA). However, our experience demonstrates otherwise. We present 2 cases of accidental left lower lobe PA occlusion during upper lobectomy causing ischaemic changes to the remaining lung tissue. Both patients became septic secondary to necrosis of infarcted lung and required completion pneumonectomy. Development of collateral circulation to bypass the occluded PA may occur but is often insufficient to support the affected lung tissue. Unless the patient is medically unfit, resection of the ischaemic lung should be undertaken.

UNILATERAL PULMONARY ARTERY OCCLUSION IN MAN

1957 ◽  
Vol 34 (2) ◽  
pp. 206-227 ◽  
Author(s):  
Bernard L. Brofman ◽  
Bernard L. Charms ◽  
Paul M. Kohn ◽  
John Elder ◽  
Robert Newman ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Artery Occlusion ◽  
Unilateral Pulmonary Artery Occlusion

Preload Index: Pulmonary Artery Occlusion Pressure Versus Intrathoracic Blood Volume Monitoring During Lung Transplantation

2002 ◽  
Vol 95 (4) ◽  
pp. 835-843 ◽  
Author(s):  
Giorgio Della Rocca ◽  
Gabriella M. Costa ◽  
Cecilia Coccia ◽  
Livia Pompei ◽  
Pierangelo Di Marco ◽  
...  
Keyword(s):  
Pulmonary Artery ◽  
Lung Transplantation ◽  
Blood Volume ◽  
Pulmonary Artery Occlusion Pressure ◽  
Artery Occlusion ◽  
Intrathoracic Blood Volume ◽  
Occlusion Pressure

Interaction between serotonin and efferent vagus nerves in dog lungs

1978 ◽  
Vol 44 (2) ◽  
pp. 144-149 ◽  
Author(s):  
H. L. Hahn ◽  
A. G. Wilson ◽  
P. D. Graf ◽  
S. P. Fischer ◽  
J. A. Nadel
Keyword(s):  
Smooth Muscle ◽  
Vagal Stimulation ◽  
Transpulmonary Pressure ◽  
Pressure Amplitude ◽  
Vagus Nerves ◽  
Pulmonary Resistance ◽  
Double Lumen ◽  
Contralateral Lung ◽  
Double Lumen Catheter ◽  
Lumen Catheter

We anesthetized, paralyzed, and ventilated 32 dogs. In 16 dogs we measured total pulmonary resistance (RL) during inhalation of acetylcholine (ACh), serotonin (5-HT), and histamine (Hist) aerosols. Cooling both cervical vagi reduced the bronchoconstriction caused by 5-HT 64% (P = 0.001), reduced Hist-induced bronchoconstriction 17% (P = 0.003), and did not significantly reduce bronchoconstriction due to ACh. In seven dogs, we ventilated both lungs separately through a double-lumen catheter. Application of 5-HT to one lung increased the transpulmonary pressure amplitude in the homolateral but not in the contralateral lung. Cooling the homolateral vagus reduced this response 32% (P = 0.02). In nine dogs, we stimulated the peripheral ends of both cut cervical vagi before and during aerosol application of ACh, 5-HT, and Hist. ACh and Hist increased baseline RL 97 and 134%, respectively, without increasing the effect of vagal stimulation. 5-HT increased baseline RL only 27% but greatly augmented the effect of vagal stimulation (mean increase, 271%, P = 0.001). We conclude that 5-HT acts to potentiate vagal effects on airway smooth muscle via the efferent vagal pathway.

Overexpression of Bcl-2 attenuates apoptosis and protects against myocardial I/R injury in transgenic mice

2001 ◽  
Vol 280 (5) ◽  
pp. H2313-H2320 ◽  
Author(s):  
Zhongyi Chen ◽  
Chu Chang Chua ◽  
Ye-Shih Ho ◽  
Ronald C. Hamdy ◽  
Balvin H. L. Chua
Keyword(s):  
Coronary Artery ◽  
Lactate Dehydrogenase ◽  
Transgenic Mice ◽  
Ischemia Reperfusion ◽  
Coronary Artery Occlusion ◽  
Artery Occlusion ◽  
Fragmentation Pattern ◽  
Area At Risk ◽  
Antiapoptotic Protein

To test whether the antiapoptotic protein Bcl-2 prevents apoptosis and injury of cardiomyocytes after ischemia-reperfusion (I/R), we generated a line of transgenic mice that carried a human Bcl-2 transgene under the control of a mouse α-myosin heavy chain promoter. High levels of human Bcl-2 transcripts and 26-kDa Bcl-2 protein were expressed in the hearts of transgenic mice. Functional recovery of the transgenic hearts significantly improved when they were perfused as Langendorff preparations. This protection was accompanied by a threefold decrease in lactate dehydrogenase (LDH) released from the transgenic hearts. The transgenic mice were subjected to 50 min of ligation of the left descending anterior coronary artery followed by reperfusion. The infarct sizes, expressed as a percentage of the area at risk, were significantly smaller in the transgenic mice than in the nontransgenic mice (36.6 ± 5 vs 69.9 ± 7.3%, respectively). In hearts subjected to 30 min of coronary artery occlusion followed by 3 h of reperfusion, Bcl-2 transgenic hearts had significantly fewer terminal deoxynucleodidyl-transferase nick-end labeling-positive or in situ oligo ligation-positive myocytes and a less prominent DNA fragmentation pattern. Our results demonstrate that overexpression of Bcl-2 renders the heart more resistant to apoptosis and I/R injury.

Effect of pulmonary artery occlusion and reperfusion on extravascular fluid accumulation

1981 ◽  
Vol 50 (1) ◽  
pp. 102-106 ◽  
Author(s):  
P. S. Barie ◽  
T. S. Hakim ◽  
A. B. Malik
Keyword(s):  
Pulmonary Artery ◽  
Water Content ◽  
Left Atrial ◽  
Left Lung ◽  
Weight Ratio ◽  
Dry Weight ◽  
Left Pulmonary Artery ◽  
Artery Occlusion ◽  
Lung Water ◽  
The Right

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.

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