Chronic lung lymph fistula that only drains the left lung

1995 ◽  
Vol 269 (4) ◽  
pp. R943-R947
Author(s):  
Y. Kikuchi ◽  
H. Nakazawa ◽  
D. L. Traber
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Mediastinal Lymph Node ◽  
Pulmonary Veins ◽  
Pulmonary Arteries ◽  
Left Lung ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
The Right ◽  
Arteries And Veins

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.

scholarly journals Recovery from Hypoxic Pulmonary Hypertension in Rats

2011 ◽  
Vol 54 (2) ◽  
pp. 73-75
Author(s):  
Hana Maxová ◽  
Alena Baňasová ◽  
Viera Povýšilová ◽  
Jan Herget ◽  
Martin Vízek
Keyword(s):  
Arterial Pressure ◽  
Ventricular Hypertrophy ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Time Frame ◽  
Hypoxic Exposure ◽  
Mean Pulmonary Arterial Pressure ◽  
Male Wistar Rats ◽  
Pulmonary Arterial ◽  
The Right

To characterize the time frame of changes in pulmonary arterial pressure, right ventricular hypertrophy and morphology of small pulmonary arteries male Wistar rats were exposed to isobaric hypoxia (3 weeks, FIO2 0.1) and then let to recover on air for 1 or 5 weeks. Normoxic animals (group N) served as controls. Mean pulmonary arterial pressure (PAP), ratio of the weight of the right heart ventricle to the sum of the weights of the left ventricle and septum (RV/LV+S) and percentage of double laminated pulmonary vessels ( % DL) were measured at the end of hypoxic exposure (group H), after 1 or 5 weeks of recovery (groups 1R and 5R), and in controls kept in air (group N). Three weeks in hypoxia resulted in increase in PAP, RV/LV+S and % DL. After 1 week of recovery RV/LV+S normalized, PAP decreased, while % DL did not change. After 5 weeks in air PAP returned to control values and % DL diminished significantly but did not normalize. Our results suggest that recovery depends on the degree of HPH and that knowledge of the time-frame of recovery is important for future studies in our rat model.

scholarly journals Caveolar peroxynitrite formation impairs endothelial TRPV4 channels and elevates pulmonary arterial pressure in pulmonary hypertension

2021 ◽  
Vol 118 (17) ◽  
pp. e2023130118
Author(s):  
Zdravka Daneva ◽  
Corina Marziano ◽  
Matteo Ottolini ◽  
Yen-Lin Chen ◽  
Thomas M. Baker ◽  
...  
Keyword(s):  
Pulmonary Hypertension ◽  
Endothelial Cell ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Pulmonary Arteries ◽  
Lung Edema ◽  
Structural Protein ◽  
Caveolin 1 ◽  
Pulmonary Arterial ◽  
Trpv4 Channel

Recent studies have focused on the contribution of capillary endothelial TRPV4 channels to pulmonary pathologies, including lung edema and lung injury. However, in pulmonary hypertension (PH), small pulmonary arteries are the focus of the pathology, and endothelial TRPV4 channels in this crucial anatomy remain unexplored in PH. Here, we provide evidence that TRPV4 channels in endothelial cell caveolae maintain a low pulmonary arterial pressure under normal conditions. Moreover, the activity of caveolar TRPV4 channels is impaired in pulmonary arteries from mouse models of PH and PH patients. In PH, up-regulation of iNOS and NOX1 enzymes at endothelial cell caveolae results in the formation of the oxidant molecule peroxynitrite. Peroxynitrite, in turn, targets the structural protein caveolin-1 to reduce the activity of TRPV4 channels. These results suggest that endothelial caveolin-1–TRPV4 channel signaling lowers pulmonary arterial pressure, and impairment of endothelial caveolin-1–TRPV4 channel signaling contributes to elevated pulmonary arterial pressure in PH. Thus, inhibiting NOX1 or iNOS activity, or lowering endothelial peroxynitrite levels, may represent strategies for restoring vasodilation and pulmonary arterial pressure in PH.

Flow through zone 1 lungs utilizes alveolar corner vessels

1991 ◽  
Vol 70 (4) ◽  
pp. 1518-1523 ◽  
Author(s):  
W. J. Lamm ◽  
K. R. Kirk ◽  
W. L. Hanson ◽  
W. W. Wagner ◽  
R. K. Albert
Keyword(s):  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Lateral Position ◽  
Double Lumen Endotracheal Tube ◽  
Mean Pulmonary Arterial Pressure ◽  
Flow Through ◽  
Pulmonary Arterial ◽  
Isolated Lungs

We have previously observed flows equivalent to 15% of the resting cardiac output of rabbits occurring through isolated lungs that were completely in zone 1. To distinguish between alveolar corner vessels and alveolar septal vessels as a possible zone 1 pathway, we made in vivo microscopic observations of the subpleural alveolar capillaries in five anesthetized dogs. Videomicroscopic recordings were made via a transparent thoracic window with the animal in the right lateral position. From recordings of the uppermost surface of the left lung, alveolar septal and corner vessels were classified depending on whether they were located within or between alveoli, respectively. Observations were made with various levels of positive end-expiratory pressure (PEEP) applied only to the left lung via a double-lumen endotracheal tube. Consistent with convention, flow through septal vessels stopped when PEEP was raised to the mean pulmonary arterial pressure (the zone 1-zone 2 border). However, flow through alveolar corner vessels continued until PEEP was 8-16 cmH2O greater than mean pulmonary arterial pressure (8-16 cm into zone 1). These direct observations support the idea that alveolar corner vessels rather than patent septal vessels provide the pathway for blood flow under zone 1 conditions.

Cyclooxygenase and lipoxygenase inhibition by BW-755C reduces acrolein smoke-induced acute lung injury

1994 ◽  
Vol 77 (2) ◽  
pp. 888-895 ◽  
Author(s):  
S. P. Janssens ◽  
S. W. Musto ◽  
W. G. Hutchison ◽  
C. Spence ◽  
M. Witten ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Arterial Pressure ◽  
Pulmonary Edema ◽  
Pulmonary Arterial Pressure ◽  
Weight Ratio ◽  
Peak Inspiratory Pressure ◽  
Dry Weight ◽  
Lymph Flow ◽  
Pulmonary Arterial ◽  
Arterial Po2

Inhalation of smoke containing acrolein, the most common toxin in urban fires after carbon monoxide, causes vascular injury with non-cardiogenic pulmonary edema containing potentially edematogenic eicosanoids such as thromboxane (Tx) B2, leukotriene (LT) B4, and the sulfidopeptide LTs (LTC4, LTD4, and LTE4). To determine which eicosanoids are important in the acute lung injury, we pretreated sheep with BW-755C (a combined cyclooxygenase and lipoxygenase inhibitor), U-63557A (a specific Tx synthetase inhibitor), or indomethacin (a cyclooxygenase inhibitor) before a 10-min exposure to a synthetic smoke containing carbon particles (4 microns) with acrolein and compared the results with those from control sheep that received only carbon smoke. Acrolein smoke induced a fall in arterial PO2 and rises in peak inspiratory pressure, main pulmonary arterial pressure, pulmonary vascular resistance, lung lymph flow, and the blood-free wet-to-dry weight ratio. BW-755C delayed the rise in peak inspiratory pressure and prevented the fall in arterial PO2, the rise in lymph flow, and the rise in wet-to-dry weight ratio. Neither indomethacin nor U-63557A prevented the increase in lymph flow or wet-to-dry weight ratio, although they did blunt and delay the rise in airway pressure and did prevent the rises in pulmonary arterial pressure and pulmonary vascular resistance. Thus, cyclooxygenase products, probably Tx, are responsible for the pulmonary hypertension after acrolein smoke and to some extent for the increased airway resistance but not the pulmonary edema. Prevention of high-permeability pulmonary edema after smoke with BW-755C suggests that LTB4, may be etiologic, as previous work has eliminated LTC4, LTD4, and LTE4.

scholarly journals Hyperuricemia in patients with pulmonary hypertension: A study in a tertiary care center

2021 ◽  
Vol 6 (3) ◽  
pp. 173-177
Author(s):  
C H Raju ◽  
M Ravindranath
Keyword(s):  
Pulmonary Hypertension ◽  
Uric Acid ◽  
Arterial Pressure ◽  
Serum Uric Acid ◽  
Pulmonary Arterial Pressure ◽  
Nyha Class ◽  
High Serum ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Arterial ◽  
The Right

Pulmonary Hypertension is one of a life-threatening disease with high rate of patient mortality. Decreased cardiac output and tissue hypoxia is measured using Uric acid as a marker for assessment of pulmonary hypertension. 75 patients who were diagnosed with a mean pulmonary arterial pressure of >22mmHg were categorized as group A and 75 healthy patients were considered to be Group B. Blood was collected for Uric acid, creatinine and total Bilirubin estimation. Pulmonary arterial systolic pressure as well as the ventricular function of the patients was evaluated using Colour Doppler ECG and a value of ≥50 mmHg, or a mean pulmonary arterial pressure (at rest) of ≥25 mmHg was taken and the right arterial pressure was calculated. Using the Simpson’s formula, the right and left ventricular ejaculation factors (RVEF, LVEF) were calculated. The serum uric acid levels among the patients were 8.3±1.4mg/dL, creatinine levels were 2.1 ± 0.5 mg/dL, and the total bilirubin levels were 1.9 ± 0.8 mg/dL all of which was significantly higher than the controls. The uric acid levels were also positively correlated to the NHYA class. The blood pressure and the pulmonary arterial pressure were also higher than that of the controls. The correlation was done between the elevated uric acid and ejection fractions and the correlation coefficients of MPAP, LVEF, RVEF and the NYHA class were all significantly associated and the values were 0.394, -0.513, -0.467 and 0.38 respectively. High serum uric acid levels is significantly associated with higher blood pressure, pulmonary arterial pressure and NYHA class. High serum uric acid levels can be a reliable prognostic marker for the detection of pulmonary hypertension. Early therapy may help in the reduction of mortality rate.

Ventilation-perfusion relationships with high cardiac output in lobar atelectasis

1981 ◽  
Vol 50 (2) ◽  
pp. 341-347 ◽  
Author(s):  
P. T. Schumacker ◽  
J. C. Newell ◽  
T. M. Saba ◽  
S. R. Powers
Keyword(s):  
Cardiac Output ◽  
Arterial Pressure ◽  
Pulmonary Arterial Pressure ◽  
Left Lung ◽  
Shunt Fraction ◽  
Mechanically Ventilated ◽  
Arteriovenous Fistulas ◽  
Hypoxic Vasoconstriction ◽  
Pulmonary Arterial ◽  
Mixed Venous

Pulmonary gas exchange was evaluated in 10 anesthetized mechanically ventilated dogs. Cardiac output (QT) was increased approximately 50% by opening peripheral arteriovenous fistulas. With both lungs ventilated, increasing QT increased mixed venous O2 both pressure (PO2) and pulmonary arterial pressure, but neither shunt fraction nor the distribution of ventilation-perfusion was consistently altered. During left lung atelectasis, increasing QT again increased mixed venous PO2 and pulmonary arterial pressure, but two different responses in shunt-like perfusion were measured. In four dogs, left lung atelectasis caused a shunt fraction of 46 +/- 6% that was not changed by high QT (P greater than 0.05). In six dogs, atelectasis caused a shunt fraction of 24 +/- 3% during normal QT that increased to 42 +/- 2% during high QT (P less than 0.001). Dogs whose shunt fraction during atelectasis was high and unchanged by QT had lower arterial pH (7.24 +/- 0.03) than dogs whose shunt fraction was initially lower and was increased with QT (7.36 +/- 0.02) (P less than 0.01). We conclude that increased QT can worsen shunt flow during lobar atelectasis when hypoxic vasoconstriction has been effective in limiting perfusion to the collapsed region at normal levels of QT.

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