An unusual pediatric case of tuberculosis‐associated mediastinal fibrosis with concomitant pulmonary arterial and venous occlusion

2020 ◽  
Author(s):  
Mansi Verma ◽  
Vineeta Ojha ◽  
Niraj N. Pandey ◽  
Anita Saxena ◽  
Sanjeev Kumar
Keyword(s):  
Venous Occlusion ◽  
Pediatric Case ◽  
Mediastinal Fibrosis ◽  
Pulmonary Arterial

scholarly journals Pulmonary venous occlusion and death in pulmonary arterial hypertension: survival analyses using radiographic surrogates

2011 ◽  
Vol 11 (1) ◽  
Author(s):  
Yasuko Takeda ◽  
Yutaka Takeda ◽  
Koji Yamamoto ◽  
Shigehiro Tomimoto ◽  
Tomomitsu Tani ◽  
...  
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Venous Occlusion ◽  
Survival Analyses ◽  
Pulmonary Arterial

A method for analysis of pulmonary arterial and venous occlusion data

1992 ◽  
Vol 73 (3) ◽  
pp. 1190-1195 ◽  
Author(s):  
S. H. Audi ◽  
C. A. Dawson ◽  
J. H. Linehan
Keyword(s):  
Compartmental Model ◽  
Venous Occlusion ◽  
Time Data ◽  
Equilibrium Pressure ◽  
New Approach ◽  
Lung Lobe ◽  
C Distribution ◽  
Average Slope ◽  
Arterial Inflow ◽  
Pulmonary Arterial

Recently, we presented a compartmental model of the pulmonary vascular resistance (R) and compliance (C) distribution with the configuration C1R1C2R2C3 (J. Appl. Physiol. 70: 2126–2136, 1991). This model was used to interpret the pressure vs. time data obtained after the sudden occlusion of the arterial inflow (AO), venous outflow (VO), or both inflow and outflow (DO) from an isolated dog lung lobe. In the present study, we present a new approach to the data analysis in terms of this model that is relatively simple to carry out and more robust. The data used to estimate the R′s and C′s are the steady-state arterial [Pa(0)] and venous [Pv(0)] pressures, the flow rate (Q), the area (A2) encompassed by Pa(t) after AO and the equilibrium pressure (Pd) after DO, and the average slope (m) of the Pa(t) and Pv(t) curves after VO. The following formulas can then be used to calculate the 2 R′s and 3 C′s: [Pa(0) - Pv(0)]/Q = R1 + R2 = RT, R1C1 congruent to to A2/[Pa(0) - Pd], R1 congruent to [Pa(0) - Pd]/Q, Q/m = C1 + C2 + C3 = CT, and C2 = CT - (RTC1/R2).

Distribution of lung vascular resistance after chronic systemic-to-pulmonary shunts

1985 ◽  
Vol 249 (6) ◽  
pp. H1106-H1113 ◽  
Author(s):  
R. P. Michel ◽  
T. S. Hakim ◽  
R. E. Hanson ◽  
A. R. Dobell ◽  
F. Keith ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Morphometric Measurements ◽  
Arterial Resistance ◽  
Pulmonary Arterial ◽  
The Right

Congenital cardiac shunts produce pathological lesions on the arterial side of the lung vasculature. We examined the effects of chronic shunts (14.2 +/- 1.2 mo) in 10 young dogs, between the left subclavian and the left lower lobe (LLL) artery, on pulmonary vascular pressure and flow (P-Q) relationships, segmental resistance with arterial and venous occlusion (AVO), and sensitivity to drugs. At final thoracotomy, mean LLL pulmonary arterial pressure (Ppa) was 23.2 +/- 4.3 mmHg compared with 11.9 +/- 0.9 in the right lung (P less than 0.05); two animals had LLL Ppa of 41 and 48 mmHg. The LLL artery and vein were cannulated, and pressure-flow (P-Q) and AVO measurements were made and compared with previous control LLL (n = 11) and contralateral right lower lobe (RLL, n = 5). Responses to serotonin, histamine, and vasodilators (diltiazem and isoproterenol) were evaluated. Comparisons of morphometric measurements were made between LLL and RLL. We found a significant increase in arterial resistance as measured with AVO and a hypersensitivity to serotonin in the shunt LLL, without changes in total pulmonary vascular resistance or P-Q measurements; vasodilators had a small effect only in the hypertensive lobes. Our data suggest that chronic shunts to the pulmonary circulation increase arterial resistance and sensitivity to serotonin, even in the absence of discernible morphometric changes, and that vasoconstriction may be an important precursor to the development of morphological lesions.

Modulation of vascular reactivity to serotonin in the dog lung

1991 ◽  
Vol 71 (1) ◽  
pp. 217-222 ◽  
Author(s):  
W. F. Hofman ◽  
W. F. Jackson ◽  
H. el-Kashef ◽  
I. C. Ehrhart
Keyword(s):  
Arterial Pressure ◽  
Vascular Reactivity ◽  
Pulmonary Arterial Pressure ◽  
Pressor Response ◽  
Venous Occlusion ◽  
Lung Lobe ◽  
Lower Lung ◽  
Pulmonary Arterial ◽  
Pressure Changes ◽  
Related Increase

Experiments were conducted to compare the effects of cyclooxygenase inhibition (COI) on vascular reactivity to serotonin (5-HT) in the isolated blood-perfused canine left lower lung lobe (LLL) and in isolated canine intrapulmonary lobar artery rings with and without a functional endothelium. LLLs (n = 6), perfused at constant blood flow, were challenged with bolus doses of 50, 100, and 250 micrograms 5-HT before COI, after COI with 45 microM meclofenamate, and after infusion of prostacyclin (PGI2) during COI. Lobar vascular resistance was segmentally partitioned by venous occlusion. Pulmonary arterial pressure increased from 13.5 +/- 1.0 to 16.3 +/- 0.8 cmH2O (P less than 0.01) after COI but declined to 13.1 +/- 1.1 cmH2O (P less than 0.01) subsequent to PGI2 infusion (91.3 +/- 14.5 ng.min-1.g LLL-1). The pulmonary arterial pressure changes were related to changes in postcapillary resistance. The dose-dependent pressor response to 5-HT was potentiated by COI (P less than 0.01) but reversibly attenuated (P less than 0.05) by PGI2 infusion. Isolated intrapulmonary artery rings (2–4 mm diam) exhibited a dose-related increase in contractile tension to 5-HT. The response to 5-HT was enhanced (P less than 0.05) in rings devoid of a functional endothelium. However, COI (10 microM indomethacin) did not alter (P greater than 0.05) the dose-related increase in contractile tension to 5-HT in rings with an intact endothelium. Our results suggest that both PGI2 and endothelium-derived relaxing factors modulate pulmonary vascular reactivity to 5-HT.(ABSTRACT TRUNCATED AT 250 WORDS)

Species differences in pulmonary vasoactive responses to histamine, 5-hydroxytryptamine, and KCl

1993 ◽  
Vol 74 (1) ◽  
pp. 139-146 ◽  
Author(s):  
J. D. Bradley ◽  
P. B. Zanaboni ◽  
T. E. Dahms
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Guinea Pigs ◽  
Species Differences ◽  
Venous Occlusion ◽  
Longitudinal Distribution ◽  
Critical Closing Pressure ◽  
Before And After ◽  
Pulmonary Arterial ◽  
Microvascular Resistance

Species differences in the longitudinal distribution of pulmonary vascular resistance (PVR) in response to 5-hydroxytryptamine (5-HT) or histamine (His) may be attributed to variations in the distribution of functional smooth muscle between arteries and veins estimated by the response to KCl. Isolated dog, guinea pig, or rabbit lungs were perfused at a constant flow = 55–75 ml.min-1.kg body wt-1. Pulmonary arterial (Ppa); arterial, double, and venous occlusion (Po,a; Pdo; Po,v, respectively); and pulmonary venous (Ppv) pressures were measured before and after increasing PVR by infusing His, 5-HT, or KCl. 5-HT and His increased Ppa--Pdo in rabbits but Pdo--Ppv in guinea pigs. In dogs, 5-HT increased Ppa--Po,a, but His increased Pdo--Ppv. Dynamic (Co,v) and static vascular compliance (CP-Q), as well as critical closing pressure (Pcc, the gamma-intercept of pressure-flow curves), were also measured. At baseline, Co,v was the same among species. However, CP-Q was higher than Co,v in all lungs and was significantly different among species in order of (in ml.cmH2O-1.100 g-1) rabbit (4.54 +/- 0.28) > guinea pig (3.31 +/- 0.18) > dog (2.21 +/- 0.13). Increases in Pcc correlated with increases in microvascular resistance (Po,a--Po,v) but not with increases in PVR after agonist infusion. KCl responses suggest that guinea pigs and rabbits have relatively more functional smooth muscle in venous and arterial microvessels, respectively, whereas dogs have approximately equal amounts.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of end-expiratory airway pressure on accumulation of extravascular lung water

1975 ◽  
Vol 38 (5) ◽  
pp. 907-912 ◽  
Author(s):  
R. H. Demling ◽  
N. C. Staub ◽  
L. H. Edmunds
Keyword(s):  
Hydrostatic Pressure ◽  
Arterial Pressure ◽  
Osmotic Pressure ◽  
Extravascular Lung Water ◽  
Airway Pressure ◽  
Pulmonary Arterial Pressure ◽  
Venous Occlusion ◽  
Colloid Osmotic Pressure ◽  
Lung Water ◽  
Pulmonary Arterial

The effect of end-expiratory airway pressure on the accumulation of extravascular lung water during lobar venous occlusion for 2 h was studied in closed-chest artifically ventilated dogs. Dogs were divided into two groups by end-expiratory airway pressures of 0 or 10 cmH2O. High-pressure lobar pulmonary edema was produced by lobar venous occlusion, which elevated microvascular hydrostatic pressure. After occlusion of the lobar pulmonary vein, lobar venous pressure (and microvascular hydrostatic pressure) rapidly became identical to pulmonary arterial pressure. We measured extravascular lung water (post mortem) and pulmonary arterial pressure and calculated plasma colloid osmotic pressure to determine the relationship between the accumulation of lung water and the difference between pulmonary microvascular pressure and plasma colloid osmotic pressure (net intravascular filtration pressure). At comparable net intravascular filtration pressures, dogs ventilated at the higher end-expiratory airway pressure accumulated more extravascular lung water. This study indicates that increasing end-expiratory airway pressure from zero to 10 cmH2O increases the accumulation of extravascular lung water when microvascular hydrostatic pressure is raised.

scholarly journals Critical Neonatal Congenital Heart Disease – a Rare Complication after Successful Surgical Correction

2020 ◽  
Vol 6 (4) ◽  
pp. 104-108
Author(s):  
Carmen Corina Şuteu ◽  
Iolanda Muntean ◽  
Cristina Blesneac ◽  
Marian Pop ◽  
Rodica Togănel
Keyword(s):  
Pulmonary Arterial Hypertension ◽  
Arterial Hypertension ◽  
Neonatal Period ◽  
Arterial Switch Operation ◽  
Rare Complication ◽  
Pediatric Case ◽  
Vasodilator Therapy ◽  
Switch Operation ◽  
Pulmonary Arterial ◽  
Favorable Clinical Response

AbstractPulmonary arterial hypertension (PAH) is a rare but severe complication that should be investigated in patients diagnosed with transposition of the great arteries who have undergone neonatal arterial switch operation. Early diagnosis and aggressive combination therapy for PAH could help to improve survival in these patients. We report a favorable clinical response 6 months after the initiation of vasodilator therapy in a pediatric case with transposition of the great arteries, successfully repaired in the neonatal period, who developed pulmonary arterial hypertension at the age of 5 years.

Venous occlusion measurement of pulmonary capillary pressure: effects of embolization

1987 ◽  
Vol 63 (6) ◽  
pp. 2340-2342 ◽  
Author(s):  
R. J. Roselli ◽  
R. E. Parker
Keyword(s):  
Capillary Pressure ◽  
Pulmonary Arteries ◽  
Arterial Embolization ◽  
Venous Occlusion ◽  
Pressure Effects ◽  
Pulmonary Capillary ◽  
Pulmonary Capillary Pressure ◽  
Occlusion Technique ◽  
Pulmonary Arterial ◽  
Significant Underestimation

The effects of pulmonary arterial embolization on calculated pulmonary capillary pressure as determined by the venous occlusion technique are examined using a simple pressure-flow model for the lung. It is predicted that pulmonary, arterial embolization can induce significant underestimation of pulmonary capillary pressure in flowing vessels. This underestimation is related to the percent of vessels embolized and the caliber of pulmonary arteries that are embolized (i.e., the size of the emboli). Experimental verification of these theoretical findings is necessary before the conclusions can be extended to the interpretation of venous occlusion experiments in the lung.

Effects of lung volume and alveolar surface tension on pulmonary vascular resistance

1987 ◽  
Vol 62 (4) ◽  
pp. 1622-1626 ◽  
Author(s):  
R. Y. Sun ◽  
G. F. Nieman ◽  
T. S. Hakim ◽  
H. K. Chang
Keyword(s):  
Surface Tension ◽  
Lung Volume ◽  
Pulmonary Arterial Pressure ◽  
Lower Lobe ◽  
Venous Occlusion ◽  
Alveolar Pressure ◽  
Lung Inflation ◽  
Occlusion Technique ◽  
Pulmonary Arterial ◽  
Alveolar Surface

Utilizing the arterial and venous occlusion technique, the effects of lung inflation and deflation on the resistance of alveolar and extraalveolar vessels were measured in the dog in an isolated left lower lobe preparation. The lobe was inflated and deflated slowly (45 s) at constant speed. Two volumes at equal alveolar pressure (Palv = 9.9 +/- 0.6 mmHg) and two pressures (13.8 +/- 0.8 mmHg, inflation; 4.8 +/- 0.5 mmHg, deflation) at equal volumes during inflation and deflation were studied. The total vascular pressure drop was divided into three segments: arterial (delta Pa), middle (delta Pm), and venous (delta Pv). During inflation and deflation the changes in pulmonary arterial pressure were primarily due to changes in the resistance of the alveolar vessels. At equal Palv (9.9 mmHg), delta Pm was 10.3 +/- 1.2 mmHg during deflation compared with 6.8 +/- 1.1 mmHg during inflation. At equal lung volume, delta Pm was 10.2 +/- 1.5 mmHg during inflation (Palv = 13.8 mmHg) and 5.0 +/- 0.7 mmHg during deflation (Palv = 4.8 mmHg). These measurements suggest that the alveolar pressure was transmitted more effectively to the alveolar vessels during deflation due to a lower alveolar surface tension. It was estimated that at midlung volume, the perimicrovascular pressure was 3.5–3.8 mmHg greater during deflation than during inflation.

Sign in / Sign up

Export Citation Format

Share Document