Pulmonary vascular response to leukotriene D4 in unanesthetized sheep: role of thromboxane

1986 ◽  
Vol 60 (3) ◽  
pp. 765-769 ◽  
Author(s):  
T. C. Noonan ◽  
A. B. Malik

We examined the pulmonary vascular response to an intravenous leukotriene D4 (LTD4) injection of (1 microgram X kg-1 X min-1 for 2 min) immediately followed by infusion of 0.133 microgram X kg-1 X min-1 for 15 min in awake sheep prepared with lung lymph fistulas. LTD4 resulted in rapid generation of thromboxane A2 as measured by an increase in plasma thromboxane B2 concentration. The thromboxane B2 generation was associated with increases in pulmonary arterial and pulmonary arterial wedge pressures while left atrial pressure did not change significantly. Pulmonary lymph flow (Qlym) increased (P less than 0.05) transiently from base line 6.87 +/- 1.88 (SE) ml/h to maximum value of 9.77 +/- 1.27 at 15 min following the LTD4 infusion. The maximum increase in Qlym was associated with an increase in the estimated pulmonary capillary pressure. The increase in Qlym was not associated with a change in the lymph-to-plasma protein concentration (L/P) ratio. Thromboxane synthetase inhibition with dazoxiben (an imidazole derivative) prevented thromboxane B2 generation after LTD4 and also prevented the increases in pulmonary vascular pressures and Qlym. We conclude that LTD4 in awake sheep increases resistance of large pulmonary veins. The small transient increase in Qlym can be explained by the increase in pulmonary capillary pressure. Thromboxane appears to mediate both the pulmonary hemodynamic and lymph responses to LTD4 in sheep.

1989 ◽  
Vol 67 (6) ◽  
pp. 2205-2211 ◽  
Author(s):  
Y. Yamada ◽  
M. Suzukawa ◽  
M. Chinzei ◽  
T. Chinzei ◽  
N. Kawahara ◽  
...  

In six open-chest dogs, electrocardiogram- (ECG) controlled pulmonary arterial occlusion was performed during the control period and during the infusions of serotonin and histamine. A temporal series of instantaneous pulmonary capillary pressure and the longitudinal distributions of vascular resistance and compliance were evaluated in the intact left lower lung lobe. In the control period, we found a significant phasic variation of pulmonary capillary pressure (Pc) with the cardiac cycle. The ratio of arterial to venous resistances (Ra/Rv) was 6:4, and the ratio of arterial to capillary compliances (Ca/Cc) was 1:11. During the infusions of serotonin and histamine, Pc showed similar phasic variations, despite significant hemodynamic changes induced by these agents. Serotonin predominantly increased Ra, whereas histamine predominantly increased Rv. The ratio of Rv to the total resistance decreased significantly from 0.42 to 0.32 during the infusion of serotonin and increased significantly to 0.62 during the infusion of histamine. The data suggest that phasic Pc determined by ECG-controlled arterial occlusion reflects the pulsatility in the pulmonary microvascular bed under control conditions and after alterations of the pulmonary vascular resistance by serotonin and histamine.


1999 ◽  
Vol 160 (1) ◽  
pp. 162-168 ◽  
Author(s):  
ANDREW A. PELLETT ◽  
ROYCE W. JOHNSON ◽  
GERALYNN G. MORRISON ◽  
MICHAEL S. CHAMPAGNE ◽  
BENNETT P. DeBOISBLANC ◽  
...  

1996 ◽  
Vol 80 (5) ◽  
pp. 1792-1798 ◽  
Author(s):  
A. K. Sinha ◽  
R. D. Gleed ◽  
T. S. Hakim ◽  
A. Dobson ◽  
K. J. Shannon

The object of this study was to relate pulmonary capillary pressure to arterial and wedge pressures during exercise. Pulmonary vascular pressures were measured in six standardbred horses exercising at speeds equivalent to 75, 90, and 100% of maximal heart rate. Vascular pressures were measured with transducer-tip catheters and expressed relative to esophageal pressure. Pulmonary capillary pressure was estimated by the arterial-occlusion technique modified for exercise. Mean pulmonary arterial, capillary and wedge pressures increased from 30.5 +/- 6.3, 17.8 +/- 4.3, and 13.4 +/- 1.6 mmHg, respectively, at rest, to 70.5 +/- 5.2, 42.1 +/- 5.3, and 38.4 +/- 5.6 mmHg, respectively, at maximal exercise. The largest part of the increase occurred during the first level of exertion. With exercise, the pressure across the lung barely doubled at a time when the cardiac output would have increased at least fivefold. Thus the absolute resistance in both pre- and postcapillary segments must have decreased. The capillary and wedge pressures rose similarly, whereas the difference between them did not change with exertion. The fractional resistance of the precapillary segment increased with exercise. The postcapillary resistance, initially 28% of the total pulmonary vascular resistance, fell to 9% at maximal exercise. The rise (to approximately 45 mmHg) in pulmonary capillary pressure with exertion is consistent with an increase in transvascular filtration.


1986 ◽  
Vol 61 (5) ◽  
pp. 1928-1934 ◽  
Author(s):  
T. C. Noonan ◽  
W. M. Selig ◽  
D. F. Kern ◽  
S. B. Malik

We examined the effects of leukotrienes C4 (LTC4) and D4 (LTD4) (1 microgram) on the pulmonary vascular filtration coefficient, a measure of vessel wall conductivity to water, and the alterations in pulmonary vascular resistance (PVR) in isolated-perfused guinea pig lungs. We also assessed whether LTC4 and LTD4 increased the permeability to albumin in cultured monolayers of pulmonary artery endothelial cells. In Ringer-perfused and blood-perfused lungs, LTC4 resulted in increases in pulmonary arterial pressure (Ppa) and the pulmonary capillary pressure (Pcap) measured as the equilibration pressure after simultaneous pulmonary arterial and venous occlusions. Pulmonary venous resistance (Rv) increased to a greater extent than arterial resistance (Ra) in both Ringer-perfused and blood-perused lungs challenged with LTC4. The greater increase in PVR in blood-perfused lungs corresponded with a greater elevation of lung effluent thromboxane B2 (TxB2) concentration. The LTC4-stimulated increase in PVR was prevented by pretreatment with meclofenamate (10(-4) M). LTD4 also induced rapid increases in Ppa and Pcap in both Ringer-perfused and blood-perfused lungs; however, Ppa decreased before stabilizing at a pressure higher than base line. The increases in Rv with LTD4 were greater than Ra. The LTD4-stimulated increases in Ra and Rv also paralleled the elevation in TxB2 concentration. As with LTC4, the increases in Ppa, Pcap, PVR, and TxB2 concentration were greater in blood-perfused than in Ringer-perfused lungs. Pretreatment with meclofenamate reduced the magnitude of the initial increase in Ppa, but did not prevent the response.(ABSTRACT TRUNCATED AT 250 WORDS)


1987 ◽  
Vol 63 (6) ◽  
pp. 2340-2342 ◽  
Author(s):  
R. J. Roselli ◽  
R. E. Parker

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.


1993 ◽  
Vol 77 (6) ◽  
pp. 1130???1134 ◽  
Author(s):  
Yoshitsugu Yamada ◽  
Kyoko Komatsu ◽  
Masayuki Suzukawa ◽  
Mieko Chinzei ◽  
Tsuneo Chinzei ◽  
...  

1986 ◽  
Vol 60 (6) ◽  
pp. 1980-1985 ◽  
Author(s):  
K. Y. Mustafa ◽  
W. M. Selig ◽  
K. E. Burhop ◽  
F. L. Minnear ◽  
A. B. Malik

The effects of temperature (37–45 degrees C) on pulmonary edema formation and transendothelial albumin clearance were investigated using isolated perfused guinea pig lungs and bovine pulmonary arterial endothelial cells grown to confluency on a gelatinized membrane. Perfusion of isolated lungs with Ringer-albumin solution at 37 or 41 degrees C for 90 min produced no change in lung wet-to-dry weight ratios (W/D) or in pulmonary capillary pressure (measured by the double-occlusion method). When perfused at 43 degrees C, lung wet weight increased 0.8 +/- 0.4 g over base line (final W/D = 7.43 +/- 0.7) within 90 min. Perfusion at 45 degrees C increased lung weight by 2.7 +/- 0.9 g over base line (final W/D 11.8 +/- 2.3 vs. control value of 5.2 +/- 0.23 at 37 degrees C perfusion) within 60 min. The changes in pulmonary capillary pressure were small (from a base-line value of 4.3 +/- 0.8 to 4.9 +/- 0.4 at 43 degrees C and from a base-line value of 4.9 +/- 0.8 to 5.9 +/- 0.6 at 45 degrees C). The clearance of 125I-albumin (microliter/min) across the endothelial monolayer system increased threefold (from 0.295 +/- 0.035 to 1.048 +/- 0.107) at 45 degrees C, an effect comparable to positive controls of trypsin (from 0.272 +/- 0.046 to 1.595 +/- 0.138) or oleic acid (from 0.278 +/- 0.043 to 0.672 +/- 0.26). An increase in temperature from 37 to 45 degrees C had no effect on the permeability of the gelatinized membrane alone.(ABSTRACT TRUNCATED AT 250 WORDS)


1968 ◽  
Vol 07 (02) ◽  
pp. 125-129
Author(s):  
J. Měštan ◽  
V. Aschenbrenner ◽  
A. Michaljanič

SummaryIn patients with acquired and congenital valvular heart disease correlations of the parameters of the radiocardiographic curve (filling time of the right heart, minimal pulmonary transit time, peak-to-peak pulmonary transit time, and the so-called filling time of the left heart) with the mean pulmonary artery pressure and the mean pulmonary “capillary” pressure were studied. Further, a regression equation was determined by means of which the mean pulmonary “capillary” pressure can be predicted.


1949 ◽  
Vol 2 (1) ◽  
pp. 24-29 ◽  
Author(s):  
H. K. Hellems ◽  
F. W. Haynes ◽  
L. Dexter

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