Thermal recovery after passage of the pulmonary circulation assessed by deconvolution

1988 ◽  
Vol 64 (3) ◽  
pp. 1210-1216 ◽  
Author(s):  
J. Bock ◽  
P. Deuflhard ◽  
A. Hoeft ◽  
H. Korb ◽  
H. G. Wolpers ◽  
...  
Keyword(s):  
Blood Flow ◽  
Pulmonary Circulation ◽  
Thermal Recovery ◽  
Base Line ◽  
Indocyanine Green Dye ◽  
Cold Blood ◽  
Finite Integral ◽  
Pulmonary Arterial ◽  
Extravascular Compartment

For indicator-dilution studies, complete thermal recovery after passage of heat through the pulmonary circulation would be desirable. However, the results in the literature obtained by extrapolation techniques are inconsistent. To overcome problems of the extrapolation approach, transport functions of the pulmonary circulation (including the left heart) were computed by deconvolution of pulmonary arterial and aortic pairs of thermodilution curves after central venous indicator injection (10 ml of an ice-cold blood indocyanine green dye mixture). Thermal recovery was determined as the finite integral of the transport function. Thirteen mongrel dogs under piritramid-N2O anesthesia were examined under base-line conditions, in orthostasis to alter the distribution of pulmonary blood flow (9 dogs), and in oleic acid edema (8 dogs). Using the deconvolution approach, thermal recovery was 0.97 ± 0.04 under base-line conditions, 0.96 ± 0.03 in orthostasis, and 0.96 ± 0.05 in pulmonary edema. Thermal recovery determined from extrapolated dilution curves was greater than 100% in all groups, a physically impossible finding. It is concluded that thermal recovery is incomplete but insensitive with respect to the distribution of blood flow and to the size of the extravascular compartment. Monoexponential extrapolation is unsuited for the determination of thermal recovery.

Effect of high intra-alveolar O2 tensions on pulmonary circulation in perfused lungs of dogs

1965 ◽  
Vol 208 (1) ◽  
pp. 130-138 ◽  
Author(s):  
G. J. A. Cropp
Keyword(s):  
Blood Flow ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Time Course ◽  
Systemic Circulation ◽  
The Body ◽  
Arterial Blood ◽  
Pulmonary Parenchyma ◽  
Pulmonary Arterial

The resistance to blood flow in the pulmonary circulation of dogs (PVR) increased when their lungs were ventilated with 95–100% oxygen and were perfused with blood that recirculated only through the pulmonary circulation; the systemic circulation was perfused independently. This increase in PVR occurred even when nerves were cut or blocked but was abolished by inhaled isopropylarterenol aerosol. Elevation of intra-alveolar Po2 without increase in pulmonary arterial blood Po2 was sufficient to increase pulmonary vascular resistance. The pulmonary venules or veins were thought to be the likely site of the constriction. These reactions were qualitatively similar to those produced by injection of serotonin or histamine into the pulmonary circulation. The time course of the response and failure to obtain it when the blood was perfused through the remainder of the body before it re-entered the pulmonary circulation are compatible with a theory that high intra-alveolar O2 tension activates a vasoconstrictor material in the pulmonary parenchyma.

Increasing oxygen tension dilates fetal pulmonary circulation via endothelium-derived relaxing factor

1993 ◽  
Vol 265 (1) ◽  
pp. H376-H380 ◽  
Author(s):  
M. H. Tiktinsky ◽  
F. C. Morin
Keyword(s):  
Blood Flow ◽  
Oxygen Tension ◽  
Hyperbaric Oxygen ◽  
Pulmonary Circulation ◽  
Left Atrial ◽  
Pulmonary Blood Flow ◽  
Absolute Pressure ◽  
Relaxing Factor ◽  
Pulmonary Arterial ◽  
Endothelium Derived Relaxing Factor

We examined the role of endothelium-derived relaxing factor (EDRF) in the increase in pulmonary blood flow caused by increasing oxygen tension in the lungs of the fetus. Fetal lambs at 133 days of gestation were instrumented for intrauterine measurement of pulmonary arterial, left atrial, and amniotic fluid pressure and pulmonary blood flow. Three days later oxygen tension in the pulmonary arterial blood of the fetus was doubled by having the ewe breathe 100% oxygen at 3 atm absolute pressure. In the control fetuses (n = 5), hyperbaric oxygenation increased pulmonary blood flow eightfold. Blocking EDRF production by infusing 45 mg of NG-monomethyl-L-arginine into the superior vena cava of the fetus over 5 min starting 30 min after the beginning of hyperbaric oxygen reversed the increase in pulmonary blood flow (n = 5). Blocking EDRF production by infusing NG-nitro-L-arginine at 1 mg/min for 60 min starting 30 min before hyperbaric oxygen blunted the initial increase in pulmonary blood flow and eliminated it by the end of the experiment (n = 5). As hyperbaric oxygen did not significantly alter pulmonary arterial or left atrial pressure, changes in pulmonary vascular conductance paralleled those in pulmonary blood flow. We conclude that the majority of the vasodilation of the fetal pulmonary circulation caused by increasing oxygen tension is mediated by EDRF. We speculate that EDRF is involved in maintaining low vascular tone at the relatively high oxygen tension of the postnatal lung.

Acute effects of partial compression of ductus arteriosus on fetal pulmonary circulation

1989 ◽  
Vol 257 (2) ◽  
pp. H626-H634 ◽  
Author(s):  
S. H. Abman ◽  
F. J. Accurso
Keyword(s):  
Blood Flow ◽  
Pulmonary Artery ◽  
Pulmonary Vascular Resistance ◽  
Pulmonary Artery Pressure ◽  
Pulmonary Circulation ◽  
Pulmonary Blood Flow ◽  
Ductus Arteriosus ◽  
Base Line ◽  
Acute Effects ◽  
Artery Pressure

To determine the acute effects of increased pulmonary artery pressure and flow on the fetal pulmonary circulation, we studied the response of pulmonary blood flow and vascular reactivity to partial compression of the ductus arteriosus in 22 chronically prepared late-gestation fetal lambs. An inflatable occluder was placed loosely around the ductus arteriosus for compression. Partial compression of the ductus rapidly increased mean pulmonary artery pressure from 45 +/- 1 to 60 +/- 1 mmHg (mean +/- SE) and left pulmonary artery blood flow from 65 +/- 6 to 151 +/- 11 ml/min at 30 min (P less than 0.001; 12 animals). Despite keeping pulmonary artery pressure constant, pulmonary blood flow steadily declined and by 2 h was not different from base-line values. Pulmonary vascular resistance initially fell during the first 30 min of partial compression but then steadily increased and remained elevated above base-line values for at least 30 min after the release of the occluder (P less than 0.001). The decline of pulmonary vascular resistance during the first 30 min of compression was blunted after treatment with the cyclooxygenase inhibitor, meclofenamate (P less than 0.001; 6 animals). Rapid incremental ductus compressions demonstrated a decrease in the slope of the pressure-flow relationship from 3.30 +/- 0.27 (control) to 1.59 +/- 0.21 ml.min-1.mmHg-1 during the postcompression period (P less than 0.001; 12 animals). The vasodilation response to small increases of fetal PO2 was markedly blunted during the postcompression period (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Uneven driving pressures and redistribution of intrapulmonary blood flow

1982 ◽  
Vol 52 (1) ◽  
pp. 96-103
Author(s):  
J. F. Murray ◽  
J. M. Hoeffel ◽  
G. Jibelian
Keyword(s):  
Blood Flow ◽  
Oleic Acid ◽  
Pulmonary Edema ◽  
Sulfur Hexafluoride ◽  
Pulmonary Arterial Pressure ◽  
Base Line ◽  
Positive End Expiratory Pressure ◽  
Pulmonary Arterial ◽  
Normal Lungs

Pulmonary arterial pressure (Ppa) and airway pressure (Paw) change equally when Paw varies widely in normal lungs under zone 2 conditions. To evaluate the mechanism underlying the decrease in Ppa at a given Paw in edematous lungs, we measured the quantity of right-to-left shunting of blood (Qs/QT) with sulfur hexafluoride (SF6) using in situ perfused dog lungs from five control animals, five animals with bronchial occlusion, and eight animals with oleic acid-induced pulmonary edema. Under base-line conditions when positive end-expiratory pressure (PEEP) was increased from 5 to 15 cmH2O, Ppa increased because Paw was fully transmitted to Ppa. After bronchial occlusion at 5 cmH2O PEEP, observed QS/QT was less than predicted (P less than 0.01) on the basis of regional conductances, but at 15 cmH2O observed and predicted QS/QT did not differ (P greater than 0.5). In five of eight dogs with oleic acid-induced pulmonary edema. QS/QT increased when PEEP was increased. We conclude that pressure barriers that create nonuniform driving pressures cause a decrease in Ppa and a redistribution of blood flow.

Structure and function of the pulmonary circulation

2020 ◽  
pp. 3691-3695
Author(s):  
Nicholas W. Morrell
Keyword(s):  
Blood Flow ◽  
Gas Exchange ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Pulmonary Circulation ◽  
Mean Pulmonary Arterial Pressure ◽  
Pulmonary Capillaries ◽  
Small Rise ◽  
Pulmonary Arterial ◽  
And Function

The normal pulmonary circulation distributes deoxygenated blood at low pressure and high flow to the pulmonary capillaries for the purposes of gas exchange. The structure of pulmonary blood vessels varies with their function—from large elastic conductance arteries, to small muscular arteries, to thin-walled vessels involved in gas exchange. Pulmonary vascular resistance is about one-tenth of systemic vascular resistance, with the small muscular and partially muscular arteries of 50–150 µm diameter being the site of the greatest contribution to resistance. In the normal pulmonary circulation, a large increase in cardiac output causes only a small rise in mean pulmonary arterial pressure because pulmonary vascular resistance falls on exercise. Pulmonary blood flow is heterogeneous: gravity causes increased blood flow in the more dependent parts of the lung; within a horizontal region—or within an acinus—blood-flow heterogeneity is imposed by the branching pattern of the vessels.

Bronchovascular adjustments after pulmonary embolism

1980 ◽  
Vol 49 (3) ◽  
pp. 476-481 ◽  
Author(s):  
A. B. Malik ◽  
S. E. Tracy
Keyword(s):  
Pulmonary Embolism ◽  
Blood Flow ◽  
Time Course ◽  
Reference Sample ◽  
Base Line ◽  
Arteriovenous Shunts ◽  
Pulmonary Arterial ◽  
Vascular Obstruction ◽  
The Right ◽  
Sample Method

We determined the time course of bronchial blood flow alterations after pulmonary microembolization. Embolization was induced by injecting 100-micrometers-diam glass beads into the right atrium so as to increase pulmonary arterial pressure from 13.8 +/- 1.8 to 35.7 +/- 2.6 Torr in 14 dogs. The increase in pulmonary vascular resistance averaged threefold after embolization (PE). The bronchial blood flow (Qb) was measured using the reference sample method with the 15 +/- 5-micrometers-diam labeled microspheres injected into the left atrium. Simultaneous blood reference samples were collected at constant rates from a femoral artery and the pulmonary artery. The pulmonary arterial reference sample was used to quantify the contribution of peripheral arteriovenous shunts to the total pulmonary activity, and the femoral arterial reference blood was used to quantify Qb. The Qb was decreased to one-third of its base-line value at 60-min PE (P less than 0.05) but not at 5 min PE. Qb was increased 300% at 2 wk PE. The decrease in flow was associated with an increased bronchovascular resistance, whereas the increase in flow was associated with a decreased resistance. The decrease in Qb at 60 min PE may be due to release of peripheral vasoconstrictor substances associated with pulmonary embolism. The finding that bronchial perfusion increased gradually after pulmonary vascular obstruction suggests that increased flow is due to neovascularization.

Assessment of the incorporation of revascularized fibula grafts used for mandibular reconstruction with F-18-PET

2001 ◽  
Vol 40 (02) ◽  
pp. 51-58 ◽  
Author(s):  
H. Schliephake ◽  
van den Hoff ◽  
W. H. Knapp ◽  
G. Berding
Keyword(s):  
Blood Flow ◽  
Regional Blood Flow ◽  
Venous Blood ◽  
Mandibular Reconstruction ◽  
Reference Region ◽  
Osteoblastic Activity ◽  
Non Union ◽  
Range Of Values ◽  
Measured Input

Summary Aim: Determination of the range of regional blood flow and fluoride influx during normal incorporation of revascularized fibula grafts used for mandibular reconstruction. Evaluation, if healing complications are preceded by typical deviations of these parameters from the normal range. Assessment of the potential influence of using “scaled population-derived” instead of “individually measured” input functions in quantitative analysis. Methods: Dynamic F-l 8-PET images and arterialized venous blood samples were obtained in 11 patients early and late after surgery. Based on kinetic modeling regional blood flow (K1) and fluoride influx (Kmlf) were determined. Results: In uncomplicated cases, early postoperative graft K1 - but not Kmlf -exceeded that of vertebrae as reference region. Kmn values obtained in graft necrosis (n = 2) were below the ranges of values observed in uncomplicated healing (0.01 13-0.0745 ml/min/ml) as well as that of the reference region (0.0154-0.0748). Knf values in mobile non-union were in the lower range - and those in rigid non-union in the upper range of values obtained in stable union (0.021 1-0.0694). If scaled population-derived instead of measured input functions were used for quantification, mean deviations of 23 ± 17% in K1 and 12 ± 16% in Kmlf were observed. Conclusions: Normal healing of predominantly cortical bone transplants is characterized by relatively low osteoblastic activity together with increased perfusion. It may be anticipated that transplant necrosis can be identified by showing markedly reduced F− influx. In case that measured input functions are not available, quantification with scaled population-derived input functions is appropriate if expected differences in quantitative parameters exceed 70%.

Determination of renal blood flow by thermodilution method

1978 ◽  
Vol 38 (5) ◽  
pp. 495-499 ◽  
Author(s):  
Torbjörn Leivestad ◽  
Erling Brodwall ◽  
Svein Simonsen
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Thermodilution Method
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