Selected Contribution: Mechanisms that may stimulate the resolution of alveolar edema in the transplanted human lung

2002 ◽  
Vol 93 (5) ◽  
pp. 1869-1874 ◽  
Author(s):  
Lorraine B. Ware ◽  
Xiohui Fang ◽  
Yibing Wang ◽  
Tsutomu Sakuma ◽  
Timothy S. Hall ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Organ Donor ◽  
Dry Weight ◽  
Organ Donors ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Stimulation ◽  
Lung Water ◽  
Human Donor ◽  
Pharmacological Agents ◽  
Alveolar Edema

Pulmonary edema is common in organ donors and lung transplant recipients. Therefore, we assessed the responsiveness of human donor lungs to pharmacological agents that stimulate clearance of alveolar edema. Organ donors whose lungs were rejected for transplantation were studied. After resection, transport (4°C), and rewarming (37°C) of lungs, alveolar fluid clearance was measured with ( n = 8 donors) or without ( n = 23 donors) β-adrenergic stimulation. Terbutaline-stimulated clearance (10−4M) was higher than unstimulated clearance (7.1 ± 1.3 vs. 4.8 ± 2.4%/h, P < 0.01). Second, we determined whether medications given to the organ donor were associated with the extent of pulmonary edema or the rate of alveolar fluid clearance in the harvested lung. Preharvest administration of dopamine in low to moderate doses was associated with faster alveolar fluid clearance ( r = 0.62, P < 0.01). Preharvest administration of diuretics was associated with lower extravascular lung water-to-dry weight ratios. This study provides the first evidence that a β2-adrenergic agonist stimulates alveolar fluid clearance in the human donor lung. Aerosolized β2-adrenergic agonists may have therapeutic value for hastening the resolution of alveolar edema during the management of donors before resection of lungs for transplantation or in the posttransplant setting.

Edema from cyclooxygenase products of endogenous arachidonic acid in isolated lung

1989 ◽  
Vol 67 (2) ◽  
pp. 846-855 ◽  
Author(s):  
M. R. Littner ◽  
F. D. Lott
Keyword(s):  
Arachidonic Acid ◽  
Pulmonary Edema ◽  
Enzyme Inhibitor ◽  
Calcium Ionophore ◽  
Dry Weight ◽  
Lung Water ◽  
Isolated Lung ◽  
Pulmonary Arterial ◽  
Area Product ◽  
Permeability Pulmonary Edema

We infused A23187, a calcium ionophore, into the pulmonary circulation of dextran-salt-perfused isolated rabbit lungs to release endogenous arachidonic acid. This led to elevations in pulmonary arterial pressure and to pulmonary edema as measured by extravascular wet-to-dry weight ratios. The increase in pressure and edema was prevented by indomethacin, a cyclooxygenase enzyme inhibitor, and by 1-benzylimidazole, a selective inhibitor of thromboxane (Tx) A2 synthesis. Transvascular flux of 125I-albumin from vascular to extravascular spaces of the lung was not elevated by A23187 but was elevated by infusion of oleic acid, an agent known to produce permeability pulmonary edema. We confirmed that A23187 leads to elevations in cyclooxygenase products and that indomethacin and 1-benzylimidazole inhibit synthesis of all cyclooxygenase products and TxA2, respectively, by measuring perfusate levels of prostaglandin (PG) I2 as 6-ketoprostaglandin F1 alpha, PGE2, and PGF2 alpha and TxA2 as TxB2. We conclude that release of endogenous pulmonary arachidonic acid can lead to pulmonary edema from conversion of such arachidonic acid to cyclooxygenase products, most notably TxA2. This edema was most likely from a net hydrostatic accumulation of extravascular lung water with an unchanged permeability of the vascular space, since an index of permeability-surface area product (i.e., transvascular albumin flux) was not increased.

Lung mechanics in hypervolemic pulmonary edema

1975 ◽  
Vol 38 (4) ◽  
pp. 681-687 ◽  
Author(s):  
W. H. Noble ◽  
J. C. Kay ◽  
J. Obdrzalek
Keyword(s):  
Pulmonary Edema ◽  
Lung Compliance ◽  
Indicator Dilution ◽  
Lung Mechanics ◽  
Dilution Technique ◽  
Lung Water ◽  
Electron Microscopic ◽  
Indicator Dilution Technique ◽  
Double Indicator Dilution ◽  
Alveolar Edema

Extravascular thermal volume of the lung (ETVL) is a double indicator dilution technique of use in measuring pulmonary edema. ETVL and lung mechanics measurements were followed to find a less invasive monitor of pulmonary edema than the double indicator dilution technique. Pulmonary edema was induced by overloading the dogs' circulation with dextran. Phases of overload were defined on the basis of a previous electron microscopic study (Noble et al., Can. Anesthetists Soc. J. 21:275, 1974) of lung biopsies relating anatomic changes to physiologic measurements of ETVL and central blood volume (CBV). Congestion occurred when CBV was elevated and ETVL was not, interstitial edema when ETVL was elevated but smaller than 60% above control and alveolar edema when ETVL greater than 85% above control. Once the dogs were in alveolar edema, they were mechanically ventilated with 4, 8, 12, and 16 cmH2O end-tidal pressure (CPPV). Mean functional residual capacity (FRC) for all 15 dogs did not change up to the time CPPV was applied. Pulmonary resistance did not rise until alveolar edema was present. Once in pulmonary edema, lung compliance always fell as lung water increased. In individual dogs, the compliance fall was directly proportional to the rising lung water. However, the variations in slope and beginning point among dogs made it difficult to predict the amount of lung water from dynamic compliance values. PaO2 fell markedly in alveolar edema as a result of a widened A-a gradient. CPPV did not decrease lung water but did increase FRC and PaO2.

Smoke aldehyde component influences pulmonary edema

1992 ◽  
Vol 72 (2) ◽  
pp. 555-561 ◽  
Author(s):  
C. A. Hales ◽  
S. W. Musto ◽  
S. Janssens ◽  
W. Jung ◽  
D. A. Quinn ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Weight Ratio ◽  
Dry Weight ◽  
Leukotriene B4 ◽  
Smoke Inhalation ◽  
High Dose ◽  
Lung Water ◽  
Protein Ratio ◽  
Arterial Blood ◽  
Lung Lymph

The pulmonary edema of smoke inhalation is caused by the toxins of smoke and not the heat. We investigated the potential of smoke consisting of carbon in combination with either acrolein or formaldehyde (both common components of smoke) to cause pulmonary edema in anesthetized sheep. Seven animals received acrolein smoke, seven animals received a low-dose formaldehyde smoke, and five animals received a high-dose formaldehyde smoke. Pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output were not affected by smoke in any group. Peak airway pressure increased after acrolein (14 +/- 1 to 21 +/- 2 mmHg; P less than 0.05) and after low- and high-dose formaldehyde (14 +/- 1 to 21 +/- 1 and 20 +/- 1 mmHg, respectively; both P less than 0.05). The partial pressure of O2 in arterial blood fell sharply after acrolein [219 +/- 29 to 86 +/- 9 (SE) Torr; P less than 0.05] but not after formaldehyde. Only acrolein resulted in a rise in lung lymph flow (6.5 +/- 2.2 to 17.9 +/- 2.6 ml/h; P less than 0.05). Lung lymph-to-plasma protein ratio was unchanged for all three groups, but clearance of lymph protein was increased after acrolein. After acrolein, the blood-free extravascular lung water-to-lung dry weight ratio was elevated (P less than 0.05) compared with both low- and high-dose formaldehyde groups (4.8 +/- 0.4 to 3.3 +/- 0.2 and 3.6 +/- 0.2, respectively). Lymph clearance (ng/h) of thromboxane B2, leukotriene B4, and the sulfidopeptide leukotrienes was elevated after acrolein but not formaldehyde.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Contribution ofα- andβ-Adrenergic Mechanisms to the Development of Pulmonary Edema

Scientifica ◽  
2012 ◽  
Vol 2012 ◽  
pp. 1-11 ◽  
Author(s):  
Beate Rassler
Keyword(s):  
Pulmonary Edema ◽  
Experimental Models ◽  
Neurogenic Pulmonary Edema ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Agonists ◽  
Alveolar Space ◽  
Adrenergic Stimulation ◽  
Abundant Protein ◽  
Different Types ◽  
Protein Rich

Endogenous or exogenous catecholamines can induce pulmonary edema (PE). This may occur in human pathologic conditions such as in pheochromocytoma or in neurogenic pulmonary edema (NPE) but can also be provoked after experimental administration of adrenergic agonists. PE can result from stimulation with different types of adrenergic stimulation. With -adrenergic treatment, it develops more rapidly, is more severe with abundant protein-rich fluid in the alveolar space, and is accompanied by strong generalized inflammation in the lung. Similar detrimental effects of -adrenergic stimulation have repeatedly been described and are considered to play a pivotal role in NPE or in PE in patients with pheochromocytoma. Although -adrenergic agonists have often been reported to prevent or attenuate PE by enhancing alveolar fluid clearance, PE may also be induced by -adrenergic treatment as can be observed in tocolysis. In experimental models, infusion of -adrenergic agonists induces less severe PE than -adrenergic stimulation. The present paper addresses the current understanding of the possible contribution of - and -adrenergic pathways to the development of PE.

Alveolar fluid clearance in late-gestational guinea pigs after labor induction: mechanisms and regulation

2001 ◽  
Vol 280 (4) ◽  
pp. L606-L616 ◽  
Author(s):  
Andreas Norlin ◽  
Hans G. Folkesson
Keyword(s):  
Cesarean Section ◽  
Guinea Pigs ◽  
Positive Airway Pressure ◽  
Fetal Lung ◽  
Clinical Implications ◽  
Alveolar Fluid Clearance ◽  
Adrenergic Stimulation ◽  
Albumin Solution ◽  
Induced Labor ◽  
Pharmacological Agents

We tested the hypothesis that labor-induced epinephrine release would stimulate alveolar fluid clearance in preterm fetuses. Preterm fetuses were obtained by cesarean section from timed-pregnant guinea pigs at 61–69 days postconception. Fetal guinea pigs were euthanized and placed on continuous positive airway pressure oxygenation, and an isosmolar 5% albumin solution was instilled. Alveolar fluid clearance was measured over 1 h. The fetal lung began to absorb fluid at 64–66 days postconception, and at birth, alveolar fluid clearance quadrupled. Baseline alveolar fluid clearance when present was sensitive to propranolol inhibition and depended on β-adrenergic stimulation. Measurements of plasma epinephrine in fetal animals confirmed high epinephrine levels in 66- to 69-day postconception fetuses. Prenatal alveolar fluid clearance when present was highly amiloride sensitive, suggesting that amiloride-sensitive Na+ channels were critical. Oxytocin-induced labor initiated an amiloride- and propranolol-sensitive net alveolar fluid clearance in 61-day-gestation animals. Moreover, oxytocin induced significant epinephrine release in all fetuses. These results have clinical implications for infants delivered by cesarean section before the onset of labor. Use of pharmacological agents to induce labor may reduce the occurrence and severity of perinatal respiratory distress.

Effect of histamine and propranolol on extravascular lung water

1984 ◽  
Vol 246 (1) ◽  
pp. H69-H73
Author(s):  
J. S. Schwartz ◽  
R. G. Konopka ◽  
R. G. Spragg
Keyword(s):  
Pulmonary Edema ◽  
Extravascular Lung Water ◽  
Adrenergic Receptors ◽  
Weight Ratio ◽  
Dry Weight ◽  
Systemic Circulation ◽  
Current Evidence ◽  
Beta Blockade ◽  
Lung Water ◽  
Wet Weight

The ability of an intravenous infusion of 21 micrograms X kg-1 X min-1 histamine diphosphate to cause pulmonary edema was studied in dogs in which beta-blockade either was or was not in effect, since current evidence suggests that beta-blockade can prevent catecholamines from antagonizing the vascular permeability effect of histamine in the systemic circulation. Mixed venous histamine levels ranging from 140 to 580 ng/ml were achieved; norepinephrine and epinephrine levels increased significantly, although in animals receiving propranolol, heart rate remained depressed. Neither lung wet weight-to dry weight ratio nor extravascular lung water increased in animals receiving histamine or histamine and propranolol. We conclude that the inability of histamine to produce substantial pulmonary edema cannot be explained on the basis of catecholamine stimulation of beta-adrenergic receptors within the lung.

Oxygen radicals participate in alloxan-induced pulmonary EDEMA

1990 ◽  
Vol 48 (3) ◽  
pp. 298-299
Author(s):  
Tomoo Kawada ◽  
Michio Arakawa ◽  
Kenjiro Kambara ◽  
Takashi Segawa ◽  
Fumio Ando ◽  
...  
Keyword(s):  
Pulmonary Edema ◽  
Oxygen Radicals ◽  
Bolus Injection ◽  
Physiological Saline ◽  
Baseline Period ◽  
Alveolar Epithelial Cells ◽  
Control Group ◽  
Intervention Period ◽  
Lung Water ◽  
Electron Microscopic

We know that alloxan causes increased-permeability pulmonary edema and that alloxan generates oxygen radicals (H2O2, O2−, ·OH) in blood. Therefore, we hypothesize that alloxan-generated oxygen radicals damage pulmonary capillary endothelial cells, and, possibly, alveolar epithelial cells as well. We examined whether oxygen radical scavengers, such as catalase or dimethylsulfoxide (DMSO), protected against alloxaninduced pulmonary edema.Five dogs in each following group were anesthetized: control group: physiological saline (20ml/kg/h); alloxan group: physiological saline + alloxan (75mg/kg) bolus injection at the beginning of the experiment; catalase group: physiological saline + catalase (150,000u/kg) bolus injection before injection of alloxan; DMSO group: physiological saline + DMSO (0.4mg/kg) bolus injection before alloxan. All dogs had 30-min baseline period and 3-h intervention period. Hemodynamics and circulating substances were measured at the specific points of time. At the end of intervention period, the dogs were killed and had the lungs removed for electron microscopic study and lung water measurement with direct destructive method.

Measurement of pulmonary edema in intact dogs by transthoracic gamma-ray attenuation

1979 ◽  
Vol 47 (6) ◽  
pp. 1228-1233 ◽  
Author(s):  
D. S. Simon ◽  
J. F. Murray ◽  
N. C. Staub
Keyword(s):  
Pulmonary Edema ◽  
Time Course ◽  
Gamma Ray ◽  
High Sensitivity ◽  
Lung Edema ◽  
Lung Water ◽  
Vascular Congestion ◽  
Isolated Lung ◽  
Wide Range ◽  
Gamma Ray Attenuation

We evaluated the attenuation of the 122 keV gamma ray of cobalt-57 across the thorax of anesthetized dogs as a method for following the time course of lung water changes in acute pulmonary edema induced by either increased microvascular permeability or increased microvascular hydrostatic pressure. The gamma rays traversed the thorax centered on the seventh rib laterally where the lung mass in the beam path was greatest. Calibration measurements in isolated lung lobes demonstrated the high sensitivity and inherent accuracy of the method over a wide range of lung water contents. In control dogs reproducibility averaged +/-3%. Increased permeability edema led to large rapid increases in the transthoracic gamma ray attenuation (TGA), while increased pressure caused an immediate, modest increase in TGA (vascular congestion) followed by a slow further increase over 2 h. There was a fairly good correlation between the increase in extravascular lung water and the change in TGA. The method is simple, safe, and noninvasive and appears to be useful for following the time course of lung water accumulation in generalized lung edema in anesthetized animals.

scholarly journals Ethical and Legal Implications of Elective Ventilation and Organ Transplantation: “Medicalization” of Dying versus Medical Mission

2014 ◽  
Vol 2014 ◽  
pp. 1-5 ◽  
Author(s):  
Paola Frati ◽  
Vittorio Fineschi ◽  
Matteo Gulino ◽  
Gianluca Montanari Vergallo ◽  
Natale Mario Di Luca ◽  
...  
Keyword(s):  
Organ Donation ◽  
Organ Donor ◽  
Legal Framework ◽  
Organ Donors ◽  
Organ Perfusion ◽  
Medical Mission ◽  
Legal Implications ◽  
Legal Context ◽  
Successful Transplantation ◽  
Italian Context

A critical controversy surrounds the type of allowable interventions to be carried out in patients who are potential organ donors, in an attempt to improve organ perfusion and successful transplantation. The main goal is to transplant an organ in conditions as close as possible to its physiological live state. “Elective ventilation” (EV), that is, the use of ventilation for the sole purpose of retrieving the organs of patients close to death, is an option which offsets the shortage of organ donation. We have analyzed the legal context of the dying process of the organ donor and the feasibility of EV in the Italian context. There is no legal framework regulating the practice of EV, neither is any real information given to the general public. A public debate has yet to be initiated. In the Italian cultural and legislative scenario, we believe that, under some circumstances (i.e., the expressed wishes of the patient, even in the form of advance directives), the use of EV does not violate the principle of beneficence. We believe that the crux of the matter lies in the need to explore the real determination and will of the patient and his/her orientation towards the specific aim of organ donation.

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