Adverse effects of prostacyclin used to perfuse isolated lung lobes

1982 ◽  
Vol 242 (5) ◽  
pp. H745-H750 ◽  
Author(s):  
M. M. Krausz ◽  
T. Utsunomiya ◽  
L. L. Levine ◽  
B. Dunham ◽  
D. Shepro ◽  
...  
Keyword(s):  
Hydrolysis Product ◽  
Weight Ratio ◽  
Dry Weight ◽  
Antiplatelet Antibody ◽  
Lung Lobe ◽  
Isolated Lung ◽  
Stable Product ◽  
Wet Weight ◽  
Pulmonary Arterial ◽  
Foreign Surface

To test the hypothesis that preservation of circulating platelets would prolong the function of an isolated perfused canine lung lobe, prostacyclin (PGI2) was added to the perfusate. Platelet count in heparinized controls (n = 7) fell to 44,500 platelets/mm3, lower than 136,000 platelets/mm3 seen with 1 microgram/min PGI2 (n = 7, P less than 0.005). Surprisingly, with PGI2, thromboxane B2 (TXB2) the stable product of thromboxane A2 (TXA2), rose from 0.07 to 0.25 ng/ml, a level higher than controls (P less than 0.005). PGI2, in comparison to controls, also led to higher pulmonary arterial pressure, an increase in lobe weight, an increase in wet weight-dry weight ratio, an increase in physiological shunt, and a decrease in compliance (P less than 0.005). Further, with PGI2 there was hemorrhagic edema. Infusion of the PGI2 hydrolysis product 6-keto-prostaglandin F1 alpha (n = 2) led to results similar to controls. Adverse PGI2 effects were eliminated by pretreatment with ibuprofen (12.5 mg/kg, n = 5) or an antiplatelet antibody (n = 6). Infusion of PGI2 into a lobar pulmonary artery of an intact animal was without effect on the lung (n = 2). These results show that platelets exposed to a foreign surface will aggregate and be lost from the circulation. PGI2 prevents platelet loss but not the synthesis of TXA2. This vasoconstrictor is likely to be the cause of pulmonary hypertension and hemorrhagic pulmonary edema.

The Relation of Oxygen Consumption to Body Size and to Temperature in the Larvae of Chironomus Riparius Meigen

1958 ◽  
Vol 35 (2) ◽  
pp. 383-395
Author(s):  
R. W. EDWARDS
Keyword(s):  
Oxygen Consumption ◽  
Body Size ◽  
Dry Matter ◽  
Larval Instar ◽  
Weight Ratio ◽  
Dry Weight ◽  
Chironomus Riparius ◽  
Consumption Rates ◽  
Rate Of Oxygen Consumption ◽  
Wet Weight

1. The oxygen consumption rates of 3rd- and 4th-instar larvae of Chironomus riparius have been measured at 10 and 20° C. using a constant-volume respirometer. 2. The oxygen consumption is approximately proportional to the 0.7 power of the dry weight: it is not proportional to the estimated surface area. 3. This relationship between oxygen consumption and dry weight is the same at 10 and at 20° C.. 4. The rate of oxygen consumption at 20° C. is greater than at 10° C. by a factor of 2.6. 5. During growth the percentage of dry matter of 4th-instar larvae increases from 10 to 16 and the specific gravity from 1.030 to 1.043. 6. The change in the dry weight/wet weight ratio during the 4 larval instar supports the theory of heterauxesis. 7. At 20° C., ‘summer’ larvae respire faster than ‘winter’ larvae.

Bathing Solution Tonicity and Potassium Transport by the Midgut of the Tobacco Hornworm Manduca Sexta

1979 ◽  
Vol 78 (1) ◽  
pp. 213-223
Author(s):  
DAVID F. MOFFETT
Keyword(s):  
Manduca Sexta ◽  
Short Circuit ◽  
Weight Ratio ◽  
Short Circuit Current ◽  
Dry Weight ◽  
Potassium Transport ◽  
Bathing Solution ◽  
Histological Studies ◽  
Wet Weight ◽  
Small Solute

Potassium transport by the isolated midgut of Manduca larvae, as measured by the short circuit current, is inhibited by substitution of small organic solutes (M.W. < 340) for the sucrose normally included in bathing solution formulated for this tissue. Other solutes of molecular weight equal to or greater than sucrose are essentially as effective as sucrose in promoting the short circuit current. Equilibration of midgut in solutions containing the small solute mannitol results in a decrease in the dry weight/wet weight ratio of the tissue, suggesting that the small solutes can penetrate into areas of the tissue which are not accessible to sucrose. Histological studies suggest that sites of swelling in the presence of mannitol include both cytoplasm and goblet cell lumen. The inhibition of the short circuit current is rapidly reversible on return to bathing solution containing sucrose or another large solute. The effect of small solutes probably does not involve compromise of the energy source for potassium transport since oxygen uptake is unchanged in the presence of a small solute.

Mechanisms of increased pulmonary microvascular permeability induced by FMLP in isolated rabbit lungs

1992 ◽  
Vol 73 (5) ◽  
pp. 2074-2082 ◽  
Author(s):  
H. Tanaka ◽  
J. D. Bradley ◽  
L. J. Baudendistel ◽  
T. E. Dahms
Keyword(s):  
Polymorphonuclear Leukocytes ◽  
Weight Ratio ◽  
Dry Weight ◽  
Microvascular Permeability ◽  
Cyclooxygenase Inhibitors ◽  
Myeloperoxidase Activity ◽  
Oxygen Species ◽  
Chemotactic Peptide ◽  
Isolated Lung ◽  
Baseline Values

We observed that the chemotactic peptide N-formyl-L-methionyl-L-leucyl-L- phenylalanine (FMLP) induced pulmonary edema when polymorphonuclear leukocytes (PMNs) were added to isolated constant-flow buffer-perfused rabbit lungs. This study was designed to test the hypothesis that PMNs activated by FMLP induced lung injury by the modulation of reactive oxygen species (ROS), cyclooxygenase products, or cysteinyl leukotrienes (LTs). Addition of FMLP alone did not increase microvascular permeability (Kf). When PMNs were added to the isolated lung, FMLP caused an 80% increase in Kf. Wet-to-dry weight ratio was also significantly increased with PMNs + FMLP compared with FMLP only. There was a significant positive correlation between total myeloperoxidase activity in lung tissue and Kf values after FMLP (30 min). Pretreatment with two dissimilar cyclooxygenase inhibitors, meclofenamate or ibuprofen, had no effect on the PMN + FMLP-induced increase in Kf. However, the ROS inhibitor catalase and the nonantioxidant LT synthesis blocker MK 886 inhibited the PMN + FMLP increase in Kf. Perfusate levels of LTs (LTC4, -D4, and -E4) were significantly increased from baseline values 30 min after FMLP. Both MK 886 and catalase suppressed the elevation of LTs after PMN + FMLP. These results indicate that FMLP increased a pulmonary microvascular permeability in isolated buffer-perfused rabbit lungs that is PMN dependent and mediated by LT produced possibly by a result of ROS production.

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.

Liver ischemia-reperfusion increases pulmonary permeability in rat: role of circulating xanthine oxidase

1995 ◽  
Vol 268 (6) ◽  
pp. G988-G996 ◽  
Author(s):  
A. Weinbroum ◽  
V. G. Nielsen ◽  
S. Tan ◽  
S. Gelman ◽  
S. Matalon ◽  
...  
Keyword(s):  
Xanthine Oxidase ◽  
Viral Infections ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
Dry Weight ◽  
Oxygen Species ◽  
Hepatic Ischemia ◽  
Hepatic Diseases ◽  
Isolated Lung ◽  
Lung Preparation

Reactive oxygen species play an important role in pathogenesis of a variety of pathological processes, e.g., ischemia-reperfusion, acute viral infections, thermal injury, hepatic diseases, and acute lung injury. Xanthine oxidase (XO) may be a significant source of these cytotoxic oxygen species. We tested the hypothesis that hepatic ischemia-reperfusion releases xanthine dehydrogenase + XO (XDH + XO) into the circulation and that circulating XO damages isolated perfused lung. Isolated liver + lung preparation was perfused with Krebs-Henseleit buffer to minimize confounding effects of circulating neutrophils. In one group, livers were rendered globally ischemic for 2 h and then reperfused (I/R). In another group, livers were pretreated with allopurinol and perfused with buffer containing additional allopurinol (I/R + Allo). After 2 h of ischemia, an isolated lung was connected to liver, and liver + lung preparation was reperfused in series for 15 min. Liver reperfusion was terminated, and lung was recirculated with liver effluent for 45 min. Capillary filtration coefficient (ml.min-1.cmH2O-1.100 g lung dry wt-1) was 2.0 +/- 0.3 and 1.9 +/- 0.4 in control and I/R + Allo lungs, respectively, and 9.0 +/- 1.2 in I/R lungs (P < 0.001). Lung wet-to-dry weight ratio in control and I/R + Allo lungs was 8.6 +/- 0.3 and 9.1 +/- 0.5, respectively, and 14.9 +/- 1.1 in I/R lungs (P < 0.01). Control and I/R + Allo bronchoalveolar lavage protein content was < 1.0 mg/ml compared with 32.6 +/- 8.4 mg/ml in I/R group.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Role of neutrophils in xanthine/xanthine oxidase-induced oxidant injury in isolated rabbit lungs

1999 ◽  
Vol 87 (6) ◽  
pp. 2319-2325 ◽  
Author(s):  
Masashi Kishi ◽  
Lois F. Richard ◽  
Robert O. Webster ◽  
Thomas E. Dahms
Keyword(s):  
Lung Injury ◽  
Xanthine Oxidase ◽  
Neutrophil Elastase ◽  
Weight Ratio ◽  
Dry Weight ◽  
Neutrophil Elastase Inhibitor ◽  
Fluid Filtration ◽  
Elastase Inhibitor ◽  
Pulmonary Arterial

Reactive oxygen species have been shown to play an important role in the pathogenesis of lung injury. This study was designed to clarify the role of intrapulmonary neutrophils in the development of xanthine/xanthine oxidase (X/XO)-induced lung injury in isolated buffer-perfused rabbit lungs. We measured microvascular fluid filtration coefficient ( K f) and wet-to-dry weight ratio to assess lung injury. X/XO induced a significant increase in K f and wet-to-dry weight ratio in neutrophil-replete lungs, whereas the lung injury was attenuated in neutrophil-depleted lungs. A neutrophil elastase inhibitor, ONO-5046, also attenuated the lung injury. In addition, X/XO induced a transient pulmonary arterial pressure (Ppa) increase. The thromboxane inhibitor OKY-046 attenuated the Ppa increase but did not alter the increase in permeability. Neutrophil depletion reduced the K f increase but had no effect on the Ppa increase. These results suggest that intrapulmonary neutrophils activated by X/XO play a major role in development of the lung injury, that neutrophil elastase is involved in the injury, and that the X/XO-induced vasoconstriction is independent of intrapulmonary neutrophils.

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.

Lung endothelial and epithelial permeability after platelet-activating factor

1987 ◽  
Vol 63 (5) ◽  
pp. 1770-1775 ◽  
Author(s):  
R. W. Bolin ◽  
T. R. Martin ◽  
R. K. Albert
Keyword(s):  
Protein Concentration ◽  
Platelet Activating Factor ◽  
Endothelial Permeability ◽  
Dry Weight ◽  
Fluid Filtration ◽  
Vascular Space ◽  
Constant Rate ◽  
Wet Weight ◽  
Pulmonary Arterial ◽  
Intravascular Pressure

We investigated whether platelet-activating factor (PAF) increased epithelial or endothelial permeability in isolated-perfused rabbit lungs. PAF was either injected into the pulmonary artery or instilled into the airway of lungs perfused with Tyrode's solution containing 1% bovine serum albumin. The effect of adding neutrophils or platelets to the perfusate was also tested. Perfusion was maintained 20–40 min after adding PAF and then a fluid filtration coefficient (Kf) was determined to assess vascular permeability. At the end of each experiment, one lung was lavaged, and the lavagate protein concentration (BALP) was determined. Wet weight-to-dry weight ratios (W/D) were determined on the other lung. PAF added to the vascular space increased peak pulmonary arterial pressure (Ppa) from 13.5 +/- 3.1 (mean +/- SE) to 24.2 +/- 3.3 cmH2O (P less than 0.05). The effect was amplified by platelets [Ppa to 70.8 +/- 8.0 cmH2O (P less than 0.05)] but not by neutrophils [Ppa to 22.0 +/- 1.4 cmH2O (P less than 0.05)]. Minimal changes in Ppa were observed after instilling PAF into the airway. The Kf, W/D, and BALP of untreated lungs were not increased by injecting PAF into the vasculature or into the air space. The effect of PAF on Kf, W/D, and BALP was unaltered by adding platelets or neutrophils to the perfusate. PAF increases intravascular pressure (at a constant rate of perfusion) but does not increase epithelial or endothelial permeability in isolated-perfused rabbit lungs.

scholarly journals Changes in lung permeability after chronic pulmonary artery obstruction

2006 ◽  
Vol 100 (4) ◽  
pp. 1224-1229 ◽  
Author(s):  
Elizabeth M. Wagner ◽  
Gulnura Karagulova ◽  
John Jenkins ◽  
John Bishai ◽  
Jessica McClintock
Keyword(s):  
Pulmonary Artery ◽  
Evans Blue ◽  
Left Lung ◽  
Weight Ratio ◽  
Dry Weight ◽  
Blue Dye ◽  
Artery Ligation ◽  
Wet Weight ◽  
Pulmonary Artery Obstruction ◽  
Artery Obstruction

We have shown that left pulmonary artery ligation (LPAL) in mice causes a prompt angiogenic response, with new systemic vessels from intercostal arteries penetrating the pleura within 6 days. Because angiogenic vessels in other organs have been shown to exhibit increased permeability, we studied vascular permeability (Evans blue dye extravasation, lung wet weight-to-dry weight ratio, and lavaged protein) in naive C57BL/6 mice and 4 h, and 14 and 21 days after LPAL (4–6 mice/time point). We also measured radiolabel clearance as an index of functional perfusion after LPAL. Tracer clearance from the left lung was maximal by 6 days after LPAL and not different from right lungs. Thus a functional vasculature is established before 6 days of LPAL that results in normal tracer clearance. By 21 days after LPAL, Evans blue-albumin was significantly increased in the left lung relative to both 4 h (no vasculature) and 14 days after LPAL. Only after 21 days of LPAL was left lung wet weight-to-dry weight ratio significantly different from naive lungs. Additionally, lavaged protein was significantly increased both 4 h and 21 days after LPAL relative to control mice. Thus, using three different methods, results consistently demonstrated increased permeability to protein and water 21 days after LPAL. Although changes in surface area of perfusion might affect the interpretation of these results, blood flow measured with labeled microspheres indicated no change in left lung perfusion between 14 and 21 days of LPAL. Thus the lung vasculature, remodeled as a consequence of chronic pulmonary artery obstruction, demonstrates increased water and protein permeability.

Age-bodyweight relationships to lung growth in the F344 rat as indexed by lung weight measurements

1986 ◽  
Vol 20 (3) ◽  
pp. 189-194 ◽  
Author(s):  
S. I. Tillery ◽  
B. E. Lehnert
Keyword(s):  
Dry Weight ◽  
Lung Growth ◽  
Lung Weight ◽  
Lung Lobe ◽  
F344 Rat ◽  
Wet Weight ◽  
The Individual ◽  
The Right ◽  
F344 Rats ◽  
Lung Lobes

Measurements of the total lung weights and the individual weights of the lung lobes of male F344 rats ranging in age from about 30 days to 140 days or more were made in order to determine how lung growth and the growths of the individual lung lobes relate to bodyweight over the course of maturation of this species. Additionally, in this study we also (1) compared how each lung lobe grows relative to total lung growth, (2) evaluated the ratios of lung dry weight to wet weight and (3) obtained information on the weights of the trachea and extra-hilar main-stem bronchi as the F344 rat matures. The wet weights WLT of the trachea-lung preparations and the pooled lobe weights WPL as functions of rat bodyweight WB could be readily described by the following logarithmic expressions: WLT = 0·596 ln WB - 1·923, r = 0·95; WPL = 0·464 ln WB - 1·566, r = 0·96. Expressed as percentages of the pooled lobe weights, the individual lobes remained at constant values as the animals grew with the exception of the right caudal lobe which decreased between bodyweights of 72 and 96 g; absolute wet weight measurements of the individual lobes indicated that the right cranial, right middle and right intermediate lobes actually decreased in weight between bodyweights of 300 and 385 g. The dry weights of the lobes consistently represented approximately 22% of the wet weights regardless of animal age or bodyweight, and on average the airways represented about 20% of the weights of the intact airway-lung preparations over the course of animal maturation.

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