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Query: UMLS:C0034063 (pulmonary edema)
10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is widely accepted that extravascular lung thermal volume estimated by the double indicator dilution method with heat as a diffusible indicator reliably reflects pulmonary extravascular water volume. Theoretically, as a premise, the indicator should be preserved during its pulmonary circulation. We therefore investigated the thermal conservation during pulmonary circulation; that is, whether there was good agreement in the cardiac outputs "wherever" the thermodilution curves were recorded; for instance, the pulmonary artery trunk (PAT), giving COPAT,heat and the aortic root (Ao), giving COAo,heat. In the present study, we observed a total of 59 pairs of cardiac outputs in dogs (n = 13), including dogs with overt pulmonary edema, produced either by dextran infusion or by alloxan administration. We also studied a total of 23 pairs of cardiac outputs of human subjects (n = 16) with ischemic heart disease or mild mitral stenosis. A mixture of ice-cold 5% glucose solution and indocyanine green was rapidly injected into the right atrium. The thermodilution curve was immediately recorded in the pulmonary artery trunk, and the thermodilution and dye dilution curves were recorded in the aorta using a conventional Swan-Ganz catheter. The cardiac outputs were calculated manually following the Stewart-Hamilton principle. The results were as follows: In dogs, COPAT,heat averaged 2.47 +/- 1.21 L/min (mean +/- SD), COAo,heat averaged 2.44 +/- 1.12 L/min and the difference was not significant (0.3 less than p less than 0.5). The regression equation was COPAT,heat = 1.01 X COAo,heat + 0.02 (n = 59, r = 0.93, p less than 0.001) and the correlation coefficient was excellent.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Double indicator dilution method using heat and dye to measure pulmonary extravascular water volume]. 391 10

During single pass indicator studies across the lungs [(14)C]urea remains in the vascular compartment, but its molecular size and solubility suggest it might escape abnormally permeable vessels. To test the hypothesis that [(14)C]urea might be used to distinguish pulmonary edema due to acutely increased intravascular pressure from that due to vascular damage by alloxan, we studied [(51)Cr]erythrocytes (r), [(125)I]albumin (a), [(14)C]urea (u), and tritiated water as dilution indicators in the pulmonary circulation of anesthetized dogs. In addition, the adequacy of albumin as an intravascular indicator was evaluated. Indicator curves, blood gases, hematocrit, and vascular pressures were determined during a base-line period and repeated 30 and 60 min after treatment in five groups of dogs: (a) saline control. (b) alloxan edema. (c) epinephrine infusion, (d) volume overload, and (e) left atrial (LA) balloon obstruction.Groups b, d, and e developed a similar degree of edema judging by wet/dry lung weights and histology. Groups a and c did not develop edema. In alloxan edema, differences between the mean transit time volume of u and r (V(v-r)) increased over base line at 30 (P < 0.001) and 60 min (P < 0.02); the differences between the mean transit time volume of a and r (V(e-r)) increased slightly at 30 (P < 0.03) and 60 min (P < 0.02); and V(u-r) significantly exceeded V(a-r) at 30 (mean difference = 9 ml, P < 0.02) and 60 min (mean difference = 11, P < 0.04). In none of the other groups did V(u-r) significantly exceed V(a-r). Thus, comparison of V(u-r) with V(a-r) may permit distinction between "high pressure" and "increased permeability" pulmonary edema. Albumin was not a consistently reliable indicator of intravascular volume as compared with composite red cell and albumin curve.
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PMID:In vivo assessment of pulmonary vascular integrity in experimental pulmonary edema. 457 97

The type J receptors are stimulated during pulmonary congestion produced by occluding the aorta or left a-v junction which causes the left atrial pressure to rise with consequent rise in pulmonary artery pressure. Such acute congestion can be maintained only for brief periods (1-2 min). Longer lasting congestion leading eventually to pulmonary oedema is produced by injecting alloxan into the right atrium or right ventricle. A marked rise in pulmonary artery pressure follows the injection and after a lag there follows intense excitation of the type J receptors. It was concluded that this excitation was due to a rise in pulmonary capillary pressure and increase in permeability of the capillary membrane. Recent experiments have revealed that a considerable increase in activity can also be produced by injecting plastic microemboli (diameter 50 minus-plus 10 micrometers, i.v.). This increase occurs a few minutes after the rise in pulmonary artery pressure and is not due to a direct action of the microemboli on the endings nor can it be due to increased capillary permeability. Here, there can be no doubt that the increase in activity is a consequence of the rise in pulmonary artery pressure leading to a rise in pulmonary capillary pressure. This causes increase in interstitial volume leading to excitation of the endings. It was postulated that the endings were located in collagen tissue which acts like a sponge. Recently electronmicroscopic evidence has been obtained showing the presence of non-medullated sensory fibres in this collagen tissue but the precise structure of the endings (presumably type J) and their physical relation to the collagen tissue still remains to be established.
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PMID:Mechanism of excitation of type J receptors. 469 99

1. The responses of type J pulmonary receptors (identified according to existing criteria) were studied in anaesthetized cats by recording impulses in individual vagal afferent fibres whose conduction velocity ranged from 0.8 to 7 m/sec.2. Measurements of actual latencies between insufflation of halothane or ether into the lungs and the excitation of the endings, and the latencies before and after circulatory arrest have established that the endings are located in the interstitial tissues close to the pulmonary capillaries. Mainly for this reason, the term juxta-pulmonary capillary receptors (i.e. type J receptors) has been applied to these endings in preference to the term K deflation receptors used hitherto.3. The endings were stimulated by pulmonary congestion produced by occlusion of the aorta or left a-v junction for short periods. They were markedly stimulated during pulmonary congestion following injection of alloxan (150 mg/kg) or the addition of chlorine to the inspired air. This excitation was associated with a marked rise in pulmonary artery pressure and the occurrence of pulmonary oedema. However, the actual onset of excitation occurred some time after the rise in pressure and it was in fact more closely related to fall in pulmonary compliance. The frequency of discharge averaged over about 10-20 sec (in order to take the periods of relative inactivity into account) was 7.5 impulses/sec in 10 fibres (range 0.6-19 impulses/sec; S.D. 6.3). This is intense stimulation of the endings and the congestion so produced is therefore regarded as a severe stimulus for the endings.4. The pattern of excitation was variable. In some fibres the activity consisted of periodic bursts of impulses which seemed to be set off during the deflation phase of artificial respiration, sometimes during the inflation phase. This periodic activity was not due to contraction of smooth muscle as the endings are not stimulated following injection of histamine (into the right ventricle) which is known to stimulate smooth muscles in the alveolar ducts and respiratory bronchioles.5. It is postulated that the actual stimulus for the endings is a rise in interstitial pressure or volume produced by a rise in pulmonary capillary pressure. Evidence has been gathered to show that the latter rises during muscular exercise; this rise must stimulate the endings. It was therefore postulated that stimulation of the endings should cause reflex inhibition of limb muscles (for terminating exercise).
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PMID:Mechanism of stimulation of type J pulmonary receptors. 538 24

This study was done to determine the effect of permeability pulmonary edema on proton nuclear magnetic resonance (NMR) relaxation times. Permeability edema was induced in rats by the intravenous injection of alloxan in saline. Control animals received only saline. The rats were ventilated through a tracheostomy; and after a time sufficient for the edema to become uniform, they were sacrificed. T1, and T2 and extravascular lung water were measured on lung samples. A linear relationship was found between the relaxation times and the extravascular lung water. Any diffuse alveolar process including pulmonary edema can increase proton density as well. The T1 and T2 relaxation times may be used to distinguish among different causes of increased proton density in the lung.
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PMID:The effect of pulmonary edema on proton nuclear magnetic resonance relaxation times. 632 45

Pulmonary edema caused by increased membrane permeability was created in dogs by alloxan and infusion of saline solution. Pulmonary extravascular water volume was measured gravimetrically using the supernatant hemoglobin concentration to estimate red cell mass in the calculation of residual pulmonary blood volume. Three groups were studied for two hours: a control group, a group given alloxan and mechanical ventilation without positive end-expiratory pressure (PEEP), and a group given alloxan and mechanical ventilation with 10 cm H2O of PEEP. After two hours, alloxan caused moderately severe pulmonary edema in the two experimental groups, but PEEP had no effect on the accumulation of pulmonary extravascular water volume. No sustained differences in pulmonary or systemic hemodynamics were present throughout two hours of pulmonary edema. The pulmonary shunt was increased in the group without PEEP but was similar in the control group and the group with PEEP. No significant changes in alveolar dead space were noted among the three groups.
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PMID:Effect of positive end-expiratory pressure on lung water in pulmonary edema caused by increased membrane permeability. 634 23

The extravascular thermal volume of the lung (ETV) has been measured in dogs as the difference between mean transit time (t) volumes for heat and indocyanine green dye across the pulmonary circulation, calculated as the product of thermal dilution cardiac output (CO) and the difference in t for aortic indicator-dilution curves generated by right and left atrial injections. ETV measurements were compared with the extravascular lung mass (ELM): in 21 normal dogs, ETV/ELM = 1.11 +/- 0.14 (SD); in 17 dogs with hydrostatic pulmonary edema (up to 21 g/kg), ETV/ELM = 0.90 +/- 0.11; and in 27 dogs with alloxan pulmonary edema (up to 51 g/kg); ETV/ELM = 0.93 +/- 0.13. For all 65 dogs the mean ETVELM was 0.98 +/- 0.15, and the liner regression was ETV (ml/kg) = 0.90 ELM (g/kg) + 0.86 +/- 2.25 (SEE; r = 0.96). Calculations based on measurements of lung specific heat predict that ETV/ELM should equal 0.984. With acute changes in pulmonary hemodynamics, ETV was reduced by reductions in pulmonary arterial pressure (Ppa) sufficient to produce zone 1 conditions at the top of the lung. However, ETV was not affected by increases in CO (mean = 50%) produced by nitroprusside or by increases in Ppa and pulmonary blood volume (mean = 27%) produced by partial mitral valve obstruction. Distortion of the thermal dilution curve due to position of the arterial thermistor appears to be the greatest source of variability and overestimation. Simultaneous measurements from pairs of thermistors differed by 14% (range 0.4-50%).
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PMID:Effect of edema and hemodynamic changes on extravascular thermal volume of the lung. 637 89

To determine the effect of the type of lung injury on the thermodilution estimation of extravascular lung water, we produced pulmonary edema in 25 anesthetized dogs by injection of alloxan or alpha-naphthylthiourea (ANTU) into the pulmonary circulation or by instillation of hydrochloric acid (HCI) into the airway. HCl injury was bilateral, unilateral with tidal volume equal in each lung, or unilateral with equal airway pressure. Extravascular thermal volume (ETV) was measured at base line and 4 h after lung injury, and the final measurement was compared with the postmortem determination of extravascular lung mass (ELM). In 11 of 15 animals with HCl injury final ETV was less than the base-line measurement. The ratio of final ETV to ELM for all HCl animal (group I) averaged 0.31 +/- 0.14, which was different from the value for animals with alloxan or ANTU injury (group II), 1.04 +/- 0.14 (P less than 0.01). Extravascular lung water per gram of blood-free dry tissue was not different for the two groups (8.1 +/- 1.2 and 8.7 +/- 2.6 for I and II, respectively), indicating equally severe lung injury; however, shunt fraction was less in group I (P less than 0.01). ETV/ELM correlated with the shunt fraction for group I (r = 0.70) but not for group II (r = 0.32). These findings indicate that ETV underestimates lung water after HCl injury due to the redistribution of pulmonary blood flow away from edematous areas.
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PMID:Type of lung injury influences the thermal-dye estimation of extravascular lung water. 643 8

We studied the early detection of alloxan-induced pulmonary injury by magnetic resonance imaging in vivo. Permeability edema was induced in ten rats by intravenous injection of alloxan at 100 mg/kg. T1-and T2-weighted images were acquired in five rats every 30 min for 120 min after alloxan injection. Five rats served as controls. The rats were sacrificed immediately after imaging and examined microscopically. CT images were also acquired in five rats every 30 min for 120 min after alloxan injection. Five rats served as controls. The rats were sacrificed immediately after imaging, and the wet-to-dry ratio of the lung was measured. In T1-weighted images, relative signal intensity from the lung with permeability edema rose from 30 min to 120 min, and was greater than that from normal lung every time. In T2-weighted images, there was no statistically significant difference in relative signal intensity of the lung between permeability edema and the control during 120 min. In CT images, there was also no statistically significant difference in lung density between permeability edema and the control during 120 min. There was no statistically significant difference in the wet-to-dry lung ratio between edematous lung and normal lung. In histological study, mild congestion and interstitial edema were observed in edematous lung. These results suggest the potential capability of MR imaging in detecting the early phase of permeability pulmonary edema.
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PMID:[Experimental study on early detection of alloxan-induced pulmonary injury by magnetic resonance imaging]. 747 47

We examined the relationship between the incidence of ultrastructural changes in the alveolar septum and the extravascular lung water content. Pulmonary edema was induced in 18 mongrel dogs by either dextran (n = 12) or alloxan (n = 6) administration. Six other dogs served as controls. Extravascular lung water content was measured by the thermal-dye double indicator dilution method. Specimens of lung tissue were examined with an electron microscope, and the incidence of 13 types of pathological changes in the alveolar septum was studied. For each type of pathological change, the incidence was correlated with the magnitude of lung water content. The following results were obtained. The incidence of edematous changes in the alveolar interstitium (widening of the interstitial space, and dispersion and disarray of collagen fibres in the interstitial space) was well correlated with lung water content (r = 0.78, p < 0.01, and r = 0.84, p < 0.01, respectively). The correlation was not significant in the remaining types of changes. We conclude that the incidence of the pathological changes in the alveolar septum is increased along with the increase in the content of lung water in both dextran- and alloxan-induced experimental pulmonary edema in dogs.
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PMID:Ultrastructural substrates for increased lung water content in experimental pulmonary edema. 768 Feb 50


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