T2 of endotoxin lung injury with and without methylprednisolone treatment.

NMR relaxation times (T1 and T2) and the water content (WC) of in vitro rat lungs were measured during the course of endotoxin lung injury in rats. Measurements of normal lungs, untreated endotoxin-injured lungs, and endotoxin-injured lungs treated with methylprednisolone (MPSL) were compared. The untreated endotoxin lungs showed prolongation of the fast and slow T2 components (T2f and T2s), but no significant changes in T1 or water content. Also, there was no correlation between 1/WC and relaxation rates or between T1 and T2. MPSL treatment prevented T2f and T2s prolongation; however, the duration of MPSL effectiveness was limited. Animals which were treated with MPSL more than 7 h prior to measurements showed T2 prolongation. This study indicates that NMR relaxation times, particularly T2, can be useful in evaluating lung injuries and their treatments.

Experimental inhalation injury with concomitant surface burn: dextran resuscitation improves lung water and oxygenation.

UNLABELLED: The role of extravascular lung water (EVLW) in the pathogenesis of inhalation injury (INH) when associated with concomitant major burn (B) remains controversial. Previous experimental models have investigated isolated INH without surface burn. This study measured the effects of isolated and combined INH on EVLW and pO2 in a porcine experimental model. The beneficial effects of early resuscitation with dextran-40 (DEX) were assessed, using a control group receiving standard Parkland formula (LR). In the first part of the study (INH vs. INH + B), a group of animals with a standardized INH was compared to a group also receiving a standardized 40% BSA third-degree surface burn (n = 8, each group). With serial measurements for 5 hours, EVLW was only modestly increased unless INH was accompanied by surface burn: 20.3 +/- 4.2 vs. 32.0 +/- 4.1 ml/kg at 5 hours (p less than 0.01). Similarly, pO2 fell much more dramatically in the INH + B group, 61 +/- 5 vs. 37 +/- 5 torr (p less than 0.05). The second part of the study compared standard Parkland crystalloid resuscitation with dextran-40 resuscitation in animals receiving a combined INH + B injury (LR vs. DEX, n = 8, each group). DEX resuscitation resulted in substantially lower accumulation of EVLW out to 5 hours, 34.1 +/- 5.0 vs. 13.1 +/- 3.0 ml/kg (p less than 0.01), and significantly better pO2, 35 +/- 5 vs. 64 +/- 4 torr (p less than 0.01). CONCLUSIONS: Inhalation injury did not dramatically increase EVLW in this animal model unless accompanied by concomitant major surface burn. The deterioration in EVLW and pO2 seen in the combined injury was significantly improved with DEX resuscitation when compared to standard crystalloid resuscitation. Further study is indicated and clinical trials may be warranted.

Bioimpedance: a novel method for the determination of extravascular lung water.

Extravascular lung water (EVLW) can be measured using the double indicator dilution technique (DD). However, because this method is highly invasive and complicated, its clinical used has been limited. In theory, changes in thoracic conductivity, or bioimpedance (BI), can reflect changes in EVLW. However, past studies were unable to directly quantitate changes in EVLW since the contribution of dynamic variables such as ventricular volumes, hematocrit (HCT), and EVLW to this impedance signal could not be discerned. Recent studies have shown that a thermodilution pulmonary artery catheter mounted with a fast response thermistor accurately measures right ventricular end-diastolic volume (RVEDV). With changes in the RVEDV and HCT known, the contribution of EVLW to the bioimpedance signal may be isolated and used to more directly measure changes in EVLW. This hypothesis was tested by creating acute sepsis in seven pigs by infusion of Pseudomonas aeruginosa. Changes in EVLW from baseline were measured using DD at 30 min and at 1, 2, and 4 hr and compared with the change in EVLW computed from a mathematical model comprising the measured changes in BI, RVEDV, and HCT at the same time points. Changes in EVLW using DD and BI were significantly correlated over the length of the study (r = 0.85, P less than 0.01). In early sepsis (30 min), BI overestimated EVLW when compared with DD (P less than 0.05). However, at 1, 2, and 4 hr there was no significant difference between the two methods. In conclusion, the use of bioimpedance and a volumetric catheter may provide a relatively simple and reliable method for continuously monitoring changes in EVLW in the intensive care setting.

Commercial double-indicator-dilution densitometer using heavy water: evaluation in oleic-acid pulmonary edema.

We evaluated a commercially available, double-indicator-dilution densitometric system for the estimation of pulmonary extravascular water volume in oleic acid-induced pulmonary edema. Indocyanine green and heavy water were used as the nondiffusible and diffusible tracers, respectively. Pulmonary extravascular water volume, measured with this system, was 67% of the gravimetric value (r = 0.91), which was consistent with values obtained from the radioisotope methods. The measured volume was not influenced by changes in cardiac index over a range of 1 to 4 L.min.m2. This system is less invasive than the thermal-dye technique and has potential for repeated clinical measurements of pulmonary extravascular lung water and cardiac output.

Measurement of extravascular lung water by thermal-dye dilution technique: mechanisms of cardiac output dependence.

The extent to which extravascular lung water (EVLW) is dependent on cardiac output was analysed in anaesthetized and mechanically ventilated pigs. EVLW was measured by thermal-dye dilution technique, by a fibreoptic thermistor catheter system (system 1), and by a thermistor catheter-external optical cuvette system (system 2). During baseline conditions, at which cardiac output was 3.65 l/min, and EVLW was 11.7 and 7.7 ml/kg b.w. with systems 1 and 2 respectively. A reduction of cardiac output to a mean of 1.90 l/min by the addition of halothane to the inspired gas did not significantly affect EVLW with system 1 (-5%) but increased EVLW by 39% (p less than 0.05) with system 2. An increase of cardiac output to a mean of 4.78 l/min by intravenous infusion of isoproterenol caused a small increase in EVLW with system 1 (14%; p less than 0.05) and a decrease with system 2 (10%; p less than 0.05). The dependence on cardiac output was the same whether the catheters were positioned centrally (aortic root) or peripherally (abdominal aorta). With system 1 the CO dependence was due to different time constants in thermistor and optical systems, and with appropriate phasing the dependence could be eliminated. With system 2 a large overestimation of the mean transit time difference between the two indicators was seen when cardiac output was low, resulting in overestimation of EVLW. It is concluded that the dependence of EVLW volume on cardiac output is an artefact due to technical problems in the design of the recording equipment rather than a reflection of pulmonary or vascular effects.

[Experimental study of dynamic changes in elastase-antiprotease in rabbits in the early stage of inhalation injury].

In this experiment, rabbit model with smoke inhalation injury was used. The study was designed to observe the dynamic changes of elastase activities of polymorphonuclear leukocytes (PMN), alveolar macrophages (AM) and bronchoalveolar lavage fluid (BALF); and trypsin inhibitory capacities of serum and BALF (STIC & BTIC). The relationships between these changes and acute lung injury, as well as the concomitant changes of arterial blood gas levels, lung water volume and pathomorphology of trachea and lung tissues were also observed. It was found that after injury the elastase activities of PMN and AM were markedly reduced, and the elastase activity of BALF was rapidly increased. STIC was also reduced. PaO2 progressively dropped and PaCO2 progressively increased. Animals showed respiratory distress. Pathomorphological phagocytes aggregations in lungs, pulmonary edema and pneumorrhagia were found. There were serious destructions of capillary endothelial cells, alveolar epithelial cells, basement membranes and interstitial fibers. The number of elastic fibers of parenchyma decreased. The lung water volume was markedly increased, and there was a significant correlation between the increment of extravascular lung water and the rising of elastase activity of BALF. On the basis of our observation, it is proposed that the imbalance of elastase-antiprotease may play an important role in the development of acute lung injury after smoke inhalation.

[The diagnosis of fat embolism in lungs altered by putrefaction]. / K diagnostike zhirovoiu émbolii gnilostno izmenennykh legkikh.

The results of biochemical analysis of rabbit lungs in case of death due to fat embolism and mechanical asphyxia (control) are presented. Reliable difference in lipid quantities was evident both immediately after death and in different putrefaction periods (this difference was 9-10 times greater in case of pulmonary fat embolism than in controls). The significant reduction in water content of the lungs in case of fat embolism as compared to controls was detected. Histological analysis of the putrefactive lungs can't detect fat embolism. Biochemical analysis makes it possible to diagnose fat embolism of the lungs in case of their marked putrefactive changes.

[Respiratory moisture loss and possible pathways of its regulation]. / Respiratornaia vlagopoteria i vozmozhnye puti ee reguliatsii.

Examination of healthy men and those suffering from nonspecific pulmonary diseases has shown that respiratory moisture loss is induced by situation and While "lifting" examinees in the altitude chamber 5000 m upwards intensity of the moisture loss increases to 158%. Essential individual variations of the response are shown. Pulmonary diseases (chronic bronchitis, pneumonia, lecithin synthesis disturbances) make the moisture loss higher. It is concluded that lung surfactants participate in regulation of the respiratory moisture loss. participate in regulation of the respiratory moisture loss.