Weak field influence on biomolecular changes

Model equations for the kinetics of the synthesis and decay of molecular aggregates are used to show the high sensitivity of equilibrium concentrations of high-molecular aggregates to external radiation. This phenomenon is used to explain the effects of low-intensity microwave fields on the functioning of biological systems. The experimental results on the influence of SHF-radiation on ferricyanide reduction by erythrocytes are interpreted in detail.     

Routes of protein transport into the lungs from the bronchial vascular system

In order to study the role of the bronchial vascular system in pulmonary protein transport, experiments have been performed in 6 anesthesized dogs, 16 isolated canine lungs and 10 white rats. When bilateral ligation of the bronchial arteries is performed in the anesthesized dogs, cessation of the bronchial blood stream results in decreasing protein transport and lymph outflow from the lungs. In the isolated canine lungs perfused through the pulmonary and bronchial vessels, lymph formation is determined by presence of the bronchial perfusion. As demonstrated the electron microscopical investigations with the marker of the protein transport--horseradish peroxidase--for 15 min of observation the marker does not get out of the limits of endothelium in the pulmonary capillaries. During this time horseradish peroxidase gets out of the bronchial vessels into the loose connective tissue of the lung, the lymphatic capillaries and the alveolar epithelium. Therefore, it is possible to make a conclusion on a predominated role of the protein transport in the lungs out of the bronchial vascular system as compared to the pulmonary system.     

Characterization of an acyl-coenzyme A binding protein predominantly expressed in human primitive progenitor cells

Human acyl-coenzyme A binding domain-containing member 6 (ACBD6) is a modular protein that carries an acyl-CoA binding domain at its N terminus and two ankyrin motifs at its C terminus. ACBD6 binds long-chain acyl-CoAs with a strong preference for unsaturated, C18:1-CoA and C20:4-CoA, over saturated, C16:0-CoA, acyl species. Deletion of the C terminus, which is not conserved among the members of this family, did not affect the binding capacity or the substrate specificity of the protein. ACBD6 is not a ubiquitous protein, and its expression is restricted to tissues and progenitor cells with functions in blood and vessel development. ACBD6 was detected in bone marrow, spleen, placenta, cord blood, circulating CD34+ progenitors, and embryonic-like stem cells derived from placenta. In placenta, the protein was only detected in CD34+ progenitor cells present in blood and in CD31+ endothelial cells surrounding the blood vessels. These cells were also positive for the marker CD133, and they probably constitute hemangiogenic stem cells, precursors of both blood and vessels. We propose that human ACBD6 represents a cellular marker for primitive progenitor cells with functions in hematopoiesis and vascular endothelium development.     

Intravascular macrophage depletion attenuates endotoxin lung injury in anesthetized sheep.

We recently showed that we can selectively and safely deplete most (average 85%) of the pulmonary intravascular macrophages in sheep by intravenously infusing liposomes containing dichloromethylene bisphosphonate. After a 1-h stable baseline, we made a 6-h comparison after a 30-min intravenous endotoxin infusion (1 microg/kg) between six anesthetized control lambs and six anesthetized lambs in which the intravascular macrophages had been depleted 24 h previously. Three of the control lambs had been macrophage depleted and allowed to recover their intravascular macrophage population for >/=2 wk. After depletion, both the early and late pulmonary arterial pressure rises were dramatically attenuated. Our main interest, however, was in the acute lung microvascular injury response. The early and late rises in lung lymph flow and the increase in lung lymph protein clearance (lymph flow x lymph-to-plasma protein concentration ratio) were >90% attenuated. We conclude the pulmonary intravascular macrophages are responsible for most of the endotoxin-induced pulmonary hypertension and increased lung microvascular leakiness in sheep, although the unavoidable injury of other intravascular macrophages by the depletion regime may also contribute something.     

Theoretical approach to the description of microvesicular transport in the endothelium

Theoretical consideration of mechanisms on curvature of the cell membrane, resulting in formation of microvesicles in the cells has been carried out. These mechanisms are presented as: 1) local changes of membrane surface tension at the border membranes--external medium; 2) local changes of the membrane potential; 3) hydrostatic pressure; 4) crystallization of membrane domains; 5) enzymatic changes of the lipid molecule configurations. Energy of the curved membrane and the energy of the external effects for the vesicle are estimated. Spontaneous formation of vesicles at the expense of the oscillatory mechanism is impossible. The most probable mechanism, from the energetic point of view, for vesicular formation is adsorption of surface-active substances or ions on the membrane. Thus, the processes of microvesicular mass transfer, playing an important role in transcapillary mass exchange are determined by physicochemical mechanisms. From the physico-chemical point of view adsorption of substances can be the most probable mechanism in the vesicular formation and determine intensity of vesicular transport.     

Application of respiratory heat exchange for the measurement of lung water.

A noninvasive method for measuring pulmonary blood flow and lung mass (called airway thermal volume), based on the measurements of lung heat exchange with environment, is described. The lungs function as a steady-state heat exchange system, having an inner heat source (pulmonary blood flow) and an external heat sink (ventilation). Sudden changes in the steady-state condition, such as caused by hyperventilation of dry air, lead to a new steady state after a few minutes. The expired air temperature difference between the initial and final steady states is proportional to pulmonary blood flow, whereas the rate at which the new steady state is achieved is proportional to airway thermal volume. The method was tested in 20 isolated dogs lungs, 9 perfused goat lungs, and 27 anesthetized sheep. The expired air temperature fall during hyperventilation was inversely proportional to the perfusion rate of the isolated lungs, and half-time of the temperature fall was proportional to the lung tissue mass. Experiments in anesthetized sheep showed that the measured airway thermal volume is close to the total mass of the excised lungs, including its residual blood (r = 0.98). Pulmonary edema and fluid instillation into the bronchial tree increased in the measured lung mass.     

Reliability of extravascular lung thermal volume measurements by thermal conductivity technique in sheep.

We tested the accuracy, sensitivity, and reproducibility of a new lung water computer, based on the thermal conductivity technique, in 22 anesthetized closed-chest ventilated sheep with different treatments: 1) controls (n = 8), 2) 0.05 ml/kg of oleic acid + 100 ml/kg of lactated Ringer solution (n = 6), and 3) airway instillation of saline [3.1 +/- 1.3 (SD) g/kg, n = 8]. After 4 h, we determined the extravascular lung water gravimetrically. We found a significant overall correlation between the final extravascular lung thermal volume and the gravimetric extravascular lung mass (P < 0.001). Although the average ratio of extravascular lung thermal volume to extravascular lung mass was 0.97 +/- 0.25 ml/g for all groups, the computer overestimated extravascular lung mass in controls by 10% (17 g) and underestimated it in sheep with oleic acid by 15% (95 g) and in sheep with airway instillation by 8% (37 g). The computer also underestimated the small quantities of saline placed via the airway in the alveolar space by 75% (61 g). Reproducibility of three consecutive measurements was 4.3% (SE). We conclude that the thermal conductivity technique has an ability to detect the baseline extravascular lung mass but has a poor ability to detect an accurate increment of the extravascular lung water under poor tissue perfusion in anesthetized ventilated sheep.     

Airway thermal volume in humans and its relation to body size

Serikov, Vladimir B., E. Heidi Jerome, Neal W. Fleming,Peter G. Moore, Frederick A. Stawitcke, and Norman C. Staub.Airway thermal volume in humans and its relation to body size.J. Appl. Physiol. 83(2): 668-676, 1997.The objective of this study was to investigate the influence ofvolume ventilation(E) andcardiac output () on the temperature of the expiredgas at the distal end of the endotracheal tube in anesthetized humans.In 63 mechanically ventilated adults, we used a step decrease in thehumidity of inspired gas to cool the lungs. After change from humid todry gas ventilation, the temperature of the expired gas decreased. Weevaluated the relationship between the inverse monoexponential timeconstant of the temperature fall (1/) and eitherE or . WhenE wasincreased from 5.67 ± 1.28 to 7.14 ± 1.60 (SD) l/min(P = 0.02), 1/ did not changesignificantly [from 1.25 ± 0.38 to 1.21 ± 0.51 min¹,P = 0.81]. In the 11 patients in whom changed during the study period(from 5.07 ± 1.81 to 7.38 ± 2.45 l/min,P = 0.02), 1/ increasedcorrespondingly from 0.89 ± 0.22 to 1.52 ± 0.44 min¹(P = 0.003). We calculated the airwaythermal volume (ATV) as the ratio of the measured values to 1/ and related it to the body height (BH):ATV (liters) = 0.086 BH (cm)  9.55 (r = 0.90).