Fate of air emboli in the pulmonary circulation

The lung serves an important nonrespiratory function by trapping and excreting venous air emboli. The site of trapping and the mechanism of excretion, however, are uncertain. To observe the behavior of bubbles in the pulmonary circulation, we injected venous air emboli into anesthetized dogs and videotaped their elimination from the pulmonary microcirculation by using in vivo microscopy. Small intravenous bubbles lodged exclusively in pulmonary arterioles and were eliminated from that site. To determine whether the gas was dissolving into nearby blood and then was carried to the capillaries for excretion, the rate of bubble radius change was measured during nonperfused conditions produced by balloon occlusion of lobar blood flow and compared with perfused conditions. Bubble volume decreased at the same rate during perfused and nonperfused conditions and thus was independent of regional blood flow. Molecular diffusion of gas directly across the arteriolar wall into alveolar spaces was the most likely mechanism of elimination because calculations based on the Fick equation for molecular diffusion predict an elimination rate nearly identical with those observed experimentally.     

Blood gas analysis: effect of air bubbles in syringe and delay in estimation.

Two common sources of error in blood pH and blood gas analysis were studied. The effect of delay in estimation was studied in 10 volunteers and 40 patients. Syringes were stored at 0 degree C, (crushed ice), 4 degrees C (refrigerator) and 22 degrees C (room temperature). The pressure of oxygen (PO2) fell significantly by 20 minutes at 4 degrees C and 22 degrees C but did not change significantly at 0 degree C for up to 30 minutes. Blood pH, pressure of carbon dioxide (PCO2), and base excess did not change significantly for up to 30 minutes at 4 degrees C and 22 degrees C and up to 60 minutes at 0 degrees C. The effect of air bubbles in the syringe was studied by leaving a single bubble or froth in contact with the blood for one to five minutes in 40 patients. Po2 rose significantly after two minutes'' contact with froth and two minutes'' contact with the air bubble, and PCO2 fell significantly after three minutes'' contact with the air bubble. Size of the bubble had little effect on rates of change. Blood pH, bicarbonate, TCO2, and base excess did not change significantly after up to five minutes'' contact. For accurate estimation of PO2 and PCO2 it is necessary to avoid frothing, to expel all air bubbles within two minutes, and to inject the sample into the machine within 10 minutes or store the syringe in crushed ice. The requirements for blood pH and base excess measurement are less exacting.     

Duroquinone reduction during passage through the pulmonary circulation

The lungs can substantially influence the redox status of redox-active plasma constituents. Our objective was to examine aspects of the kinetics and mechanisms that determine pulmonary disposition of redox-active compounds during passage through the pulmonary circulation. Experiments were carried out on rat and mouse lungs with 2,3,5,6-tetramethyl-1,4-benzoquinone [duroquinone (DQ)] as a model amphipathic quinone reductase substrate. We measured DQ and durohydroquinone (DQH2) concentrations in the lung venous effluent after injecting, or while infusing, DQ or DQH2 into the pulmonary arterial inflow. The maximum net rates of DQ reduction to DQH2 in the rat and mouse lungs were approximately 4.9 and 2.5 micromol. min(-1).g dry lung wt(-1), respectively. The net rate was apparently the result of freely permeating access of DQ and DQH2 to tissue sites of redox reactions, dominated by dicumarol-sensitive DQ reduction to DQH2 and cyanide-sensitive DQH2 reoxidation back to DQ. The dicumarol sensitivity along with immunodetectable expression of NAD(P)H-quinone oxidoreductase 1 (NQO1) in the rat lung tissue suggest cytoplasmic NQO1 as the dominant site of DQ reduction. The effect of cyanide on DQH2 oxidation suggests that the dominant site of oxidation is complex III of the mitochondrial electron transport chain. If one envisions DQ as a model compound for examining the disposition of amphipathic NQO1 substrates in the lungs, the results are consistent with a role for lung NQO1 in determining the redox status of such compounds in the circulation. For DQ, the effect is conversion of a redox-cycling, oxygen-activating quinone into a stable hydroquinone.     

Mathematical modelling of pulmonary gas transport

 Equations governing the transport of the gases oxygen and carbon dioxide inside the pulmonary capillaries are written down. By analysing these equations it is predicted that there will be negligible limitation to the transport of oxygen when oxygen concentration takes a normal physiological or higher value. For low values of oxygen concentration, there may be limitation to oxygen transport. It is predicted further that the quantity of carbon dioxide excreted from blood into alveolar gas is dependent on oxygen concentration, with low oxygen concentrations inhibiting the carbon dioxide transport process. The relatively slow reaction involving carbon dioxide in plasma also inhibits the excretion of carbon dioxide. These predictions are verified by solving the whole system of governing equations numerically. Received: 1 May 2002 / Revised version: 20 October 2002 / Published online: 19 March 2003 JPW was supported by a grant from the Engineering and Physical Sciences Research Council of Great Britain. Key words or phrases: Pulmonary gas transport – Haemoglobin – Saturation     

The dynamics of gas bubbles in conduits of vascular plants and implications for embolism repair

Pressure-induced tensions in the xylem, the water conducting tissue of vascular plants, can lead to embolism in the water-conducting cells. The details and mechanisms of embolism repair in vascular plants are still not well understood. In particular, experimental results which indicate that embolism repair may occur during xylem tension cause great problems with respect to current paradigms of plant water transport. The present paper deals with a theoretical analysis of interfacial effects at the pits (pores in the conduit walls), because it was suggested that gas-water interfaces at the pit pores may be involved in the repair process by hydraulically isolating the embolized conduit. The temporal behaviour of bubbles at the pit pores was especially studied since the question of whether these pit bubbles are able to persist is of crucial importance for the suggested mechanism to work. The results indicate that (1) the physical preconditions which are necessary for the suggested mechanism appear to be satisfied, (2) pit bubbles can achieve temporal stability and therefore persist and (3) dissolving of bubbles in the conduit lumen may lead to the final breakdown of the hydraulic isolation. The whole process is, however, complex and strongly dependent on the detailed anatomy of the pit and the contact angle.     

Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs

Chen, H. F., B. P. Lee, and Y. R. Kou. Mechanisms ofstimulation of vagal pulmonary C fibers by pulmonary air embolism indogs. J. Appl. Physiol. 82(3):765-771, 1997.We investigated the involvement of thecyclooxygenase metabolites and hydroxyl radical (^· OH) in thestimulation of vagal pulmonary C fibers (PCs) by pulmonary air embolism(PAE). Impulses were recorded from PCs in 51 anesthetized, open-chest,and artificially ventilated dogs. Fifty of 59 PCs were stimulated byinfusion of air into the right atrium (0.2 ml ^· kg^{1 ·} min¹for 10 min). As a group (n = 59), PCactivity increased from a baseline of 0.4 ± 0.1 to a peak of 1.7 ± 0.2 impulses/s during the period from 1 min before to 2 min afterthe termination of PAE induction. In PCs initially stimulated by PAEinduction, PAE was repeated after the intervening treatment (iv) withsaline (n = 9), ibuprofen (acyclooxygenase inhibitor; n = 11), ordimethylthiourea (a ^· OH scavenger;n = 12). The responses of PCs to PAEwere not altered by saline vehicle but were abolished by ibuprofen and significantly attenuated by dimethylthiourea. Although hyperinflation of the lungs reversed the PAE-induced bronchomotor responses, it didnot reverse the stimulation of PCs (n = 8). These results suggest that 1)cyclooxygenase products are necessary for the stimulation of PCs byPAE, whereas changes in lung mechanics are not, and2) the functional importance ofcyclooxygenase products may be mediated in part through the formationof ^· OH.

     

Water transport and the distribution of aquaporin-1 in pulmonary air spaces

Effros, R. M., C. Darin, E. R. Jacobs, R. A. Rogers, G. Krenz, and E. E. Schneeberger. Water transport and thedistribution of aquaporin-1 in pulmonary air spaces.J. Appl. Physiol. 83(3): 1002-1016, 1997.Recent evidence suggests that water transport between the pulmonary vasculature and air spaces can be inhibited byHgCl₂, an agent that inhibitswater channels (aquaporin-1 and -5) of cell membranes. In the presentstudy of isolated rat lungs, clearances of labeled(³HOH) and unlabeled water werecompared after instillation of hypotonic or hypertonic solutions intothe air spaces or injection of a hypotonic bolus into the pulmonaryartery. The clearance of ³HOHbetween the air spaces and perfusate after intratracheal instillation and from the vasculature to the tissues after pulmonary arterial injections was invariably greater than that of unlabeled water, indicating that osmotically driven transport of water is limited bypermeability of the tissue barriers rather than the rate of perfusion.Exposure to 0.5 mM HgCl₂ in theperfusate and air-space solution reduced the product of the filtrationcoefficient and surface area(P_fS)of water from the air spaces to the perfusate by 28% afterinstillation of water into the trachea. In contrast, perfusion of 0.5 mM HgCl₂ in air-filled lungs reducedP_fSof the endothelium by 86% after injections into the pulmonary artery, suggesting that much of the action of this inhibitor is on the endothelial surfaces. Confocal laser scanning microscopy demonstrated that aquaporin-1 is on mouse pulmonary endothelium. No aquaporin-1 wasfound on alveolar type I cells with immunogold transmission electronmicroscopy, but small amounts were present on some type II cells.