Exercise-induced intrapulmonary shunting of venous gas emboli does not occur after open-sea diving.

Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 m breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at approximately 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.     

Spatial distribution of collagen and elastin fibers in the lungs

Surface tension forces acting on the thin-wall alveolar septa and the collagen-elastin fiber network are major factors in lung parenchymal micromechanics. Quantitative serial section analysis and morphometric evaluations of planar sections were used to determine the spatial location of collagen and elastin fibers in Sprague-Dawley rat and normal human lung samples. A large concentration of connective tissue fibers was located in the alveolar duct wall in both species. For rats, the tissue densities of collagen and elastin fibers located within 10 microns of an alveolar duct were 13 and 9%, respectively. In human lung samples, the tissue densities of collagen and elastin fibers within 20 microns of an alveolar duct were 18 and 16%, respectively. In both species, bands of elastin fibers formed a continuous ring around each alveolar mouth. In human lungs, elastin fibers were found to penetrate significantly deeper into alveolar septal walls than they did in rat lungs. The concentration of connective tissue elements in the alveolar duct walls of both species is consistent with their proposed roles as the principal load-bearing elements of the lung parenchyma.     

Blood biochemical factors in humans resistant and susceptible to formation of venous gas emboli during decompression

Blood biochemical parameters were measured in 12 male human subjects before and after exposure to a staged decompression protocol, with simulated extravehicular activity, during 3 days. Following the exposure, significant changes occurred in several parameters, including increases in blood urea nitrogen, inorganic phosphate, potassium, and osmolality, and decreases in uric acid and creatinine. Pre-exposure blood samples from subjects who were susceptible to formation of venous gas emboli (VGE) during decompression exhibited significantly greater levels of total cholesterol, high density lipoprotein cholesterol, potassium, inorganic phosphate, calcium, and magnesium. The results indicate that, following this decompression profile, small but significant (P less than 0.05) changes occur in several blood biochemical parameters, and that levels of certain blood factors may be related to susceptibility to VGE formation during decompression.     

Spatial distribution of mast cells in chronic venous leg ulcers

Chronic venous leg ulcers (CVUs) show chronic inflammation but different pathological changes occur in different parts of the ulcer. There is a lack of re-epithelialisation and defective matrix deposition in the ulcer base but epidermal hyperproliferation and increased matrix deposition in the surrounding skin. The role of mast cells in wound healing, inflammation, fibrosis and epidermal hyperproliferation has been extensively studied but less is known about their role in CVUs. In the present study, we investigated the distribution of mast cells in CVUs with specific consideration of the differences between the ulcer base and the skin surrounding the ulcer. Both histochemical and immunohistological methods were used to detect the mast cell marker tryptase in frozen sections of CVU biopsies. Mast cells were counted in the dermis of normal skin, in the ulcer base and in the skin surrounding the ulcer. Double immunofluorescence staining was used to study the location of mast cells in relation to blood vessels. In normal skin few mast cells were seen in the dermis but none in the epidermis. However in CVUs there was a significant increase in intact and degranulated mast cells in the surrounding skin and ulcer edge (184 per field, p<0.003) of CVUs and a significant reduction in the ulcer base (20.5 per field p<0.05) in comparison to normal skin (61 per field). In CVUs mast cells showed a characteristic location near the epithelial basement membrane whilst mast cell granules and phantom cells (mast cells devoid of granules) were predominantly seen in the epidermis. In the dermis, mast cells were seen associated with blood vessels. The marked increase in mast cells in the surrounding skin of CVUs and depletion of mast cells in the ulcer base could implicate mast cell mediators in the pathological changes in CVUs particularly in the epidermal and vascular changes occurring in the surrounding skin.     

Effect of aminophylline on transpulmonary passage of venous air emboli in pigs.

Aminophylline has been shown to dramatically reduce the filtering capacity of the lung in dogs during venous air embolism. Similarities have been pointed out between the cardiovascular and respiratory systems of the pig and of humans. We therefore wanted to find out whether aminophylline also modifies the transpulmonary spillover of microbubbles to the arterial circulation of the pig. Twenty-eight pigs were anesthetized with pentobarbital sodium and mechanically ventilated. Aminophylline was injected intravenously into 10 of the pigs before the introduction of air bubbles into the right ventricle, while the other 18 pigs served as controls. A transesophageal echocardiographic probe was used to detect eventual air bubbles in the left atrium or in the aorta. Pigs received either air infusion, at rates varying from 0.05 to 0.20 ml.kg-1.min-1, or calibrated microbubbles, 5-300 microns diam. We found that aminophylline-treated pigs did not show any change in spillover incidence compared with controls. Furthermore, in both groups the spillover during continuous air infusion seemed to be a preterminal event, because the pigs had very low arterial pressure when arterial bubbles were observed. Finally, there was an increase in mean pulmonary arterial pressure from 18 +/- 3.4 to 26 +/- 2.2 (SD) mmHg (n = 4, P less than 0.01) in aminophylline-treated pigs after a bolus injection of microbubbles (less than or equal to 50 microns, total volume less than 0.5 ml). Our results suggest that aminophylline does not modify the transpulmonary passage of microbubbles in this porcine model. In addition, it would seem that the pulmonary circulation of the pig is sensitive to very small volumes of air, when injected as microbubbles.     

Bubble splitting in bifurcating tubes: a model study of cardiovascular gas emboli transport.

The transport of long gas bubbles, suspended in liquid, through symmetric bifurcations, is investigated experimentally and theoretically as a model of cardiovascular gas bubble transport in air embolism and gas embolotherapy. The relevant dimensionless parameters in the models match the corresponding values for arteries and arterioles. The effects of roll angle (the angle the plane of the bifurcation makes with the horizontal), capillary number (a dimensionless indicator of flow), and bubble volume (or length) on the splitting of bubbles as they pass through the bifurcation are examined. Splitting is observed to be more homogenous at higher capillary numbers and lower roll angles. It is shown that, at nonzero roll angles, there is a critical value of the capillary number below which the bubbles do not split and are transported entirely into the upper branch. The value of the critical capillary number increases with roll angle and parent tube diameter. A unique bubble motion is observed at the critical capillary number and for slightly slower flows: the bubble begins to split, the meniscus in the lower branch then moves backward, and finally the entire bubble enters the upper branch. These findings suggest that, in large vessels, emboli tend to be transported upward unless flow is unusually strong but that a more homogeneous distribution of emboli occurs in smaller vessels. This corresponds to previous observations that air emboli tend to lodge in the upper regions of the lungs and suggests that relatively uniform infarction of tumors by gas embolotherapy may be possible.     

Simplified models for gas exchange in the human lungs

This paper presents a hierarchy of models with increasing complexity for gas exchange in the human lungs. The models span from a single compartment, inflexible lung to a single compartment, flexible lung with pulmonary gas exchange. It is shown how the models are related to well-known models in the literature. A long-term purpose of this work is to study nonlinear phenomena seen in the cardio-respiratory system (for example, synchronization between ventilation rate and heart rate, and Cheyne-Stokes respiration). The models developed in this paper can be regarded as the controlled system (plant) and provide a mathematical framework to link between "molecular-level", and "systems-level" models. It is shown how changes in molecular level affect the alveolar partial pressure. Two assumptions that have previously been made are re-examined: (1) the hidden assumption that the air flow through the mouth is equal to the rate of volume change in the lungs, and, (2) the assumption that the process of oxygen binding to hemoglobin is near equilibrium. Conditions under which these assumptions are valid are studied. All the parameters in the models, except two, are physiologically realistic. Numerical results are consistent with published experimental observations.     

香溪河大型底栖无脊椎动物空间分布

2005年7月至2006年6月,通过对大型底栖无脊椎动物的量化检测,对三峡水库湖北库区最大河流香溪河的大型底栖无脊椎动物空间分布进行了研究.结果表明：四节蜉、高翔蜉、短尾石蝇为香溪河水系大型底栖动物优势类群;香溪河各支流间生境特征及大型底栖无脊椎动物群落结构差异较大;功能摄食类群密度相对丰度的变化能够反映不同的栖境特征.对生物多样性指数及优势类群耐污值的比较表明,大型底栖动物栖境为九冲河最好,香溪河干流次之,高岚河和古夫河较差.典型对应分析表明：铵态氮对香溪河大型底栖动物群落结构影响显著;pH值、浊度、水深、二氧化硅、电导和碱度对九冲河大型底栖动物群落结构影响显著;浊度对高岚河大型底栖动物群落结构影响显著;铵态氮和硝酸盐氮对古夫河大型底栖动物群落结构影响显著.     

Pulmonary venous pressure increases during alveolar hypoxia in isolated lungs of newborn pigs.

The purpose of this study was to determine whether pulmonary venous pressure increases during alveolar hypoxia in lungs of newborn pigs. We isolated and perfused with blood the lungs from seven newborn pigs, 6-7 days old. We maintained blood flow constant at 50 ml.min-1.kg-1 and continuously monitored pulmonary arterial and left atrial pressures. Using the micropuncture technique, we measured pressures in 10 to 60-microns-diam venules during inflation with normoxic (21% O2-69-74% N2-5-10% CO2) and hypoxic (90-95% N2-5-10% CO2) gas mixtures. PO2 was 142 +/- 21 Torr during normoxia and 20 +/- 4 Torr during hypoxia. During micropuncture we inflated the lungs to a constant airway pressure of 5 cmH2O and kept left atrial pressure greater than airway pressure (zone 3). During hypoxia, pulmonary arterial pressure increased by 69 +/- 24% and pressure in small venules increased by 40 +/- 23%. These results are similar to those obtained with newborn lambs and ferrets but differ from results with newborn rabbits. The site of hypoxic vasoconstriction in newborn lungs is species dependent.     

Impedance, gas mixing, and bimodal ventilation in constricted lungs.

To evaluate the effect of increasing smooth muscle activation on the distribution of ventilation, lung impedance and expired gas concentrations were measured during a 16-breath He-washin maneuver in five nonasthmatic subjects at baseline and after each of three doses of aerosolized methacholine. Values of dynamic lung elastance (El,dyn), the curvature of washin plots, and the normalized slope of phase III (S(N)) were obtained. At the highest dose, El,dyn was 2.6 times the control value and S(N) for the 16th breath was 0.65 liter(-1). A previously described model of a constricted terminal airway was extended to include variable muscle activation, and the extended model was tested against these data. The model predicts that the constricted airway has two stable states. The impedances of the two stable states are independent of smooth muscle activation, but driving pressure and the number of airways in the high-resistance state increase with increasing muscle activation. Model predictions and experimental data agree well. We conclude that, as a result of the bistability of the terminal airways, the ventilation distribution in the constricted lung is bimodal.     

Spatial distribution of hypoxic pulmonary vasoconstriction in the supine pig.

Hypoxic pulmonary vasoconstriction (HPV) serves to maintain optimal gas exchange by decreasing perfusion to hypoxic regions. However, global hypoxia and nonuniform HPV may result in overperfusion of poorly constricted regions leading to local edema seen in high-altitude pulmonary edema. To quantify the spatial distribution of HPV and its response to regional Po2 (Pr(O2)) among small lung regions, five pigs were anesthetized and mechanically ventilated in the supine posture. The animals were ventilated with an inspired O2 fraction (Fi(O2)) of 0.50 and 0.21 and then (in random order) 0.15, 0.12, and 0.09. Regional blood flow (Q) and alveolar ventilation (Va) were measured by using intravenous infusion of 15 microm and inhalation of 1-microm fluorescent microspheres, respectively. Pr(O2) was calculated for each piece at each Fi(O2). Lung pieces differed in their Q response to hypoxia in a manner related to their initial Va/Q with Fi(O2) = 0.21. Reducing Fi(O2) < 0.15 decreased Q to the initially high Va/Q (higher Pr(O2)) regions and forced Q into the low Va/Q (dorsal-caudal) regions. Resistance increased in most lung pieces as Pr(O2) decreased, reaching a maximum resistance when Pr(O2) is between 40 and 50 Torr. Local resistance decreased at PrO2 < 40 Torr. Pieces were statistically clustered with respect to their relative Q response pattern to each Fi(O2). Some clusters were shown to be spatially organized. We conclude that HPV is spatially heterogeneous. The heterogeneity of Q response may be related, in part, to the heterogeneity of baseline Va/Q.     

Analysis of stress distribution in the alveolar septa of normal and simulated emphysematic lungs.

The alveolar septum consists of a skeleton of fine collagen and elastin fibers, which are interlaced with a capillary network. Its mechanical characteristics play an important role in the overall performance of the lung. An alveolar sac model was developed for numerical analysis of the internal stress distribution and septal displacements within the alveoli of both normal and emphysematic saline-filled lungs. A scanning electron micrograph of the parenchyma was digitized to yield a geometric replica of a typical two-dimensional alveolar sac. The stress-strain relationship of the alveolar tissue was adopted from experimental data. The model was solved by using commercial finite-element software for quasi-static loading of alveolar pressure. Investigation of the state of stresses and displacements in a healthy lung simulation yielded values that compared well with experimentally reported data. Alteration of the mechanical characteristics of the alveolar septa to simulate elastin destruction in the emphysematic model induced significant stress concentrations (e.g., at a lung volume of 60% total capacity, tensions at certain parts in an emphysematic lung were up to 6 times higher than those in a normal lung). The combination of highly elevated stress sites together with the cyclic loading of breathing may explain the observed progressive damage to elastin fibers in emphysematic patients.