Respiratory Medium Research Articles

Evaluation of SCO1 deletion on Saccharomyces cerevisiae metabolism through a proteomic approach

The Saccharomyces cerevisiae gene SCO1 has been shown to play an essential role in copper delivery to cytochrome c oxidase. Biochemical studies demonstrated specific transfer of copper from Cox17p to Sco1p, and physical interactions between the Sco1p and Cox2p. Deletion of SCO1 yeast gene results in a respiratory deficient phenotype. This study aims to gain a more detailed insight on the effects of SCO1 deletion on S. cerevisiae metabolism. We compared, using a proteomic approach, the protein pattern of SCO1 null mutant strain and wild-type BY4741 strain grown on fermentable and on nonfermentable carbon sources. The analysis showed that on nonfermentable medium, the SCO1 mutant displayed a protein profile similar to that of actively fermenting yeast cells. Indeed, on 3% glycerol, this mutant displayed an increase of some glycolytic and fermentative enzymes such as glyceraldehyde-3-phosphate dehydrogenase 1, enolase 2, pyruvate decarboxylase 1, and alcohol dehydrogenase 1. These data were supported by immunoblotting and enzyme activity assay. Moreover, the ethanol assay and the oxygen consumption measurement demonstrated a fermentative activity in SCO1 mutant on respiratory medium. Our results suggest that on nonfermentable carbon source, the lack of Sco1p causes a metabolic shift from respiration to fermentation.

Diagnosis and treatment of neurogenic pulmonary edema in children with severe hand, foot and mouth disease

Severe hand foot and mouth disease can lead to death when accompanied by neurogenic pulmonary edema. Early identifying involvement of central nervous system, focusing on the evidences of excited sympathetic nerve tension and high risks of neurogenic pulmonary edema, monitoring respiratory rate,dyspnea, cyanosis, fine and medium rales in lungs are critical to prognosis. Managing fluid loading strictly, decreasing intracranial hypertension, supporting actively respiratory function and strengthening airway management are key points for the treatment of neurogenic pulmonary edema. Key words: Severe hand foot and mouth disease ; Neurogenic pulmonary edema; Diagnosis; Treatment

Prenatal Maternal Stress and Cord Blood Innate and Adaptive Cytokine Responses in an Inner-City Cohort

Stress-elicited disruption of immunity begins in utero. Associations among prenatal maternal stress and cord blood mononuclear cell (CBMC) cytokine responses were prospectively examined in the Urban Environment and Childhood Asthma Study (n = 557 families). Prenatal maternal stress included financial hardship, difficult life circumstances, community violence, and neighborhood/block and housing conditions. Factor analysis produced latent variables representing three contexts: individual stressors and ecological-level strains (housing problems and neighborhood problems), which were combined to create a composite cumulative stress indicator. CBMCs were incubated with innate (lipopolysaccharide, polyinosinic-polycytidylic acid, cytosine-phosphate-guanine dinucleotides, peptidoglycan) and adaptive (tetanus, dust mite, cockroach) stimuli, respiratory syncytial virus, phytohemagglutinin, or medium alone. Cytokines were measured using multiplex ELISAs. Using linear regression, associations among increasing cumulative stress and cytokine responses were examined, adjusting for sociodemographic factors, parity, season of birth, maternal asthma and steroid use, and potential pathway variables (prenatal smoking, birth weight for gestational age). Mothers were primarily minorities (Black [71%], Latino [19%]) with an income less than $15,000 (69%). Mothers with the highest cumulative stress were older and more likely to have asthma and deliver lower birth weight infants. Higher prenatal stress was related to increased IL-8 production after microbial (CpG, PIC, peptidoglycan) stimuli and increased tumor necrosis factor-alpha to microbial stimuli (CpG, PIC). In the adaptive panel, higher stress was associated with increased IL-13 after dust mite stimulation and reduced phytohemagglutinin-induced IFN-gamma. Prenatal stress was associated with altered innate and adaptive immune responses in CBMCs. Stress-induced perinatal immunomodulation may impact the expression of allergic disease in these children.

Yeast Colony Survival Depends on Metabolic Adaptation and Cell Differentiation Rather Than on Stress Defense

Enzymes scavenging reactive oxygen species (ROS) are important for cell protection during stress and aging. A deficiency in these enzymes leads to ROS imbalance, causing various disorders in many organisms, including yeast. In contrast to liquid cultures, where fitness of the yeast population depends on its ROS scavenging capability, the present study suggests that Saccharomyces cerevisiae cells growing in colonies capable of ammonia signaling use a broader protective strategy. Instead of maintaining high levels of antioxidant enzymes for ROS detoxification, colonies activate an alternative metabolism that prevents ROS production. Colonies of the strain deficient in cytosolic superoxide dismutase Sod1p thus developed the same way as wild type colonies. They produced comparable levels of ammonia and underwent similar developmental changes (expression of genes of alternative metabolism and center margin differentiation in ROS production, cell death occurrence, and activities of stress defense enzymes) and did not accumulate stress-resistant suppressants. An absence of cytosolic catalase Ctt1p, however, brought colonies developmental problems, which were even more prominent in the absence of mitochondrial Sod2p. sod2Delta and ctt1Delta colonies failed in ammonia production and sufficient activation of the alternative metabolism and were incapable of center margin differentiation, but they did not increase ROS levels. These new data indicate that colony disorders are not accompanied by ROS burst but could be a consequence of metabolic defects, which, however, could be elicited by imbalance in ROS produced in early developmental phases. Sod2p and homeostasis of ROS may participate in regulatory events leading to ammonia signaling.

Predator or prey? The dive response to aerial and aquatic predators of Arafura filesnakes

In air-breathing aquatic animals, predation is a strong selection pressure that may be reduced by modification to diving patterns. The risk of predation increases with time spent at the surface, thus shorter, more frequent surfacing events or longer, less frequent surfacing events would decrease predation risk. A reduction in time spent on the surface can be achieved by use of bimodal respiration, which is an ability to extend dive duration using dissolved oxygen to supplement aerially acquired oxygen. Air is a more efficient respiratory medium; however, under predation pressure, the cost of surfacing increases and the reliance on aquatic gas exchange should therefore increase. We tested whether the bimodally respiring filesnake (Acrochordus arafurae) changed its diving behaviour under simulated aerial (model bird) and aquatic (large fish) predation. Aerial predation did not alter dive or surface duration, percentage time surfacing or activity. However, a greater number of longer dives were observed with fewer long surface intervals, suggesting an increase in the use of aquatic gas exchange. The diel diving patterns (short night dives, long day dives) may provide an in-built antipredatory response to aerial predation. The threat of aquatic predation produced atypical antipredator behaviour, with longer surface intervals, shorter dives and increased activity, indicating that piscivorous filesnakes may have identified the predatory fish as prey rather than a predator.

The influence of feeding on aerial and aquatic oxygen consumption, nitrogenous waste excretion, and metabolic fuel usage in the African lungfish, Protopterus annectens

We studied the utilization of air versus water as a respiratory medium for O2consumption (Mo2) in the bimodally breathing African lungfish, Protopterus annectens (Owen, 1839), (151.2 ± 3.7 g) at 26–28 °C. We also investigated the impact of a single meal on this respiratory allocation and nitrogenous waste excretion in lungfish entrained to a 48 h feeding cycle. Correction for the “microbial blank” was found to be critically important in assessing the aquatic component of Mo2. After correction, total Mo2was low (~1000 μmol·kg–1·h–1), and lungfish took about 40% of Mo2from water and 60% from air. Following a meal of chironomid larvae (3.3% of body mass), Mo2values from both air and water increased in proportion over the first 3 h and continued to increase to a peak at 5–8 h postfeeding, at which point total Mo2(still 40% from water) was approximately 2.5-fold greater than the prefeeding level. When the same fish, entrained to the same 48 h feeding regime, were fasted, Mo2declined then later increased prior to the next anticipated feeding. In fed fish, the elevation in Mo2relative to fasted values was approximately 3-fold at 0–3 h and 9-fold at 5–8 h. This specific dynamic action (SDA) effect lasted until 23–26 h and amounted to only 9.5% of the oxycalorific content of the ingested meal. N-waste efflux was only slightly elevated after feeding, where there was a tendency for greater urea–N excretion (significant at 42–48 h); however, the lungfish remained ammoniotelic overall during the 48 h postfeeding period.

Transmembrane Transport and Release of GABA in the Brain of Rats Subjected to Postnatal Hypoxia

We studied the effects of early postnatal hypoxia on the efficiency of active GABA transport through the plasma membrane of synaptic terminals (synaptosomes) isolated from the cerebral cortex, hippocampus, and thalamus of rats and on non-stimulated and Ca2+-stimulated GABA release. The state of hypoxia was induced by exposure of 10- to 12-day-old rats to a respiratory medium with low O2 content (4% О2 and 96% N2) for 12 min (up to the initiation of clonico-tonic seizures). Animals were taken in the experiment 8 to 9 weeks after an episode of hypoxic stress. The intensity of transmembrane transport of GABA was estimated according to accumulation of [3Н]GABA in a coarse synaptosomal fraction. The process was characterized by calculation of the Michaelis constant K m and also of the initial (within the 1st min) and maximum rates of accumulation of [3Н]GABA. The means of the initial rate of [3Н]GABA accumulation in preparations from the thalamus, cortex, and hippocampus were 205.5 ± 8.8, 266.2 ± 29.6, and 302.3 ± 31.2 pmol/min⋅mg protein, respectively. Hypoxic stress influenced the rates of accumulation of [3Н]GABA in synaptic terminals from the cortex and hippocampus but not in those from the thalamus. According to the characteristics of the response to hypoxic stress, all experimental animals could be classified into two groups. In some rats, accumulation of [3Н]GABA in both cortical and hippocampal synaptosomes decreased insignificantly (by about 15%), while in other animals this parameter increased significantly (by nearly 50%) for the cortex and decreased by 21.5%, on average, for the hippocampus. The affinity of the transporter with respect to [3Н]GABA in the cortex and hippocampus was nearly the same and showed no changes under the influence of hypoxia. The non-stimulated release of [3Н]GABA after the influence of hypoxia increased in all structures, while the depolarization-induced Ca2+-dependent release of [3Н]GABA was intensified only in synaptosomes from the cerebral cortex. The mechanisms of development of modifications of GABA-ergic processes under the influence of hypoxic stress in the course of the perinatal period are discussed.

Functional Mitochondria Are Required for α-Synuclein Toxicity in Aging Yeast

alpha-Synuclein is one of the principal toxic triggers of Parkinson disease, an age-associated neurodegeneration. Using old yeast as a model of alpha-synuclein expression in post-mitotic cells, we show that alpha-synuclein toxicity depends on chronological aging and results in apoptosis as well as necrosis. Neither disruption of key components of the unfolded protein response nor deletion of proapoptotic key players (including the yeast caspase YCA1, the apoptosis-inducing factor AIF1, or the serine protease OMI) did prevent alpha-synuclein-induced cell killing. However, abrogation of mitochondrial DNA (rho(0)) inhibited alpha-synuclein-induced reactive oxygen species formation and subsequent apoptotic cell death. Thus, introducing an aging yeast model of alpha-synuclein toxicity, we demonstrate a strict requirement of functional mitochondria.

The response of the tidepool sculpin, Oligocottus maculosus, to hypoxia in laboratory, mesocosm and field environments

Animals living in the intertidal zone experience regular, predictable fluctuations in physical parameters including temperature, oxygen and salinity and rely on behavioural, physiological and biochemical mechanisms to cope with environmental variation. In the present study, behavioural strategies induced by aquatic hypoxia (e.g. emergence) were performed at similar oxygen tensions across laboratory, mesocosm and field environments; the number of individuals performing these behaviours at any one time was similar in mesocosms and the field. The use of aquatic surface respiration (ASR) was more plastic than emergence behaviour, occurring at a lower oxygen tension in juveniles than adults and being influenced by the addition of alarm substance. Oxygen uptake was lower in air than in water in adults but, in contrast, oxygen uptake was not influenced by the respiratory medium in juveniles. In the laboratory, 72 h of forced emergence did not affect whole body concentrations of lactate but when ASR and emergence were prevented within mesocosm environments there was a significant elevation of lactate. The present study highlights the benefits of transcending traditional laboratory/field boundaries allowing the responses of laboratory-held animals to environmental fluctuation to be integrated with how these animals perform in their natural environment.

Malate metabolism in Hoya carnosa mitochondria and its role in photosynthesis during CAM phase III

This study investigated the respiratory properties and the role of the mitochondria isolated from one phosphoenolpyruvate carboxykinase (PCK)-CAM plant, Hoya carnosa, in malate metabolism during CAM phase III. The mitochondria showed high malate dehydrogenase (mMDH) and aspartate amino transferase (mAST), and a significant amount of malic enzyme (mME) activities. H. carnosa readily oxidized malate via mME and mMDH in the presence of some cofactors such as thiamine pyrophosphate (TPP), coenzyme A (CoA) or NAD(+). A high respiration rate of malate oxidation was observed at pH 7.2 with NAD(+) and glutamate (Glu). Providing AST and Glu simultaneously into the respiratory medium strongly increased the rates of malate oxidation, and this oxidation was gradually inhibited by an inhibitor of alpha-ketoglutarate (alpha-KG) carrier, pyridoxal-5'-phosphate (PLP). The mitochondria readily oxidized aspartate (Asp) or alpha-KG individually with low rates, while they oxidized Asp and alpha-KG simultaneously with high rates, and this simultaneous oxidation was also inhibited by PLP. By measuring the capacity of the mitochondrial shuttle, it was found that the OAA produced via mMDH seemed not to be transported outside the mitochondria, but mAST interconverted OAA and Glu to Asp and alpha-KG, respectively, and exported them out via a malate-aspartate (malate-Asp) shuttle. The data in this research suggest that during phase III of PCK-CAM, H. carnosa mitochondria oxidized malate via both mME and the mMDH systems depending on metabolic requirements. However, malate metabolism by the mMDH system did not operate via a malate-OAA shuttle similarly to Ananas comosus mitochondria, but it operated via a malate-Asp shuttle similarly to Kalanchoë daigremontiana mitochondria.

Prenyldiphosphate synthase, subunit 1 (PDSS1) and OH-benzoate polyprenyltransferase (COQ2) mutations in ubiquinone deficiency and oxidative phosphorylation disorders

Coenzyme Q10 (CoQ10) plays a pivotal role in oxidative phosphorylation (OXPHOS), as it distributes electrons among the various dehydrogenases and the cytochrome segments of the respiratory chain. We have identified 2 novel inborn errors of CoQ10 biosynthesis in 2 distinct families. In both cases, enzymologic studies showed that quinone-dependent OXPHOS activities were in the range of the lowest control values, while OXPHOS enzyme activities were normal. CoQ10 deficiency was confirmed by restoration of normal OXPHOS activities after addition of quinone. A genome-wide search for homozygosity in family 1 identified a region of chromosome 10 encompassing the gene prenyldiphosphate synthase, subunit 1 (PDSS1), which encodes the human ortholog of the yeast COQ1 gene, a key enzyme of CoQ10 synthesis. Sequencing of PDSS1 identified a homozygous nucleotide substitution modifying a conserved amino acid of the protein (D308E). In the second family, direct sequencing of OH-benzoate polyprenyltransferase (COQ2), the human ortholog of the yeast COQ2 gene, identified a single base pair frameshift deletion resulting in a premature stop codon (c.1198delT, N401fsX415). Transformation of yeast Deltacoq1 and Deltacoq2 strains by mutant yeast COQ1 and mutant human COQ2 genes, respectively, resulted in defective growth on respiratory medium, indicating that these mutations are indeed the cause of OXPHOS deficiency.

TOTAL LIQUID VENTILATION IN PRETERM LAMBS: REPORT OF IN VIVO TESTS OF A VENTILATOR PROTOTYPE

The purpose of this study was to perform in vivo animal tests of a novel ventilator prototype for Total Liquid Ventilation (TLV). A total of 17 preterm lambs (gestational age 110±5 days; body weight 3.1±1.2kg), under general anesthesia, were instrumented to record hemodynamic values and gas exchange which were monitored throughout the experiments. Tracheostomy and intratracheal intubation were performed, as well as instrumentation with ex uterus intrapartum treatment (EXIT) support. All fetuses were maintained connected to the placental circulation for the first 10 minutes of ventilation. After complete extraction and disconnection from the mother circulation, the lambs were ventilated for 6 hours. Eleven lambs were ventilated with the prototype ventilator (TLV group); the other 6 lambs (gas ventilation, GV group) were ventilated, as control, with a conventional mechanical ventilator (Siemens Servoventilator 900B). The TLV prototype consists of a volume-controlled, pressure-limited ventilator; it comprises a double-piston system performing respiratory cycles and an uncoupled refresh circuit to achieve perfluorocarbon (PFC) filtration, thermo-regulation, oxygenation, and CO2washout. TLV was performed using PFC FC77 (3M Corp.). At the end of each experiment, fetal lungs were excised and processed for light microscopy to verify airway and lung parenchyma condition. Adequate oxygenation was achieved, while hypercapnia was shown in both groups. Mean arterial pO2 and pCO2 were respectively 72.6 mmHg and 77.8 mmHg, in the TLV group, while 86.6 mmHg and 67.9 mmHg, in the GV group. Higher mortality occurred in the gas ventilation group (67%) than in the TLV group (45%). The histological analyses highlighted a more homogeneous distribution of the respiratory medium in the TLV-ventilated animals (49.3%) with respect to the control group (38.8%) and the histological analyses showed minimal signs of inflammation of the airways and lung parenchyma in the TLV-ventilated animals. The outcomes of the experiments showed the capacity of the TLV ventilator to support the life of very preterm neonatal animals, on the other hand it could be useful to refine the approach to the firsts breathes to minimize the possible lungs damages and improve distribution of the respiratory medium.

Decreased Protein Accretion in Pigs with Viral and Bacterial Pneumonia Is Associated with Increased Myostatin Expression in Muscle

Chronic respiratory infections reduce growth in pigs but protein accretion (PA) during an ongoing multifactorial respiratory infection has not been determined, and the mechanisms underlying growth inhibition are largely unknown. The objectives of this study were to determine whether viral and bacterial pneumonia in young pigs decrease PA, increase serum IL-1beta and IL-6, and increase myostatin (MSTN) mRNA in biceps femoris and triceps muscles. Mycoplasma hyopneumoniae (Mh) or medium was given intratracheally at 4 wk of age, Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) or medium was given intranasally at 6 wk of age, and pigs were killed 7 or 14 d after PRRSV inoculation for body composition analysis. PRRSV but not Mh induced a marked increase (P < 0.01) in IL-1beta, IL-6, and MSTN mRNA and a decrease (P < 0.01) in food intake, daily weight gain, PA, and lipid accretion. PRRSV also reduced (P < 0.01) myofiber area in the biceps femoris. Food intake, weight gain, PA, and weight of biceps femoris and triceps muscles were negatively correlated (r = -0.4 to -0.8, P < 0.05) with serum IL-1beta and IL-6 and with MSTN mRNA in muscle. These results suggest that the magnitude of increases in inflammatory cytokines during a respiratory infection may be predictive of decreases in PA and growth. They further suggest that during infection growth of skeletal muscle is limited in part by myostatin.

Oxygen and carbon dioxide sensitivity of ventilation in amphibious crabs, Cardisoma guanhumi, breathing air and water

Amphibious crabs, Cardisoma guanhumi, were acclimated to breathing either air or water and exposed to altered levels of oxygen and/or carbon dioxide in the medium. Hypercapnia (22, 36 and 73 torr CO2) stimulated a significant hypercapnic ventilatory response (HCVR) in both groups of crabs, with a much greater effect on scaphognathite frequency (ΔfSC=+700%) in air-breathing crabs than water-breathing crabs (ΔfSC=+100%). In contrast, hyperoxia induced significant hypoventilation in both sets of crabs. However, simultaneous hyperoxia and hypercapnia triggered a greater than 10-fold increase in fSC in air-breathing crabs but no change in water-breathing crabs. For water-breathing crabs hypoxia simultaneous with hypercapnia triggered the same response as hypoxia alone—bradycardia (−50%), and a significant increase in fSC at moderate exposures but not at the more extreme levels. The response of air-breathing crabs to hypoxia concurrent with hypercapnia was proportionally closer to the response to hypercapnia alone than to hypoxia. Thus, C. guanhumi were more sensitive to ambient CO2 than O2 when breathing air, characteristic of fully terrestrial species, and more sensitive to ambient O2 when breathing water, characteristic of fully aquatic species. C. guanhumi possesses both an O2- and a CO2-based ventilatory drive whether breathing air or water, but the relative importance switches when the respiratory medium is altered.

Oxygen and carbon dioxide sensitivity of ventilation in amphibious crabs, Cardisoma guanhumi, breathing air and water

Amphibious crabs, Cardisoma guanhumi, were acclimated to breathing either air or water and exposed to altered levels of oxygen and/or carbon dioxide in the medium. Hypercapnia (22, 36 and 73 torr CO 2) stimulated a significant hypercapnic ventilatory response (HCVR) in both groups of crabs, with a much greater effect on scaphognathite frequency (Δ f SC=+700%) in air-breathing crabs than water-breathing crabs (Δ f SC=+100%). In contrast, hyperoxia induced significant hypoventilation in both sets of crabs. However, simultaneous hyperoxia and hypercapnia triggered a greater than 10-fold increase in f SC in air-breathing crabs but no change in water-breathing crabs. For water-breathing crabs hypoxia simultaneous with hypercapnia triggered the same response as hypoxia alone—bradycardia (−50%), and a significant increase in f SC at moderate exposures but not at the more extreme levels. The response of air-breathing crabs to hypoxia concurrent with hypercapnia was proportionally closer to the response to hypercapnia alone than to hypoxia. Thus, C. guanhumi were more sensitive to ambient CO 2 than O 2 when breathing air, characteristic of fully terrestrial species, and more sensitive to ambient O 2 when breathing water, characteristic of fully aquatic species. C. guanhumi possesses both an O 2- and a CO 2-based ventilatory drive whether breathing air or water, but the relative importance switches when the respiratory medium is altered.

QO Site Deficiency Can Be Compensated by Extragenic Mutations in the Hinge Region of the Iron-Sulfur Protein in the bc1 Complex of Saccharomyces cerevisiae

The mitochondrial bc(1) complex catalyzes the oxidation of ubiquinol and the reduction of cytochrome (cyt) c. The cyt b mutation A144F has been introduced in yeast by the biolistic method. This residue is located in the cyt b cd(1) amphipathic helix in the quinol-oxidizing (Q(O)) site. The resulting mutant was respiration-deficient and was affected in the quinol binding and electron transfer rates at the Q(O) site. An intragenic suppressor mutation was selected (A144F+F179L) that partially alleviated the defect of quinol oxidation of the original mutant A144F. The suppressor mutation F179L, located at less than 4 A from A144F, is likely to compensate directly the steric hindrance caused by phenylalanine at position 144. A second set of suppressor mutations was obtained, which also partially restored the quinol oxidation activity of the bc(1) complex. They were located about 20 A from A144F in the hinge region of the iron-sulfur protein (ISP) between residues 85 and 92. This flexible region is crucial for the movement of the ISP between cyt b and cyt c(1) during enzyme turnover. Our results suggested that the compensatory effect of the mutations in ISP was due to the repositioning of this subunit on cyt b during quinol oxidation. This genetic and biochemical study thus revealed the close interaction between the cyt b cd(1) helix in the quinol-oxidizing Q(O) site and the ISP via the flexible hinge region and that fine-tuning of the Q(O) site catalysis can be achieved by subtle changes in the linker domain of the ISP.

Liquid ventilation: an adjunct for respiratory management

Although significant advances in respiratory care have reduced mortality of patients with respiratory failure, morbidity persists, often resulting from iatrogenic mechanisms. Mechanical ventilation with gas has been shown to initiate as well as exacerbate underlying lung injury, resulting in progressive structural damage and release of inflammatory mediators within the lung. Alternative means to support pulmonary gas exchange while preserving lung structure and function are therefore required. Perfluorochemical (PFC) liquids are currently used clinically in a number of ways, such as intravascular PFC emulsions for volume expansion/oxygen carrying/angiography and intracavitary neat PFC liquid for image contrast enhancement or vitreous fluid replacement. As a novel approach to replace gas as the respiratory medium, liquid assisted ventilation (LAV) with PFC liquids has been investigated as an alternative respiratory modality for over 30 years. Currently, there are several theoretical and practical applications of LAV in the immature or mature lung at risk for acute respiratory distress and injury associated with mechanical ventilation.

Liquid ventilation

Liquid ventilation

Structure, function and evolution of the gas exchangers: comparative perspectives.

Over the evolutionary continuum, animals have faced similar fundamental challenges of acquiring molecular oxygen for aerobic metabolism. Under limitations and constraints imposed by factors such as phylogeny, behaviour, body size and environment, they have responded differently in founding optimal respiratory structures. A quintessence of the aphorism that 'necessity is the mother of invention', gas exchangers have been inaugurated through stiff cost-benefit analyses that have evoked transaction of trade-offs and compromises. Cogent structural-functional correlations occur in constructions of gas exchangers: within and between taxa, morphological complexity and respiratory efficiency increase with metabolic capacities and oxygen needs. Highly active, small endotherms have relatively better-refined gas exchangers compared with large, inactive ectotherms. Respiratory structures have developed from the plain cell membrane of the primeval prokaryotic unicells to complex multifunctional ones of the modern Metazoa. Regarding the respiratory medium used to extract oxygen from, animal life has had only two choices--water or air--within the biological range of temperature and pressure the only naturally occurring respirable fluids. In rarer cases, certain animals have adapted to using both media. Gills (evaginated gas exchangers) are the primordial respiratory organs: they are the archetypal water breathing organs. Lungs (invaginated gas exchangers) are the model air breathing organs. Bimodal (transitional) breathers occupy the water-air interface. Presentation and exposure of external (water/air) and internal (haemolymph/blood) respiratory media, features determined by geometric arrangement of the conduits, are important features for gas exchange efficiency: counter-current, cross-current, uniform pool and infinite pool designs have variably developed.

Fundamental structural aspects and features in the bioengineering of the gas exchangers: comparative perspectives.

Fundamental structural aspects and features in the bioengineering of the gas exchangers: comparative perspectives.