Olfactory preferences of Popillia japonica, Vanessa cardui, and Aphis glycines for Glycine max grown under elevated CO2

Levels of atmospheric CO(2) have been increasing steadily over the last century and are projected to increase even more dramatically in the future. Soybeans (Glycine max L.) grown under elevated levels of CO(2) have larger herbivore populations than soybeans grown under ambient levels of CO(2). Increased abundance could reflect the fact that these herbivores are drawn in by increased amounts of volatiles or changes in the composition of volatiles released by plants grown under elevated CO(2) conditions. To determine impacts of elevated CO(2) on olfactory preferences, Japanese beetles (Popillia japonica Newman) and soybean aphids (Aphis glycines Matsumura) were placed in Y-tube olfactometers with a choice between ambient levels of CO(2) gas versus elevated levels of CO(2) gas or damaged and undamaged leaves and plants grown under ambient levels of CO(2) versus damaged and undamaged plants grown under elevated levels of CO(2). All plants had been grown from seeds under ambient or elevated levels of CO(2). Painted lady butterflies (Vanessa cardui L.) were placed in an oviposition chamber with a choice between plants grown under ambient and elevated levels of CO(2). A. glycines and V. cardui showed no significant preference for plants in either treatment. P. japonica showed no significant preference between ambient levels and elevated levels of CO(2) gas. There was a significant P. japonica preference for damaged plants grown under ambient CO(2) versus undamaged plants but no preference for damaged plants grown under elevated CO(2) versus undamaged plants. P. japonica also preferred damaged plants grown under elevated levels of CO(2) versus damaged plants grown under ambient levels of CO(2). This lack of preference for damaged plants grown under elevated CO(2) versus undamaged plants could be the result of the identical elevated levels of a green leaf volatile (2-hexenal) present in all foliage grown under elevated CO(2) regardless of damage status. Green leaf volatiles are typically released from damaged leaves and are used as kairomones by many herbivorous insects for host plant location. An increase in production of volatiles in soybeans grown under elevated CO(2) conditions may lead to larger herbivore outbreaks in the future.     

Temperature, oxygen, and salt-sensing neurons in C. elegans are carbon dioxide sensors that control avoidance behavior

Homeostatic control of body fluid CO(2) is essential in animals but is poorly understood. C.?elegans relies on diffusion for gas exchange and avoids environments with elevated CO(2). We show that C.?elegans temperature, O(2), and salt-sensing neurons are also CO(2) sensors mediating CO(2) avoidance. AFD thermosensors respond to increasing CO(2) by a fall and then rise in Ca(2+) and show a Ca(2+) spike when CO(2) decreases. BAG O(2) sensors and ASE salt sensors are both activated by CO(2) and remain tonically active while high CO(2) persists. CO(2)-evoked Ca(2+) responses in AFD and BAG neurons require cGMP-gated ion channels. Atypical soluble guanylate cyclases mediating O(2) responses also contribute to BAG CO(2) responses. AFD and BAG neurons together stimulate turning when CO(2) rises and inhibit turning when CO(2) falls. Our results show that C.?elegans senses CO(2) using functionally diverse sensory neurons acting homeostatically to minimize exposure to elevated CO(2).     

End-tidal carbon dioxide tension reflects arterial carbon dioxide tension in the heat-stressed human with and without simulated hemorrhage

End-tidal carbon dioxide tension (Pet(CO(2))) is reduced during an orthostatic challenge, during heat stress, and during a combination of these two conditions. The importance of these changes is dependent on Pet(CO(2)) being an accurate surrogate for arterial carbon dioxide tension (Pa(CO(2))), the latter being the physiologically relevant variable. This study tested the hypothesis that Pet(CO(2)) provides an accurate assessment of Pa(CO(2)) during the aforementioned conditions. Comparisons between these measures were made: 1) after two levels of heat stress (N = 11); 2) during combined heat stress and simulated hemorrhage [via lower-body negative pressure (LBNP), N = 8]; and 3) during an end-tidal clamping protocol to attenuate heat stress-induced reductions in Pet(CO(2)) (N = 7). Pet(CO(2)) and Pa(CO(2)) decreased during heat stress (P < 0.001); however, there was no group difference between Pa(CO(2)) and Pet(CO(2)) (P = 0.36) nor was there a significant interaction between thermal condition and measurement technique (P = 0.06). To verify that this nonsignificant trend for the interaction was not due to a type II error, Pet(CO(2)) and Pa(CO(2)) at three distinct thermal conditions were also compared using paired t-tests, revealing no difference between Pa(CO(2)) and Pet(CO(2)) while normothermic (P = 0.14) and following a 1.0 ± 0.2°C (P = 0.21) and 1.4 ± 0.2°C (P = 0.28) increase in internal temperature. During LBNP while heat stressed, measures of Pet(CO(2)) and Pa(CO(2)) were similar (P = 0.61). Likewise, during the end-tidal carbon dioxide clamping protocol, the increases in Pet(CO(2)) (7.5 ± 2.8 mmHg) and Pa(CO(2)) (6.6 ± 3.4 mmHg) were similar (P = 0.31). These data indicate that mean Pet(CO(2)) reflects mean Pa(CO(2)) during the evaluated conditions.     

Elevated CO2 lowers relative and absolute herbivore density across all species of a scrub-oak forest

The unabated increase in global atmospheric CO(2) is expected to induce physiological changes in plants, including reduced foliar nitrogen, which are likely to affect herbivore densities. This study employs a field-based CO(2 )enrichment experiment at Kennedy Space Center, Florida, to examine plant-herbivore (insect) interactions inside eight open-topped chambers with elevated CO(2) (710 ppm) and eight control chambers with ambient CO(2). In elevated CO(2) we found decreased herbivore densities per 100 leaves, especially of leaf miners, across all five plant species we examined: the oak trees Quercus myrtifolia, Q. geminata, and Q. chapmanii, the nitrogen-fixing vine Galactia elliottii and the shrub Vaccinium myrsinites. Both direct and indirect effects of lowered plant nitrogen may influence this decrease in herbivore densities. Direct effects of lowered nitrogen resulted in increased host-plant related death and an increase in compensatory feeding: per capita herbivore leaf consumption in elevated CO(2) was higher than in ambient CO(2). Indirectly, compensatory feeding may have prolonged herbivore development and increased exposure to natural enemies. For all leaf miners we examined, mortality from natural enemies increased in elevated CO(2). These increases in host-plant induced mortality and in attack rates by natural enemies decreased leaf miner survivorship, causing a reduction in leaf miner density per 100 leaves. Despite increased leaf production in elevated CO(2) from the carbon fertilization effect, absolute herbivore abundance per chamber was also reduced in elevated CO(2). Because insects cause premature leaf abscission, we also thought that leaf abscission would be decreased in elevated CO(2). However, for all plant species, leaf abscission was increased in elevated CO(2), suggesting a direct effect of CO(2) on leaf abscission that outweighs the indirect effects of reduced insect densities on leaf abscission.     

高浓度CO_2诱导的小麦叶片毫秒延迟发光的振荡

当空气中CO_2浓度增至较高水平（5％）时,小麦叶片毫秒延迟发光（ms－DLE）显示出强烈的振荡。若再通入正常空气,DLE仍恢复到原有水平。当将空气中的CO2含量从无增加亚空气水平时,DLE下降但不伴随明显振荡,而继续增高CO2浓度会诱导振荡出现,该振荡随CO2浓度增高而加强。解联剂尼日利亚菌素可以消除CO2诱导的DLE振荡。     

Elevated CO(2) induces biochemical and ultrastructural changes in leaves of the C(4) cereal sorghum

We analyzed the impact of growth at either 350 (ambient) or 700 (elevated) microL L(-1) CO(2) on key elements of the C(4) pathway (photosynthesis, carbon isotope discrimination, and leaf anatomy) using the C(4) cereal sorghum (Sorghum bicolor L. Moench.). Gas-exchange analysis of the CO(2) response of photosynthesis indicated that both carboxylation efficiency and the CO(2) saturated rate of photosynthesis were lower in plants grown at elevated relative to ambient CO(2). This was accompanied by a 49% reduction in the phosphoenolpyruvate carboxylase content of leaves (area basis) in the elevated CO(2)-grown plants, but no change in Rubisco content. Despite the lower phosphoenolpyruvate carboxylase content, there was a 3-fold increase in C isotope discrimination in leaves of plants grown at elevated CO(2) and bundle sheath leakiness was estimated to be 24% and 33%, respectively, for the ambient and elevated CO(2)-grown plants. However, we could detect no difference in quantum yield. The ratio of quantum yield of CO(2) fixation to PSII efficiency was lower in plants grown at elevated CO(2), but only when leaf internal was below 50 microL L(-1). This suggests a reduction in the efficiency of the C(4) cycle when [CO(2)] is low, and also implies increased electron transport to acceptors other than CO(2). Analysis of leaf sections using a transmission electron microscope indicated a 2-fold decrease in the thickness of the bundle sheath cell walls in plants grown at elevated relative to ambient CO(2). These results suggest that significant acclimation to increased CO(2) concentrations occurs in sorghum.     

Carbon monoxide actuates O(2)-limited heme degradation in the rat brain

The biochemical paradigm for carbon monoxide (CO) is driven by the century-old Warburg hypothesis: CO alters O(2)-dependent functions by binding heme proteins in competitive relation to 1/oxygen partial pressure (PO(2)). High PO(2) thus hastens CO elimination and toxicity resolution, but with more O(2), CO-exposed tissues paradoxically experience less oxidative stress. To help resolve this paradox we tested the Warburg hypothesis using a highly sensitive gas-reduction method to track CO uptake and elimination in brain, heart, and skeletal muscle in situ during and after exogenous CO administration. We found that CO administration does increase tissue CO concentration, but not in strict relation to 1/PO(2). Tissue gas uptake and elimination lag behind blood CO as predicted, but 1/PO(2) vs. [CO] fails even at hyperbaric PO(2). Mechanistically, we established in the brain that cytosol heme concentration increases 10-fold after CO exposure, which sustains intracellular CO content by providing substrate for heme oxygenase (HO) activated after hypoxia when O(2) is resupplied to cells rich in reduced pyridine nucleotides. We further demonstrate by analysis of CO production rates that this heme stress is not due to HO inhibition and that heme accumulation is facilitated by low brain PO(2). The latter becomes rate limiting for HO activity even at physiological PO(2), and the heme stress leads to doubling of brain HO-1 protein. We thus reveal novel biochemical actions of both CO and O(2) that must be accounted for when evaluating oxidative stress and biological signaling by these gases.     

Passive entry of CO2 and its energy-dependent intracellular conversion to HCO3- in cyanobacteria are driven by a photosystem I-generated deltamuH+

CO(2) entry into Synechococcus sp. PCC7942 cells was drastically inhibited by the water channel blocker p-chloromercuriphenylsulfonic acid suggesting that CO(2) uptake is, for the most part, passive via aquaporins with subsequent energy-dependent conversion to HCO3(-). Dependence of CO(2) uptake on photosynthetic electron transport via photosystem I (PSI) was confirmed by experiments with electron transport inhibitors, electron donors and acceptors, and a mutant lacking PSI activity. CO(2) uptake was drastically inhibited by the uncouplers carbonyl cyanide m-chlorophenylhydrazone (CCCP) and ammonia but substantially less so by the inhibitors of ATP formation arsenate and N, N,-dicyclohexylcarbodiimide (DCCD). Thus a DeltamuH(+) generated by photosynthetic PSI electron transport apparently serves as the direct source of energy for CO(2) uptake. Under low light intensity, the rate of CO(2) uptake by a high-CO(2)-requiring mutant of Synechococcus sp. PCC7942, at a CO(2) concentration below its threshold for CO(2) fixation, was higher than that of the wild type. At saturating light intensity, net CO(2) uptake was similar in the wild type and in the mutant IL-3 suggesting common limitation by the rate of conversion of CO(2) to HCO3(-). These findings are consistent with a model postulating that electron transport-dependent formation of alkaline domains on the thylakoid membrane energizes intracellular conversion of CO(2) to HCO3(-).     

Transcranial Doppler estimation of cerebral blood flow and cerebrovascular conductance during modified rebreathing.

Clinical transcranial Doppler assessment of cerebral vasomotor reactivity (CVMR) uses linear regression of cerebral blood flow velocity (CBFV) vs. end-tidal CO(2) (Pet(CO(2))) under steady-state conditions. However, the cerebral blood flow (CBF)-Pet(CO(2)) relationship is nonlinear, even for moderate changes in CO(2). Moreover, CBF is increased by increases in arterial blood pressure (ABP) during hypercapnia. We used a modified rebreathing protocol to estimate CVMR during transient breath-by-breath changes in CBFV and Pet(CO(2)). Ten healthy subjects (6 men) performed 15 s of hyperventilation followed by 5 min of rebreathing, with supplemental O(2) to maintain arterial oxygen saturation constant. To minimize effects of changes in ABP on CVMR estimation, cerebrovascular conductance index (CVCi) was calculated. CBFV-Pet(CO(2)) and CVCi-Pet(CO(2)) relationships were quantified by both linear and nonlinear logistic regression. In three subjects, muscle sympathetic nerve activity was recorded. From hyperventilation to rebreathing, robust changes occurred in Pet(CO(2)) (20-61 Torr), CBFV (-44 to +104% of baseline), CVCi (-39 to +64%), and ABP (-19 to +23%) (all P < 0.01). Muscle sympathetic nerve activity increased by 446% during hypercapnia. The linear regression slope of CVCi vs. Pet(CO(2)) was less steep than that of CBFV (3 vs. 5%/Torr; P = 0.01). Logistic regression of CBF-Pet(CO(2)) (r(2) = 0.97) and CVCi-Pet(CO(2)) (r(2) = 0.93) was superior to linear regression (r(2) = 0.91, r(2) = 0.85; P = 0.01). CVMR was maximal (6-8%/Torr) for Pet(CO(2)) of 40-50 Torr. In conclusion, CBFV and CVCi responses to transient changes in Pet(CO(2)) can be described by a nonlinear logistic function, indicating that CVMR estimation varies within the range from hypocapnia to hypercapnia. Furthermore, quantification of the CVCi-Pet(CO(2)) relationship may minimize the effects of changes in ABP on the estimation of CVMR. The method developed provides insight into CVMR under transient breath-by-breath changes in CO(2).     

Effect of mild carboxy-hemoglobin on exercising skeletal muscle: intravascular and intracellular evidence

We studied muscle blood flow, muscle oxygen uptake (VO(2)), net muscle CO uptake, Mb saturation, and intracellular bioenergetics during incremental single leg knee-extensor exercise in five healthy young subjects in conditions of normoxia, hypoxia (H; 11% O(2)), normoxia + CO (CO(norm)), and 100% O(2) + CO (CO(hyper)). Maximum work rates and maximal oxygen uptake (VO(2 max)) were equally reduced by approximately 14% in H, CO(norm), and CO(hyper). The reduction in arterial oxygen content (Ca(O(2))) (approximately 20%) resulted in an elevated blood flow (Q) in the CO and H trials. Net muscle CO uptake was attenuated in the CO trials. Suprasystolic cuff measurements of the deoxy-Mb signal were not different in terms of the rate of signal rise or maximum signal attained with and without CO. At maximal exercise, calculated mean capillary PO(2) was most reduced in H and resulted in the lowest Mb-associated PO(2). Reductions in ATP, PCr, and pH during H, CO(norm), and CO(hyper) occurred earlier during progressive exercise than in normoxia. Thus the effects of reduced Ca(O(2)) due to mild CO poisoning are similar to H.     

Sympathetic regulation of the human cerebrovascular response to carbon dioxide

Although the cerebrovasculature is known to be exquisitely sensitive to CO(2), there is no consensus on whether the sympathetic nervous system plays a role in regulating cerebrovascular responses to changes in arterial CO(2). To address this question, we investigated human cerebrovascular CO(2) reactivity in healthy participants randomly assigned to the α(1)-adrenoreceptor blockade group (9 participants; oral prazosin, 0.05 mg/kg) or the placebo control (9 participants) group. We recorded mean arterial blood pressure (MAP), heart rate (HR), mean middle cerebral artery flow velocity (MCA(V mean)), and partial pressure of end-tidal CO(2) (Pet(CO(2))) during 5% CO(2) inhalation and voluntary hyperventilation. CO(2) reactivity was quantified as the slope of the linear relationship between breath-to-breath Pet(CO(2)) and the average MCAv(mean) within successive breathes after accounting for MAP as a covariate. Prazosin did not alter resting HR, Pet(CO(2)), MAP, or MCA(V mean). The reduction in hypocapnic CO(2) reactivity following prazosin (-0.48 ± 0.093 cm·s(-1)·mmHg(-1)) was greater compared with placebo (-0.19 ± 0.087 cm·s(-1)·mmHg(-1); P < 0.05 for interaction). In contrast, the change in hypercapnic CO(2) reactivity following prazosin (-0.23 cm·s(-1)·mmHg(-1)) was similar to placebo (-0.31 cm·s(-1)·mmHg(-1); P = 0.50 for interaction). These data indicate that the sympathetic nervous system contributes to CO(2) reactivity via α(1)-adrenoreceptors; blocking this pathway with prazosin reduces CO(2) reactivity to hypocapnia but not hypercapnia.     

Oral [13C]bicarbonate measurement of CO2 stores and dynamics in children and adults

During exercise, less additional CO2 is stored per kilogram body weight in children than in adults, suggesting that children have a smaller capacity to store metabolically produced CO2. To examine this, tracer doses of [13C]bicarbonate were administered orally to 10 children (8-12 yr) and 12 adults (25-40 yr) at rest. Washout of 13CO2 in breath was analyzed to estimate recovery of tracer, mean residence time (MRT), and size of CO2 stores. CO2 production (VCO2) was also measured breath by breath using gas exchange techniques. Recovery did not differ significantly between children [73 +/- 13% (SD)] and adults (71 +/- 9%). MRT was shorter in children (42 +/- 7 min) compared with adults (66 +/- 15 min, P less than 0.001). VCO2 per kilogram was higher in the children (5.4 +/- 0.9 ml.min-1.kg-1) compared with adults (3.1 +/- 0.5, P less than 0.0001). Tracer estimate of CO2 production was correlated to VCO2 (r = 0.86, P less than 0.0001) and when corrected for mean recovery accurately predicted the VCO2 to within 3 +/- 14%. There was no difference in the estimate of resting CO2 stores between children (222 +/- 52 ml CO2/kg) and adults (203 +/- 42 ml CO2/kg). We conclude that orally administered [13C]bicarbonate can be used to assess CO2 transport dynamics. The data do not support the hypothesis of lower CO2 stores under resting conditions in children.     

Real-time monitoring of nasal mucosal pH during carbon dioxide stimulation: implications for stimulus dynamics

Carbon dioxide is a commonly employed irritant test compound in nasal chemesthetic studies because it is essentially free of olfactory stimulus properties. CO(2) is thought to act via hydration to H(2)CO(3) and dissociation to H(+) in nasal mucus, with resulting activation of acid sensors. However, transient changes in nasal mucosal pH have not been documented during CO(2) stimulation in humans. We placed a small pH probe on the floor of the right anterior nasal cavity during CO(2) stimulation in eight human subjects with historically high (>30%) and low (< or =20%) CO(2) detection thresholds. Three second pulses of CO(2) (15-45% v/v) paired with air in random order (12-15 s inter-stimulus interval; 60 s inter-trial interval) were administered by nasal cannula at 5 l/min. in an ascending series. For each subject, both a CO(2) detection threshold and suprathreshold psychophysical ratings [psi; labeled magnitude scale] were generated. All subjects showed phasic drops in pH associated with CO(2) stimulation (DeltapH). For all subjects combined, a positive correlation was apparent between applied [CO(2)] and both DeltapH and psi, as well as between DeltapH and psi themselves (P < 0.0001 for each comparison). Subjects with historically low CO(2) thresholds showed steeper dose-response curves for psi as a function of both applied [CO(2)] and DeltapH, but not for DeltapH as a function of applied [CO(2)]. For the six of eight subjects with measurable pH changes at threshold, DeltapH was positively related to log [CO(2) threshold] (P < 0.01). These data imply that variability in CO(2) detection thresholds and suprathreshold rating may derive from intrinsic differences in neural sensitivity, rather than differences in stimulus activation to hydrogen ion.     

Topical inhibition of nasal carbonic anhydrase affects the CO2 detection threshold in rats

Previous studies indicate that Long-Evans rats can be operantly trained to discriminate inspired CO(2) concentrations as low as 0.5%. This ability has been proposed to be due to the presence of CO(2)-sensitive olfactory receptors that contain the enzyme carbonic anhydrase (CA). The objectives of the present study were as follows: 1) to determine whether Zucker rats could be operantly conditioned to discriminate low concentrations of CO(2) from control air and 2) to determine the rats' CO(2) detection thresholds before and after nasal perfusion of mammalian Ringers or methazolamide, a CA inhibitor. Rats were operantly trained to discriminate between 25% CO(2) and control air (0% CO(2)) and were then subjected to various CO(2) concentrations (0.5-12.5%) to determine their CO(2) detection thresholds. The average (+/-standard error of mean) baseline CO(2) detection threshold of 7 Zucker rats was 0.48 +/- 0.07% CO(2), whereas the average CO(2) detection thresholds after nasal perfusion of either mammalian Ringers or 10(-2) M methazolamide were 1.41 +/- 0.30% and 5.92 +/- 0.70% CO(2), respectively. The average CO(2) detection threshold after methazolamide was significantly greater (P<0.0001) than the baseline detection threshold. These findings demonstrate that like Long-Evans rats, Zucker rats can be trained to discriminate low concentrations of CO(2) and that inhibition of nasal CA reduces the ability of the rats to detect low concentrations (3.5% and below) but not higher concentrations of CO(2) (12.5%). These results add to the growing evidence that olfactory neurons exhibiting CA activity are CO(2) chemoreceptors sensitive to physiological concentrations of CO(2).     

Effect of CO2 on LPS-induced cytokine responses in rat alveolar macrophages

Alveolar macrophages (AM) may be exposed to a range of CO(2) and pH levels depending on their location in the alveoli and the health of the lung. Cytokines produced by AM contribute to inflammation in acute lung injury (ALI). Current ventilatory practices for the management of ALI favor low tidal volumes, which can give rise to increases in CO(2) and changes in pH of the alveolar microenvironment. Here we examined the effect of CO(2) on cytokine release from LPS-stimulated rat AM. AM were incubated for 1-4 h under different atmospheric gas mixtures ranging from 2.5-20% CO(2). To distinguish between effects of pH and CO(2), the culture media were also buffered to pH 7.2 with NaHCO(3). Cell metabolic activity, but not cell viability, decreased and increased significantly after 4 h at 20 and 2.5% CO(2), respectively. Increasing CO(2) decreased TNF-alpha secretion but had no effect on lysate TNF-alpha. Buffering the media abated the effects of CO(2) on TNF-alpha secretion. CO(2) increased cytokine-induced neutrophil chemoattractant factor-1 secretion only when the pH was buffered to 7.2. Effects of CO(2) on cytokine responses were reversible. In conclusion, the effects of CO(2) on cytokine lysate levels and/or secretion in AM are cytokine specific and, depending on both the cytokine and the immediate microenvironment, may be beneficial or detrimental to ALI.     

Modulation of the heteromeric Kir4.1-Kir5.1 channels by P(CO(2)) at physiological levels

Several inward rectifier K(+) (Kir) channels are pH-sensitive, making them potential candidates for CO(2) chemoreception in cells. However, there is no evidence showing that Kir channels change their activity at near physiological level of P(CO(2)), as most previous studies were done using high concentrations of CO(2). It is known that the heteromeric Kir4.1-Kir5.1 channels are highly sensitive to intracellular protons with pKa value right at the physiological pH level. Such a pKa value may allow these channels to regulate membrane potentials with modest changes in P(CO(2)). To test this hypothesis, we studied the Kir4.1-Kir5.1 currents expressed in Xenopus oocytes and membrane potentials in the presence and absence of bicarbonate. Evident inhibition of these currents (by approximately 5%) was seen with P(CO(2)) as low as 8 torr. Higher P(CO(2)) levels (23-60 torr) produced stronger inhibitions (by 30-40%). The inhibitions led to graded depolarizations (5-45 mV with P(CO(2)) 8-60 torr). Similar effects were observed in the presence of 24 mM bicarbonate and 5% CO(2). Indeed, the Kir4.1-Kir5.1 currents were enhanced with 3% CO(2) and suppressed with 8% CO(2) in voltage clamp, resulting in hyper- (-9 mV) and depolarization (16 mV) in current clamp, respectively. With physiological concentration of extracellular K(+), the Kir4.1-Kir5.1 channels conduct substantial outward currents that were similarly inhibited by CO(2) as their inward rectifying currents. These results therefore indicate that the heteromeric Kir4.1-Kir5.1 channels are modulated by a modest change in P(CO(2)) levels. Such a modulation alters cellular excitability, and enables the cell to detect hypercapnia and hypocapnia in the presence of bicarbonate.     

Leaf O(2) uptake in the dark is independent of coincident CO(2) partial pressure

Elevated CO(2), in the dark, is sometimes reported to inhibit leaf respiration, with respiration usually measured as CO(2) efflux. Oxygen uptake may be a better gauge of respiration because non-respiratory processes can affect dark CO(2) efflux in elevated CO(2). Two methods of quantifying O(2) uptake indicated that leaf respiration was unaffected by coincident CO(2) level in the dark.     

Chemoreflex control of breathing during wakefulness in healthy men and women.

This study used a modified CO(2) rebreathing procedure to examine the effect of gender on the chemoreflex control of breathing during wakefulness in healthy men (n = 14) and women (n = 14). Women were tested in the follicular phase of the menstrual cycle. During rebreathing trials, subjects hyperventilated to reduce the partial pressure of end-tidal CO(2) (Pet(CO(2))) below 25 Torr and were then switched to a rebreathing bag containing a normocapnic hypoxic or hyperoxic gas mixture. During the trial, Pet(CO(2)) increased, while O(2) was maintained at a constant level. The point at which ventilation began to rise as Pet(CO(2)) increased was identified as the ventilatory recruitment threshold (VRT). Ventilation below the VRT was measured, and the slope of the ventilatory response above the VRT was determined. Gender had no effect on the hyperoxic or hypoxic VRT for CO(2). Central chemoreflex sensitivity was significantly greater in men than women but not after correction for forced vital capacity. Measures of peripheral chemoreflex sensitivity were similar between genders. However, the slope of the tidal volume (Vt) response to hyperoxic and hypoxic CO(2) rebreathing (corrected and uncorrected) was greater in men than women, respectively. We conclude that central chemoreflex sensitivity is greater in men compared with women as reflected by differences in ventilatory (uncorrected) and Vt (corrected and uncorrected) responses to CO(2). However, gender has no significant effect on the central chemoreflex VRT for CO(2). The peripheral chemoreflex control of breathing during wakefulness is similar between men and women.     

Changes in respiratory mitochondrial machinery and cytochrome and alternative pathway activities in response to energy demand underlie the acclimation of respiration to elevated CO2 in the invasive Opuntia ficus-indica

Studies on long-term effects of plants grown at elevated CO(2) are scarce and mechanisms of such responses are largely unknown. To gain mechanistic understanding on respiratory acclimation to elevated CO(2), the Crassulacean acid metabolism Mediterranean invasive Opuntia ficus-indica Miller was grown at various CO(2) concentrations. Respiration rates, maximum activity of cytochrome c oxidase, and active mitochondrial number consistently decreased in plants grown at elevated CO(2) during the 9 months of the study when compared to ambient plants. Plant growth at elevated CO(2) also reduced cytochrome pathway activity, but increased the activity of the alternative pathway. Despite all these effects seen in plants grown at high CO(2), the specific oxygen uptake rate per unit of active mitochondria was the same for plants grown at ambient and elevated CO(2). Although decreases in photorespiration activity have been pointed out as a factor contributing to the long-term acclimation of plant respiration to growth at elevated CO(2), the homeostatic maintenance of specific respiratory rate per unit of mitochondria in response to high CO(2) suggests that photorespiratory activity may play a small role on the long-term acclimation of respiration to elevated CO(2). However, despite growth enhancement and as a result of the inhibition in cytochrome pathway activity by elevated CO(2), total mitochondrial ATP production was decreased by plant growth at elevated CO(2) when compared to ambient-grown plants. Because plant growth at elevated CO(2) increased biomass but reduced respiratory machinery, activity, and ATP yields while maintaining O(2) consumption rates per unit of mitochondria, we suggest that acclimation to elevated CO(2) results from physiological adjustment of respiration to tissue ATP demand, which may not be entirely driven by nitrogen metabolism as previously suggested.     

Determination of log P for pressurized carbon dioxide and its characterization as a medium for enzyme reaction

The log P value of pressurized CO(2) at 50 degrees C was determined from the solubility of 1-octanol in CO(2) and compared with other solvent parameters such as permittivity, epsilon, and polarity parameter, E(T)(30). The log P indicated that pressurized CO(2) is rather hydrophilic although it seems hydrophobic being judged from epsilon(r) and E(T)(30). With a change in pressure from 3 to 11.8 MPa, the log P changed from 0.9 to 2.0 while epsilon(r) and E(T)(30) changed only slightly. The log P was linearly correlated to the logarithm of the solubility of water among organic solvents. Pressurized CO(2) was located close to the linear correlation line among the solvents at high pressure (>11 MPa) but its location deviated to the hydrophilic side with a decrease in pressure. Lipase-catalyzed esterification of stearic acid with ethanol and hydrolysis of ethyl stearate were carried out in pressurized CO(2), benzene (log P = 2.0), and n-hexane (log P = 3.5). In spite of the lowest log P value for CO(2), the reaction rate in CO(2) was the highest among solvents tested in pressure range over 10 MPa. The reaction rate was strongly dependent on pressure of CO(2).