Glutathione peroxidase activity and release of glutathione from oxygen-deficient perfused rat heart.

The effect of cellular hypoxia on glutathione levels in rat hearts was determined. Hearts perfused with 95% N₂–5% CO₂ demonstrated a significant decrease in tissue reduced glutathione content when compared to control hearts perfused with 95% O₂–5% CO₂. The hypoxic perfusate contained reduced glutathione and its release was time dependent over a period of 60 minutes. The cellular depletion of oxidized glutathione and its release into coronary effluent were less evident with respect to reduced glutathione. Moreover during hypoxic perfusion we have observed a decrease of cytosol glutathione peroxidase activity. These results suggest that severe oxygen-deprivation causes in myocardial cells a significant perturbation of glutathione metabolism.     

Prostacyclin (PGI2) mediates hypoxic relaxation of bovine coronary arterial strips

Bovine coronary arterial strips (BCA) exhibiting spontaneous tone, relax in response to a decrease in the PO₂ of the batching medium. Experiments were performed to determine if prostaglandins (PGs) mediate the oxygen-induced changes in tension. BCA were equilibrated in Krebs-bicarbonate solution at 37 °C gassed with 95% O₂, 5% CO₂ and tension was measured isometrically. When the PO₂ of the bathing medium was decreased, BCA exhibited reversible reductions in tension. Switching from 95% O₂, 5% CO₂ to 95% N₂, 5% CO₂ (anoxia) elicited an initial relaxation followed by a contraction. In contrast, a change to 5% O₂, 5% CO₂, 90% N₂ (hypoxia) was followed by a sustained relaxation. Re-introduction of O₂ to anoxic strips produced a biphasic response: relaxation followed by contraction. Indomethacin or eicosatetraynoic acid (EYA) increased tone and inhibited the relaxation produced by anoxia or hypoxia. Indomethacin or EYA did not inhibit the relaxation of anoxic strips during re-introduction of O₂, but did inhibit the contraction partially. Relaxation of arterial strips to arachidonic acid (AA) was similar to relaxation to prostacyclin (PGI₂). Anoxia limited the relaxation to AA but not to PGI₂. We conclude that PG synthesis contributes to the basal tone and the hypoxia-induced relaxation of CBA. In addition, hypoxia, unless severe, does not prevent the conversion of AA to PGI₁.     

Ventilatory response of the diamondback water snake,Natrix rhombifera to hypoxia, hypercapnia and increased oxygen demand

Summary Simultaneous measurements of ventilatory frequency, tidal volume, O₂ uptake, CO₂ output and cardiac frequency were made in the diamondback water snake,Natrix rhombifera while breathing hypoxic (15% to 5% O₂ in N₂) or hypercarbic (2% to 10% CO₂ and 21% O₂ in N₂) gases. The snakes responded to hypoxia by increasing tidal volume and decreasing ventilatory frequency resulting in little change in ventilation (50% increase at 5% inspired O₂), or O₂ uptake and only a light increase in CO₂ output. Hypercarbia to 4.2% inspired CO₂ resulted in a slight hyperventilation but ventilation was depressed at 6.3% inspired CO₂ and became erratic at higher concentrations. The resting rate of O₂ uptake was maintained throughout hypercapnia. Heart rate increased during hypoxia and decreased during hypercapnia. Cutaneous O₂ uptake increased during extreme hypoxia (5% inspired O₂) and cutaneous CO₂ output increased during hypercapnia, probably due to changes in the body-to-ambient gas gradients (Crawford and Schultetus, 1970). Both pulmonary oxygen uptake and ventilation were dramatically increased immediately following 10–15 min experimental dives. The increased ventilation was achieved primarily through an increased tidal volume.     

Effects of hypoxia on lipolysis in isolated rat myocardial cells

Summary The effect of hypoxia on myocardial lipolysis (glycerol release) was investigated in freshly isolated, calcium-tolerant rat ventricular myocytes. Hypoxia was produced by gassing the incubation medium (Joklik-minimum essential medium, supplemented with 1.2 mM MgSO₄, 1 mM DL-carnitine, 1.5 mM CaCl₂ and 0.6 mM palmitate bound to 0.15 mM fatty acid free bovine serum albumin) with 95% N₂–5% CO,. Control (normoxic) incubations were carried out under air-5% CO₂ atmosphere. Basal glycerol release increased from 46.6 ± 3.0 nmol/106 cells · 30 min in normoxia to 64.5 ± 4.3 nmol/10⁶ cells · 30 min in hypoxia (p < 0.05). Addition of isoprenaline (10 M) resulted in a significant (p < 0.05) stimulation of the glycerol release both in normoxia and in hypoxia, but the enhancement above basal rates was apparently lower in hypoxia (8.7 ± 2.5 nmol/10⁶ cells · 30 min) than in normoxia (12.2 ± 2.7 nmol/106 cells · 30 min). Furthermore, whereas the isoprenaline-induced rise in lipolysis both in normoxia and hypoxia was prevented by inclusion of propranolol (10 M), propranolol did not affect the hypoxia-induced increase in lipolysis. Thus, the above findings suggest that myocardial lipolysis may be stimulated by local non-adrenergic mechanisms during hypoxia.     

Acute hypoxia alters eicosanoid production of perfused pulmonary artery endothelial cells in culture

Hypoxia alters vascular tone which regulates regional blood flow in the pulmonary circulation. Endothelial derived eicosanoids alter vascular tone and blood flow and have been implicated as modulators of hypoxic pulmonary vasoconstriction. Eicosanoid production was measured in cultured bovine pulmonary endothelial cells during constant flow and pressure perfusion at two oxygen tensions (hypoxia: 4% O₂, 5% CO₂, 91% N₂; normoxia: 21% O₂, 5% CO₂, 74% N₂). Endothelial cells were grown to confluence on microcarrier beads. Cell cartridges (N=8) containing 2 ml of microcarrier beads ( 5 × 10⁶ cells) were constantly perfused (3 ml/min) with Krebs' solutions (pH 7.4, T 37°C) equilibrated with each gas mixture. After a ten minute equilibration period, lipids were extracted (C₁₈ Sep Pak®) from twenty minute aliquots of perfusate over three hours (nine aliquots per cartridge). Eicosanoids (6-keto PGF_1α; TXB₂; and total leukotriene [LT - LTC₄, LTD₄, LTE₄, LTF₄]) were assayed by radioimmunoassay. Eicosanoid production did not vary over time. 6-keto PGF_1α production was increased during hypoxia (normoxia 291 ± 27 vs hypoxia 395 ± 35 ng/min/gm protein; p < 0.01). Thromboxane production (normoxia 19 ± 2 vs hypoxia 20 ± 2 ng/min/gm protein) and total leukotriene production (normoxia 363 ± 35 vs hypoxia 329 ± 29 ng/min/gm protein) did not change with hypoxia. These data demonstrated that oxygen increased endothelial prostacyclin production but did not effect thromboxane or leukotriene production.     

Influence of the estrous cycle on hypoxic failure in the female rat heart

Background: Clinical studies have shown that fluctuation in the plasma concentrations of estrogen during the menstrual cycle has an effect on myocardial health in premenopausal women. When estrogen levels are low, the number of ischemic events experienced is increased.Objective: To determine whether the increased ischemic events reported with low plasma estrogen concentrations in women could be reproduced in an animal model, cardiac function was measured during hypoxia in the female rat at different time points of the estrous cycle.Methods: Hearts from female Sprague-Dawley rats were perfused in the working mode at the diestrous (low estrogen; n = 7) and proestrous (high estrogen; n = 6) phases of the estrous cycle, confirmed by plasma estradiol concentrations. Hearts were perfused under aerobic conditions with 5.5 mM glucose, 100 μU/mL insulin, and 1.2 mM palmitate, followed by a 30-minute period of hypoxia with 95% N₂-5% CO₂ gassing.Results: There were no significant differences in heart function between diestrous and proestrous groups prior to hypoxia. However, hypoxia induced perturbations in function that were dependent on the estrous cycle. Reductions in left ventricular systolic and diastolic pressure occurred with hypoxia, but no significant differences in these pressures were observed between groups. Left ventricular pulse pressure and coronary flow also decreased significantly during hypoxia (both, P < 0.05), but hearts from the proestrous group maintained a significantly higher pulse pressure (P < 0.05). Hearts from the proestrous group also maintained significantly higher rates of coronary flow during hypoxia (P < 0.05), compared with hearts from the diestrous group. However, despite the effect of proestrus, correlation coefficients between plasma estradiol concentrations and indices of cardiac function were not significant.Conclusions: Our findings indicate that the estrous cycle of the female rat affects cardiac function during hypoxia. This model may be useful to study the impact of the estrous cycle on metabolic and cardiovascular function.     

Inhibition of hypoxic coronary vasoconstriction by pinacidil

Acute hypoxia causes constriction of isolated coronary arteries from several species. The present study was designed to test whether pinacidil, a potassium channel opener, inhibits hypoxiainduced contraction of porcine isolated coronary arteries. Coronary arterial rings were suspended in organ baths for isometric tension recording. Hypoxic contractions were evoked by rapidly changing the gas mixture from 95% O₂/5% CO₂ to 95% N₂/5% CO₂ in preparations partially contracted with KC1. Pretreatment with pinacidil (10⁻⁶ to 10⁻⁴ M) caused concentration-dependent inhibition of the contractile response to hypoxia. The inhibitory effect of pinacidil was attenuated by the k_atp channel blocker, glibenclamide (10⁻⁶ M). In rings contracted with acetylcholine, glibenclamide caused a rightward shift in the concentration-response curve to pinacidil while having no effect on the vasorelaxant responses to sodium nitroprusside and diltiazem, thus confirming the specificity of glibenclamide for potassium channel opener-mediated responses. Taken together, the data indicate that pinacidil prevents hypoxia-induced contraction of porcine coronary arteries, and that the effect of pinacidil may be mediated by the opening of glibenclamide-sensitive potassium channels.     

Modification of alveolar hyperoxia induced pulmonary vasodilatation by indomethacin

Decrease in pulmonary vascular resistance was observed in neonatal minature pigs breathing 100% O₂ or 95% O₂:5% CO₂. The pulmonary vasodilator response to hyperoxia ventilation was reduced by indomethacin in the intact animal and in the isolated perfused lung preparation. In the isolated perfused lung preparation, it was also shown that lung alveolar pO₂ rather than pulmonary arterial pO₂ was responsible for the pulmonary vasodilation. The study suggests that alveolar hyperoxia induced decrease in pulmonary vascular resistance may be mediated in part by release of prostaglandins. The relevance of this study with oxygen therapy in newborn infants is also discussed.     

Effect of hypoxia and reoxygenation on the formation and release of reactive oxygen species by porcine pulmonary artery endothelial cells

Endothelial cells are critical targets in both hypoxia-and reoxygenation-mediated lung injury. Reactive O₂ species (ROS) have been implicated in the pathogenesis of hypoxic and reoxygenation lung injury, and xanthine dehydrogenase/oxidase (XDH/XO) is a major generator of the ROS. Porcine pulmonary artery endothelial cells (PAEC) have no detectable XDH/XO. This study was undertaken to examine (1) ROS production by hypoxic porcine PAEC and their mitochondria and (2) ROS production and injury in reoxygenated PAEC lacking XDH/XO activity. Intracellular H₂O₂ generation and extracellular H₂O₂ and O/₂ release were measured after exposure to normoxia (room air-5% CO₂), hypoxia (0% O₂ -95% N-5% CO₂), or hypoxia followed by normoxia or hyperoxia (95% O₂-5% CO₂). Exposure to hypoxia results in significant reductions in intracellular H₂ O₂ formation and extracellular release of H₂ O₂ and O₂ by PAEC and mitochondria. The reductions occur with as little as a 2 h exposure and progress with continued exposure. During reoxygenation, cytotoxicity was not observed, and the production of ROS by PAEC and their mitochondria never exceeded levels observed in normoxic cells. The absence of XDH/XO may prevent porcine PAEC from developing injury and increased ROS production during reoxygenation. © 1995 Wiley-Liss, Inc.     

Phosphatidylserine synthesis in rat cerebral cortex: effects of hypoxia,hypocapnia and development

Phosphatidylserine, which is necessary for protein kinase C activity, is synthesized in mammalian tissues by the Ca²⁺-dependent base exchange enzyme. The synthesis of phosphatidylserine is greater in slices or homogenates of rat cerebral cortex subjected to hypoxia by N₂ treatment when compared with O₂ plus 5% CO₂. An intermediate effect was observed when the treatment was done with N₂ plus 5% CO₂. Incorporation rates were dependent on Ca²⁺ in Krebs-Henseleit Ringer bicarbonate medium, being greater with 2 mM Ca²⁺ than with the same medium prepared without Ca²⁺. The increase of phosphatidylserine synthesis, due to hypoxia, was, on the contrary, more evident in the medium lacking added Ca²⁺. Similar results were obtained with the homogenates. This suggests that elevation of intracellular Ca²⁺, caused by hypocapnia and hypoxia, may be responsible for the greater incorporation of serine into phosphatidylserine. In both cerebrocortical slices and homogenate, [¹⁴C]serine incorporation decreased with development both in O₂ plus 5% CO₂ and N₂-treated preparations. However, in younger rats (14–18 days) hypoxia induced a lesser increase of phosphatidylserine than in 40 day old animals. We suggest that a regulatory mechanisms for phosphatidylserine synthesis is established during development and that N₂-treatment can increase phosphatidylserine synthesis by interfering with this regulatory mechanism.Abbreviations KRB Krebs-Henseleit Ringer bicarbonate - KRP Krebs Ringer phosphate - PS serine glycerophospholipids     

Plant Life History and Residue Chemistry Influences Emissions of CO2 and N2O From Soil – Perspectives for Genetically Modified Cell Wall Mutants

Vascular plants have lignified tissues that transport water, minerals, and photosynthetic products throughout the plant. They are the dominant primary producers in terrestrial ecosystems and capture significant quantities of atmospheric carbon dioxide (CO₂) through photosynthesis. Some of the fixed CO₂ is respired by the plant directly, with additional CO₂ lost from rhizodeposits metabolized by root-associated soil microorganisms. Microbially-mediated mineralization of organic nitrogen (N) from plant byproducts (rhizodeposits, dead plant residues) followed by nitrification generates another greenhouse gas, nitrous oxide (N₂O). In anaerobic soils, reduction of nitrate by microbial denitrifiers also produces N₂O. The plant-microbial interactions that result in CO₂ and N₂O emissions from soil could be affected by genetic modification. Down-regulation of genes controlling lignin biosynthesis to achieve lower lignin concentration or a lower guaiacyl:syringyl (G:S) ratio in above-ground biomass is anticipated to produce forage crops with greater digestibility, improve short rotation woody crops for the wood-pulping industry and create second generation biofuel crops with low ligno-cellulosic content, but unharvested residues from such crops are expected to decompose quickly, potentially increasing CO₂ and N₂O emissions from soil. The objective of this review are the following: 1) to describe how plants influence CO₂ and N₂O emissions from soil during their life cycle; 2) to explain how plant residue chemistry affects its mineralization, contributing to CO₂ and N₂O emissions from soil; and 3) to show how modification of plant lignin biosynthesis could influence CO₂ and N₂O emissions from soil, based on experimental data from genetically modified cell wall mutants of Arabidopsis thaliana. Conceptual models of plants with modified lignin biosynthesis show how changes in phenology, morphology and biomass production alter the allocation of photosynthetic products and carbon (C) losses through rhizodeposition and respiration during their life cycle, and the chemical composition of plant residues. Feedbacks on the soil environment (mineral N concentration, soil moisture, microbial communities, aggregation) affecting CO₂ and N₂O emissions are described. Down-regulation of the Cinnamoyl CoA Reductase 1 (CCR1) gene is an excellent target for highly digestable forages and biofuel crops, but A. thaliana with this mutation has lower plant biomass and fertility, prolonged vegetative growth and plant residues that are more susceptible to biodegradation, leading to greater CO₂ and N₂O emissions from soil in the short term. The challenge in future crop breeding efforts will be to select tissue-specific genes for lignin biosynthesis that meet commercial demands without compromising soil CO₂ and N₂O emission goals.     

Quantitative analysis of feedforward sympathetic coronary vasodilation in exercising dogs.

Recent experiments demonstrate that feedforward sympathetic beta-adrenoceptor coronary vasodilation occurs during exercise. The present study quantitatively examined the contributions of epinephrine and norepinephrine to exercise coronary hyperemia and tested the hypothesis that circulating epinephrine causes feedforward beta-receptor-mediated coronary dilation. Dogs (n = 10) were chronically instrumented with a circumflex coronary artery flow transducer and catheters in the aorta and coronary sinus. During strenuous treadmill exercise, myocardial oxygen consumption increased by approximately 3.9-fold, coronary blood flow increased by approximately 3.6-fold, and arterial plasma epinephrine concentration increased by approximately 2.4-fold over resting levels. At arterial concentrations matching those during strenuous exercise, epinephrine infused at rest (n = 6) produced modest increases (18%) in flow and myocardial oxygen consumption but no evidence of direct beta-adrenoceptor-mediated coronary vasodilation. Arterial norepinephrine concentration increased by approximately 5. 4-fold during exercise, and coronary venous norepinephrine was always higher than arterial, indicating norepinephrine release from cardiac sympathetic nerves. With the use of a mathematical model of cardiac capillary norepinephrine transport, these norepinephrine concentrations predict an average interstitial norepinephrine concentration of approximately 12 nM during strenuous exercise. Published dose-response data indicate that this norepinephrine concentration increases isolated coronary arteriolar conductance by approximately 67%, which can account for approximately 25% of the increase in flow observed during exercise. It is concluded that a significant portion of coronary exercise hyperemia ( approximately 25%) can be accounted for by direct feedforward beta-adrenoceptor coronary vascular effects of norepinephrine, with little effect from circulating epinephrine.     

孤儿核受体Nur77对缺/复氧损伤中心肌细胞自噬的调节

目的:研究孤儿核受体Nur77对缺/复氧损伤中心肌细胞自噬的调节作用。方法:差速贴壁法分离乳鼠心肌细胞,经免疫荧光染色鉴定纯度。缺氧(1%O_2、5%CO_2和94%N_2)培养12 h后,常氧培养2 h构建心肌细胞缺/复氧损伤。实时定量PCR和western blot的方法检测Nur77的表达变化。通过siRNA转染抑制心肌细胞nur77表达,通过自噬标志蛋白表达改变作为细胞自噬水平的变化。结果:原代分离的心肌细胞纯度95%以上。缺氧12 h和缺/复氧(12 h/2 h)刺激后,心肌细胞中Nur77表达都明显升高(P0.01)。与缺氧组相比,缺/复氧组细胞质中的水平明显增加(P0.01),细胞核中Nur77水平无明显变化。抑制Nur77后,缺/复氧组自噬水平明显降低,缺氧组心肌细胞自噬水平无明显变化。结论:Nur77参与缺/复氧损伤中心肌细胞自噬水平的调节。     

Proliferative and secretory activity of human umbilical endothelial cells cultivated under various hypoxia conditions

In this study, we examined the impact of 3-day hypoxia of different degrees on the viability, proliferation, and secretory activity of endothelial cells from human umbilical vein (HUVEC). A gas mixture of three components was used (%): 1) 10 O₂, 5 CO₂, and 85 Ar; 2) 5 O₂, 5 CO₂, and 80 Ar; and 3) 1 O₂, 5 CO₂, and 94 Ar. Cells cultivated in a CO₂ incubator in atmospheric oxygen (21% O₂) served as control. It was found that 3-day HUVEC cultivation at 1% O₂ increased NO synthesis; enhanced secretion of endothelin-1, IL-6, IL-8, TNF-alpha, sVCAM-1, sE-cadherin, sE-selectin, VEGF-A, and bFGF; and inhibited proliferation. HUVEC cultivated under 10% O₂ and 5% O₂ exhibited the lowest level of basal secretion of these substances and increased proliferative activity. These cells cultivated under conditions of atmospheric oxygen for 3 days displayed activated secretion of NO, IL-6, IL-8, and von Willebrand factor; the activation was higher than at 10% O₂ and 5% CO₂. Thus, the gaseous medium with reduced oxygen content (5%) is a more physiological condition for HUVEC cultivation. An increase in the amount of oxygen up to the atmospheric level causes endotheliocyte activation; the cells exhibit the features of endothelial dysfunction. Oxygen content reduced to 1% induces endothelial dysfunction and reduced proliferative potential.     

Relationships between cardiac hyperactivity, oxygen tension, and release of vasodilator material in coronary autoregulation of guinea-pig hearts

Increases in cardiac activity induce autoregulatory coronary vasodilation. The intermediate steps which trigger this process are thought to be myocardial hypoxia which induces the release of vasodilator mediator(s). The present study examines the relationships between mechanical activity, oxygen tension, and release of vasodilator material in isolated perfused hearts. Guinea-pig isolated hearts were perfused in series, the effluent from donor hearts being regassed prior to entry to recipient hearts. Histamine (1 microgram) and isoproterenol (10 ng) increased the rate and tension of donor hearts and produced predominant coronary vasodilator responses which were followed by the appearance of vasodilator material in the recipient (falls in perfusion pressure, 9.8 +/- 1.1 and 9.1 +/- 2.5 mmHg) (1 mmHg = 133.322 Pa). Exposure of donor hearts to hypoxia also caused vasodilatation and release of vasodilator material (fall in pressure, 11.4 +/- 1.6 mmHg). Pacing-induced tachycardia (6 Hz) of donor hearts promoted the release of vasodilator material, the fall in recipient heart pressure being 11.5 +/- 1.8 mmHg. This was abolished by beta-adrenoceptor blockade and when donor hearts were from reserpine-pretreated guinea pigs. In was concluded that pacing released endogenous catecholamines which in turn released the vasodilator material. Pacing per se did not cause vasodilatation or release of the vasodilator. The Po2 of perfusates from donor hearts was reduced by pacing at 5 Hz (25.7 +/- 5.2 mmHg) and by isoproterenol (10 ng, 32.0 +/- 3.7 mmHg), indicative of an elevated oxygen extraction. The isoproterenol-induced falls in Po2 were abolished by beta-adrenoceptor blockade. However, the pacing-induced falls in Po2 persisted, the values occurring before (25.7 +/- 5.2 mmHg) and after propranolol (45.7 +/- 4.5 mmHg) and before (32.1 +/- 1.1 mmHg) and after practolol (27.3 +/- 4.1 mmHg) not differing significantly (p greater than 0.05). These falls in perfusate Po2 were not accompanied by coronary vasodilatation or release of vasoactive material. Perfusate Po2 changes could therefore be dissociated from the coronary vasodilatation and vasoactive material release, suggesting that hypoxia may not be a prerequisite for the metabolic autoregulatory vasodilatation in response to myocardial hyperactivity induced by cardiac stimulants.     

Decreases in Amino Acid and Acetylcholine Metabolism During Hypoxia

Abstract: Hypoxia impairs brain function by incompletely defined mechanisms. Mild hypoxia, which impairs memory and judgment, decreases acetylcholine (ACh) synthesis, but not the levels of ATP or the adenylate energy charge. However, the effects of mild hypoxia on the synthesis of the glucosederived amino acids [alanine, aspartate, γ-amino butyric acid (GABA), glutamate, glutamine, and serine] have not been characterized. Thus, we examined the incorporation of [U-¹⁴C]glucose into these amino acids and ACh during anemic hypoxia (injection of NaNO₂), hypoxic hypoxia (15 or 10% O₂), and hypoxic hypoxia plus hypercarbia (15 or 10% O₂ with 5% CO₂). In general, the synthesis of the amino acids and of ACh declined in parallel with each type of hypoxia we studied. For example, anemic hypoxia (75 mg/kg of NaNO₂) decreased the incorporation of [U-¹⁴C]glucose into the amino acids and into ACh similarly. [Percent inhibition: ACh (57.4), alanine (34.4), aspartate (49.2), GABA (61.9). glutamine (59.2), glutamate (51.0), and serine (36.7)]. A comparison of several levels (37.5, 75, 150, 225 mg/kg of NaNO₂) of anemic hypoxia showed a parallel decrease in the flux of glucose into ACh and into the amino acids whose synthesis depends on mitochondrial oxidation: GABA (r= 0.98), glutamate (r= 0.99), aspartate (r= 0.96), and glutamine (r= 0.97). The synthesis of the amino acids not dependent on mitochondrial oxidation did not correlate as well with changes in ACh metabolism: serine (r= 0.68) and alanine (r= 0.76). The decreases in glucose incorporation into ACh and into the amino acids with hypoxic hypoxia (15% or 10% O₂) or hypoxic hypoxia with 5% CO₂ were very similar to those with the two lowest levels of anemic hypoxia. Thus, any explanation of the brain's sensitivity to a decrease in oxygen availability must include the alterations in the metabolism of the amino acid neurotransmitters as well as ACh.     

Growth of Pseudomonas fluorescens in modified atmosphere packaged tofu

Aims: The objective was to study the growth of Pseudomonas in a food product (tofu) where it typically occurs as a spoilage organism, and when this product is stored under modified atmosphere. Methods and Results: A Pseudomonas strain was isolated from the endogenous microflora of tofu. Tofu was inoculated with the strain, packaged in different gas conditions (air, 100% N₂, 30% CO₂/70% N₂ or 100% CO₂) and stored under refrigerated conditions. Microbial loads and the headspace gas composition were monitored during storage. Conclusions: The strain was capable of growing in atmospheres containing no or limited amounts of oxygen and increased amounts of carbon dioxide. Even when 100% CO₂ was used, growth could not be inhibited completely. Significance and Impact of Study: In contrast to the general characteristics of the genus Pseudomonas (strictly aerobic, highly sensitive to CO₂), it should not be expected in the food industry that removing oxygen from the food package and increasing the carbon dioxide content, combined with cold storage, will easily avoid spoilage by Pseudomonas species. Guarantee of hygienic standards and combination of strategies with other microbial growth inhibiting measures should be implemented.     

Plasma ATP during exercise: possible role in regulation of coronary blood flow

It was previously shown that red blood cells release ATP when blood oxygen tension decreases. ATP acts on microvascular endothelial cells to produce a retrograde conducted vasodilation (presumably via gap junctions) to the upstream arteriole. These observations form the basis for an ATP hypothesis of local metabolic control of coronary blood flow due to vasodilation in microvascular units where myocardial oxygen extraction is high. Dogs (n = 10) were instrumented with catheters in the aorta and coronary sinus, and a flow transducer was placed around the circumflex coronary artery. Arterial and coronary venous plasma ATP concentrations were measured at rest and during three levels of treadmill exercise by using a luciferin-luciferase assay. During exercise, myocardial oxygen consumption increased approximately 3.2-fold, coronary blood flow increased approximately 2.7-fold, and coronary venous oxygen tension decreased from 19 to 12.9 mmHg. Coronary venous plasma ATP concentration increased significantly from 31.1 to 51.2 nM (P < 0.01) during exercise. Coronary blood flow increased linearly with coronary venous ATP concentration (P < 0.01). Coronary venous-arterial plasma ATP concentration difference increased significantly during exercise (P < 0.05). The data support the hypothesis that ATP is one of the factors controlling coronary blood flow during exercise.     

Impact of modified atmospheres on respiration of last instar larvae of the rice moth,Corcyra cephalonica (Lepidoptera: Pyralidae)

Abstract

Effect of modified atmospheres (MAs) containing CO₂ at 20, 40, 60 and 80% or containing N₂ at 97 and 98% on the mortality of Corcyra cephalonica Stainton (Lepidoptera: Pyralidae) sixth instar larvae was studied to determine the LT values at 30?°C. The respiration rates of untreated and treated larvae with 60% CO₂ and/or 98% N₂ at LT₅₀ were measured using Q-Box RP1LP low range respirometry package. Total protein and triglycerides of treated and untreated larvae were assayed. Complete larval mortality was recorded after 72 and 144?h of treatment with 60% CO₂ and 98% N₂, respectively. Calculated LT₅₀ values were 39.3 at 60% CO₂ and 87.5?h at 98% N₂ MAs. Respiration quotient (RQ) in the light of consumed O₂ and produced CO₂ of untreated larvae was 1.0 while it was 0.85 at 60% CO₂ and 0.72 at 98% N₂. Duration time necessary for produced CO₂ curve to reach the maximum point (2000?ppm) was significantly shorter at untreated larvae (27.64?min) in comparison with that recorded at CO₂ (35.48?min) which also significantly less than that obtained at N₂ (98.54?min). At all treatments, total protein was decreased while triglycerides were increased in comparison with control.     

Increased shelf life of a bioherbicide through combining modified atmosphere packaging and low temperatures

The effects of air temperatures (4, 14 and 24°C) and modified atmosphere packaging (MAP) (0% CO₂/100% N₂; 20% CO₂/80% N₂ or 40% CO₂/60% N₂) on vigour of a Sclerotinia minor barley formulation during 6 months storage were evaluated. The study was performed using a multilevel factorial experimental design and response surface methodology (RSM) and aimed to determine the optimum combination of the above factors that resulted in retention of S. minor vigour during storage. Temperature and storage duration are the main factors that affect S. minor vigour. CO₂ concentration had no effect on S. minor vigour during storage. However, oxygen displacement from storage containers by CO₂ and N₂ resulted in significant decrease of vigour reduction of S. minor as compared to ambient air control. An acceptable level of S. minor vigour reduction (ALVR) during storage was developed and determined to be ALVR=31.7±14.8% (mean±95% CI). Contour plot analysis indicated that the S. minor barley formulation at 0.4 water activity could be stored for 6, 12 or 26 weeks without exceeding the upper ALVR threshold (ca. 46%) at air temperatures not higher than 20, 17 or 11°C, respectively.