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At least 19 recordsLinked to original sources
PubMed2026

Effects of acute hypoxia followed by reoxygenation on intestinal histomorphology, oxidative stress and hypoxia signaling biomarkers, and microbiota in pikeperch (Sander lucioperca).

In aquatic environments, natural and anthropogenic factors commonly reduce dissolved oxygen (DO) and trigger hypoxia, which threatens the health and survival of aquatic organisms. As an important economic fish species in China, pikeperch (Sander lucioperca) is extremely sensitive to hypoxia. However, there are relatively few reports on how hypoxia and reoxygenation affect its intestinal physiology and microbial community. Three treatment groups were set for pikeperch: normoxia (DO = 8.5 ± 0.5 mg/L), 48 h hypoxia (DO = 2.5 ± 0.1 mg/L), and reoxygenation (48 h hypoxia followed by 6 h reoxygenation at normal DO), to evaluate alterations in intestinal histopathology, tight junction gene expression, oxidative stress, hypoxia signaling molecules and intestinal microbiota composition. The results showed that hypoxia significantly decreased muscularis thickness by approximately 32.5% and reduced the expression of tight junction genes (Occludin, Claudin2, and ZO-2). Moreover, hypoxia significantly increased oxidative stress index levels (GSH-Px, CAT, and MDA), markedly upregulated the expression of Bax, Caspase3, and HIF-1α, while significantly downregulating the expression of Bcl-2, Egln1, and Egln2. Notably, reoxygenation elicited partial compensatory effects against these hypoxia-induced changes. 16S rRNA sequencing analysis revealed that hypoxic stress altered the intestinal microbial community composition of pikeperch and increased its diversity. In the hypoxia group, the abundance of the phylum Bacillota, along with the genera Halomonas and Acinetobacter, was significantly elevated, whereas in the reoxygenation group, the genus Lactobacillus increased approximately 180-fold. The results indicated that hypoxia caused intestinal oxidative damage, cell apoptosis, and intestinal microbiota dysbiosis in pikeperch, while short-term reoxygenation achieved partial recovery from these hypoxia-triggered intestinal injuries. The present research provides valuable references for in-depth exploration of the molecular mechanisms behind the response of pikeperch to acute hypoxia and reoxygenation stress, while also offering a novel perspective to understand the mechanism by which hypoxia impacts intestinal health in fish.

Animals↗
PubMed1992

Prolonged lobar hypoxia in vivo enhances the responsivity of isolated pulmonary veins to hypoxia.

The hypoxic response of pulmonary vessels isolated from eight sheep whose right apical lobes (RAL) had inspired 100% N2 for 20 h was studied. The RAL of these conscious sheep inspired hypoxic gas and the remainder of the lung inspired air. During hypoxia, RAL perfusion was 33 +/- 3% of its air value, carotid arterial PO2 averaged 86 +/- 3 mm Hg and pulmonary perfusion pressure was not significantly different from the initial control period when the RAL inspired air. At the end of the hypoxic exposure, the sheep were killed, and pulmonary artery and vein rings (0.5 to 2 mm inner diameter) were isolated from both the RAL and the right cardiac lobe, which served as the control lobe (CL). Arteries from the RAL and CL did not contract in response to 6% O2/6% CO2/88% N2 (hypoxia). In contrast, RAL veins did contract vigorously in response to hypoxia, whereas CL veins did not contract or contracted only minimally. Rubbing of the endothelium or prior incubation of RAL veins with catalase (1,200 units/ml), indomethacin (10(-5) M), or the thromboxane A2/prostaglandin H2 (TxA2/PGH2) receptor antagonist, SQ 29,548 (3 X 10(-6) M) each significantly reduced the response to hypoxia. RAL veins were also found to be more reactive than CL veins to the prostaglandin endoperoxide analogue U46619. We conclude that prolonged lobar hypoxia in vivo increases the responsivity of isolated pulmonary veins to hypoxia. These contractions may result from an increase in reactive O2 species, which in turn modify production of, metabolism of, and/or tissue responsivity to TxA2/PGH2.

Animals↗
PubMed1979

[Hypoxia and internal intensive medicine. I. Clinical aspects of acute hypoxia].

The treatment of the topic acute hypoxia and internal intensive medicine with description of the fundaments--classification and definition of hypoxia and its forms, clinic, therapeutic possibilities and oxygen therapy--becomes necessary in order to get in the entity of hypoxia and to find a common language among specialists for intensive medicine. The knowledge of a differentiated treatment of different forms of hypoxia and thus also of clinical pictures seems to be necessary under the aspect of a highly developed respirator technique and the knowledge of anaesthesiology in this field. Application of the first report is the description of the factors of the oxygen transport. Respiratory, stagnation, anaemic and histotoxic hypoxia are defined and possible causes mentioned. The clinically relevant hypoxia will mostly be a mixed form, among which the respiratory insufficiency in shock lung plays an important role in intensive medicine.

Critical Care↗
PubMed1992

Enhancement of hypoxia radioprotection and decrease of hypoxia toxicity caused by adenosine monophosphate.

It was shown in experiments on mice that the radioprotective effects of adenosine monophosphate (AMP) or of a combination of Mg aspartate and AMP join with those induced by hypobaric hypoxia. The hypotensive effects of these drugs lead probably to hypoxia in radiosensitive tissues which acts additively with hypoxia elicited by way of respiration. Furthermore, Mg aspartate and AMP decrease the toxicity of high degrees of hypobaric hypoxia. These effects can be explained by the ability of adenosine liberated from AMP and of magnesium to increase brain and heart blood perfusion and/or to mitigate excessive sympathetic activity. The pharmacological effects of AMP and Mg aspartate are thus not only radioprotective but also energy preserving and protecting vitally important organs against hypoxia toxicity. These effects may be of favourable importance in hypoxic radiotherapy.

Adenosine Monophosphate↗
PubMed1978

Profound hypoxia in Papio anubis and Macaca mulatta--physiological and neuropathological effects. I. Abrupt exposure following normoxia. II. Abrupt exposure following moderate hypoxia.

Lightly anaesthetized and spontaneously breathing P. anubis (PA) and M. mulatta (MM) inhaled at ambient pressure 3.2% oxygen (identical to 37,500 ft or 11,430 m) from air and also after pre-exposure to 14% oxygen (identical to 10,000 ft or 3,048 m). The EEG, ECG, respiratory rate, arterial and cerebral venous sinus pressures, end-tidal pO2 and pCO2 and body temperature were recorded. Arterial and cerebral venous sinus blood gases, pH and pyruvate and lactate contents were estimated. Before hypoxia, MM showed a relative hyperventilation. Profound hypoxia, from air, ended with the "last breath" at 89--205 sec in PA and at 93--570 sec in MM. Brain damage was restricted to one MM (4 exposures). Profound hypoxia after exposure to 14% oxygen ended with the "last breath" at 87--210 sec in PA and at 120 sec--94 min (including 9 exposures over 5 min) in MM. Brain damage was restricted to one MM ("last breath" at 94 min). In the two MM with brain damage there was evidence of reduction in cerebral perfusion near the end of profound hypoxia. Brain damage in one animal contrasts with the frequent and often severe brain damage in MM after equivalent sub-atmospheric decompressions preceded by exposure to moderate altitude (10,000 ft).

Animals↗
PubMed1992

Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis.

Inefficient vascular supply and the resultant reduction in tissue oxygen tension often lead to neovascularization in order to satisfy the needs of the tissue. Examples include the compensatory development of collateral blood vessels in ischaemic tissues that are otherwise quiescent for angiogenesis and angiogenesis associated with the healing of hypoxic wounds. But the presumptive hypoxia-induced angiogenic factors that mediate this feedback response have not been identified. Here we show that vascular endothelial growth factor (VEGF; also known as vascular permeability factor) probably functions as a hypoxia-inducible angiogenic factor. VEGF messenger RNA levels are dramatically increased within a few hours of exposing different cell cultures to hypoxia and return to background when normal oxygen supply is resumed. In situ analysis of tumour specimens undergoing neovascularization show that the production of VEGF is specifically induced in a subset of glioblastoma cells distinguished by their immediate proximity to necrotic foci (presumably hypoxic regions) and the clustering of capillaries alongside VEGF-producing cells.

Animals↗
PubMed1975

Labilization of lysosomes and mitochondria in situ by hypoxia and hypoxia-related factors.

Primary cultures of rat heart muscle and endothelioid cells were used to study the labilization of lysosomes and mitochondria by hypoxia, "hypoxia substitutes", and the in vivo-related factors of free fatty acid and pH. Subliminally-active levels tested were: hypoxia (1% O2/4 days), 5x10(-6)M sodium stearate: albumin in 6:1 ratio/30 min, KCN (1x10(-3)M/1 hr), 2 deoxy-glucose (3x10(-2)M/12 hr), acidosis (pH 6.9/30 min) and combinations. KCN plus 2-DG labilized the organelles in both cell types. Sensitivity to injury was in the order mitochondria greater than lysosomes and muscle cells greater than endothelioid cells.

Animals↗
PubMedDate not supplied

[Comparison of the effect of acute hypoxia on the rat liver lysosomal apparatus against a background of adaptation to hypoxia and the administration of gutimine].

Acute hypobaric hypoxia in rats (260 mm Hg., 90 min) was accompanied by a greater liver lysosomes osmotic susceptibility and by an increase in the relative content of the lysosomal enzymes (acid RNAase and acid phosphatase) in the nuclear fraction. This indicates an enrichment of the liver cell lysosomes with secondary lysosomes. No significant signs of labilization of the liver lysosomes were found. The adaptation of rats to hypoxia, as well as administration of the antihypoxant guthimin or of 1,4-bis-(3'-morpholinopropin-1'-yl-1') benzene hinder these changes to occur in the liver lysosomes during the organism reaction to hypoxia. But the effect of stabilization of the lysosomal membranes in a minor component in the antihypoxia action of the treatment.

Acid Phosphatase↗
PubMed1977

Lung mast cells in rats exposed to acute hypoxia, and chronic hypoxia with recovery.

Exposure to acute hypoxia (barometric pressure 263 mmHg) for 8 hours did not lead to increased numbers of mast cells in the lungs of rats. In contrast, in adult rats kept for 35 days at a barometric pressure of 380 mmHg there was a proliferation of mast cells around the pulmonary blood vessels and in the alveolar septa. This hyperplasia of lung mast cells in response to chronic hypoxia was reversible on removal of the hypoxic stimulus. There was a correlation between the logarithm of the perivascular lung mast cell density (defined in the paper) and the logarithm of the right ventricular weight. There was no increase in the mast cells in the carotid bodies of the hypoxic rats. Young male, old male, young female, and old female rats which had been subjected for 39 days to a barometric pressure of 380 mmHg showed a proliferation of mast cells around the pulmonary blood vessels and in the alveolar walls. This response was greatest in the adult animals and independent of their sex. In the age and sex experiment there was a correlation between the perivascular lung mast cell density and the medial thickness of the muscular pulmonary arteries. Since mast cell hyperplasia has been reported as preceding right ventricular hypertrophy, it is conceivable that mast cell proliferation in the lung may be a defence mechanism to limit the severity of hypoxic pulmonary hypertension rather than to mediate it.

Age Factors↗
PubMedDate not supplied

Studies on hypoxia: XII. Detrimental effects of synthetic polyribonucleotides on epiphyseal plates of rats exposed to hypoxia.

The effect of different doses of polyadenylic and polyuridylic acids (poly A:U) was studied in control rats and in rats exposed to hypoxia. In the control rats, administration of different doses of poly A:U did not change the thickness of the epiphyseal plate or increase the incorporation of 3H-phenylalanine as judged using radioautography. Rats exposed to hypoxia showed a significant dose-related reduction in the thickness of the epiphyseal plate and 3H-phenylalanine incorporation.

Amino Acids↗
PubMed1992

Hypoxia-selective antitumor agents. 6. 4-(Alkylamino)nitroquinolines: a new class of hypoxia-selective cytotoxins.

A series of isomeric 4-[[3-(dimethylamino)propyl]amino]nitroquinolines has been synthesized and evaluated as hypoxia-selective cytotoxins and as radiosensitizers of hypoxic cells. The compounds showed widely-differing hypersensitivity factors (ratios of cytotoxicity against wild-type and repair-deficient mammalian cells). Many compounds showed oxygen-sensitive bioreduction resulting in DNA alkylation, while others show oxygen-insensitive modes of action. Of the nitro isomers studied, the 5-nitro showed the greatest hypoxic selectivity. A series of ring-substituted analogues were then prepared, in an effort to lower its reduction potential of -286 mV. Structure-activity studies showed that the effects of substitution on reduction potential were complex, being mediated by electronic and steric effects on the nitro group, as well as by effects on quinoline pKa. Two compounds of lower reduction potential, the 3- and 8-methyl analogues, showed improved selectivity (47- and 60-fold in a clonogenic assay). These two compounds also showed the highest "in vitro therapeutic indices" of the series as hypoxic cell radiosensitizers. Despite these favorable in vitro properties, neither compound had activity against hypoxic cells in SCCVII tumors when administered at 60% of the MTD.

Animals↗
PubMed1975

Effects of hypoxia on distribution of cardiac output and organ blood flow in the rabbit. Regional vascular response to hypoxia.

The hemodynamic responses of various vascular beds in the systemic circulation to prolonged moderate hypoxia were studied in the rabbit using the radioactive microsphere method. Although cardiac output remained unchanged, there was a redistribution of blood flow in which blood was mainly diverted from the kidneys to provide greater supply to heart, brain and skeletal muscle. These regional adjustments are similar to those seen after low cardiac output due to hemorrhage or endotoxic shock.

Animals↗
PubMed1975

Influence of carbon monoxide, hypoxic hypoxia or potassium cyanide pretreatment on acute carbon monoxide and hypoxic hypoxia lethality.

Pre-exposure of mice to 500 or 1000 ppm of carbon monoxide (CO) for 4 hours resulted in a significant decrease in lethality induced by exposure to 2500 ppm of CO 24 hours later. Pre-exposure to CO had no effect on lethality induced by hypoxic hypoxia (low inspired O2 tension) or potassium cyanide (KCN). Pre-exposure to 10% O2 for 4 hours significantly decreased lethality induced 24 hours later by CO or 7% O2 exposures lethality induced 24 hours later by CO or 7% O2 exposures but had no effect on KCN-induced lethality. Pretreatment with a nonlethal dose of KCN had no significant effect on lethality induced 24 hours later by exposure to CO (2500 ppm), 7% O2 or KCN. The alterations in CO lethality were not associated with alterations in carboxyhemoglobin levels. Studies of oxygen consumption and indicators of oxygen delivery to tissues (P50 and red blood cell 2,3-diphosphoglycerate) failed to provide any evidence of pretreatment alteration. Examination of blood lactate, pyruvate and lactate/pyruvate ratios in control and pre-exposed mice after a short exposure to 2500 ppm of CO showed significantly lower lactate and lactate/pyruvate ratios in the pre-exposed mice as compared to controls. These data suggest that animals pre-exposed to 1000 ppm of CO and 10% O2 are less hypoxic than non-pre-exposed animals even through their oxygen delivery system is unchanged.

Adenosine Diphosphate↗
PubMed1977

Hypoxia in fibroblast cultures. 3. 35S-sulfate incorporation into acid mucopolysaccharides as influenced by 5% O2 hypoxia with simultaneous changes in the lactate-and H-ion concentrations.

The influence of 5% O2 hypoxia on the 35S-sulfate incorporation into different mucopolysaccharide fractions was studied in monolayer cultures of embryonic rat fibroblasts before reaching the stationary phase. Besides the O2 concentration also the pH value and lactate concentration were varied in the experiments. The results are valid for proliferating cell cultures.

Animals↗
PubMed1977

Changes in tissue glycogen stores of rats under acute and chronic hypoxia and their relationship to hypoxia tolerance.

Rats were exposed to simulated altitudes of 3658 m, 4877 m, and 7620 m, for 5 h/d for 30 d at an ambient temperature of 28 degrees C. Blood sugar and tissue glycogen levels were measured--after acute exposure and chronic exposure while either fed ad lib or fasted for 24 h--in liver, kidney, brain, heart, lungs, and skeletal muscles. Glycogen levels were decreased significantly in several tissues under chronic hypoxia in fed animals. In the animals which were fasted 24 h before sacrifice after their 1 month altitude exposure, there was a significant glycogen increase in livers but no change in other tissues. In fasted, acute-exposed animals, glycogen decreased in hearts while in other tissues its levels were unchanged. Hyperglycemia invariably accompanied all conditions of altitude exposures (in fed, fasted, acute, or chronic exposed). Glucose injected i.p. to fed rats as single doses of 20 g/kg body weight 3 h before sacrifice resulted in significantly increased glycogen in all tissues except brain. These glucose injected rats had highly increased resistance to hypoxic stress.

Altitude Sickness↗
PubMed1976

Measurement of the ventilatory response to hypoxia. A step hypoxia three-minute test.

A step hypoxia method for testing response of patients has been described. It involves a well-trained operator who must observe the patient while monitoring and adjusting alveolar oxygen and CO2 tensions. The advantages of the step test are that the time effects can be examined and that quantitative information in a steady-state can be obtained in a relatively short period of time. It can be done at several different levels of CO2.

Animals↗
PubMed1976

Effects of prior hypoxia exposure on visual target detection during later more severe hypoxia.

Three groups of 15 subjects each were exposed to 3 different combinations of intermediate (staging) altitudes and exposure times, and were then tested for visual target detection capability at a final altitude of 4300 m. All groups with staging exposure performed better at altitude and had fewer symptoms of acute mountain sickness than a fourth group which went directly to 4300 m altitude from sea level. The data showed that task factors of both viewing distance and degree of peripheral placement of the target significantly influenced detection time within all groups regardless of variations in exposure to altitude.

Adaptation, Physiological↗