FRET
发表于 2025-3-26 22:36:33
Time-Course of Ventilation, Arterial and Pulmonary CO2 Tension During CO2 Increase in Humans, 41.8 ± 38.0 and 21.6 ± 9.7 and A was 0.39 ± 0.67, 1.64 ± 1.35 and 0.17 ± 0.83 in VE, PaCO. and PvCO., respectively, with statistical difference of PaCO. from other variables, suggesting that VE and PvCO. showed same mode of change according to time but PaCO. did not.
Bouquet
发表于 2025-3-27 02:54:51
Hydrogen Sulfide (H2S): A Physiologic Mediator of Carotid Body Response to Hypoxia,harmacological inhibitors of CSE as well as CBS showed a similar phenotype in mice and rats. Like hypoxia, H2S donors stimulated the carotid body sensory activity and this response required Ca. influx via voltage-gated Ca2+ channels. Evidence is emerging implicating Ca2+ activated K+ channels in glomus cells as potential targets of H2S.
提升
发表于 2025-3-27 07:56:03
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口诀法
发表于 2025-3-27 10:05:52
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团结
发表于 2025-3-27 15:56:16
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倔强不能
发表于 2025-3-27 20:25:20
The Role of Hypoxia-Inducible Factors in Oxygen Sensing by the Carotid Body,ganese superoxide dismutase, which converts superoxide to hydrogen peroxide. Thus, IH disrupts the balance between HIF-1-dependent pro-oxidant and HIF-2-dependent anti-oxidant activities, and this loss of redox homeostasis underlies the pathogenesis of autonomic morbidities associated with IH.
平躺
发表于 2025-3-28 01:38:16
Dose Dependent Effect of Progesterone on Hypoxic Ventilatory Response in Newborn Rats,t in 12-days old pups. This response was similar between the dose of 4 and 8 mg/kg. These observations suggested that progesterone enhances in age- and dose-dependent manner the hypoxic ventilatory response in newborn rats.
CODA
发表于 2025-3-28 04:53:24
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收养
发表于 2025-3-28 08:55:39
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平息
发表于 2025-3-28 13:10:25
e-Development Toward the Knowledge Economydiated activation of the sympathetic nervous system. IH triggers increased levels of reactive oxygen species (ROS) in the carotid body, which induce increased synthesis and stability of hypoxia-inducible factor 1α (HIF-1α) and calpain-dependent degradation of HIF-2α. HIF-1 activates transcription of