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![Metabolic Implications of Single-unit Avian Intrapulmonary CO2 Chemoreceptor (IPC) Responses to Sustained Anoxia and Normoxic Recovery için kapak resmi Metabolic Implications of Single-unit Avian Intrapulmonary CO2 Chemoreceptor (IPC) Responses to Sustained Anoxia and Normoxic Recovery için kapak resmi](/client/assets/d79c3e4af2b6d196/ctx/images/no_image.png)
Metabolic Implications of Single-unit Avian Intrapulmonary CO2 Chemoreceptor (IPC) Responses to Sustained Anoxia and Normoxic Recovery
Başlık:
Metabolic Implications of Single-unit Avian Intrapulmonary CO2 Chemoreceptor (IPC) Responses to Sustained Anoxia and Normoxic Recovery
Yazar:
Low, Trevor M., author.
ISBN:
9780438015241
Yazar Ek Girişi:
Fiziksel Tanımlama:
1 electronic resource (44 pages)
Genel Not:
Source: Masters Abstracts International, Volume: 57-06M(E).
Advisors: Steven C. Hempleman Committee members: David Pierotti; Tinna Taustadóttir.
Özet:
Pilarski (et al., 2009) reported that both tonic and phasic IPC CO 2 transduction are strongly inhibited by mitochondrial electron transport system (ETS) inhibitor rotenone and glycolysis inhibitor iodoacetate, while ETS uncoupler 2,4-DNP inhibited only tonic CO2 transduction. They suggested that glycolysis may provide sufficient ATP to power phasic IPC transduction, but could not sustain tonic CO2 transduction. To investigate further, we separately ventilated and perfused the right (R) and left (L) lungs of anesthetized mallard ducks, and recorded L lung IPC responses to CO2 in 12 IPC. Ten (10) min of complete L lung anoxia produced by ligating the L pulmonary artery (LPA) and ventilating the L lung with N2 and CO2 significantly reduced mean IPC discharge CO2 responses (to 36% of control, p<0.001). We tested the effects of recovery on 10 IPC by returning venilatory O2 and blood flow to the L lung. Returning O2 to the L lung ventilating gas restored IPC responses to normal (to 95% of control, p=NS). Returning blood flow to the left lung as well as returning O2 to L lung ventilating gas caused further increase in mean IPC discharge (to 98% of control, p=NS). We conclude that IPC CO2 transduction is strongly inhibited by true anoxia (and would likely be abolished by anoxia exposure times > 10 min). Inhibition may have been due to accumulation of lactate causing intracellular acidosis, formation of reactive oxygen species (ROS), and disruption of transmembrane ionic gradients. Previous work has shown that decreased intracellular pH inhibits IPC (Bebout and Hempleman, 1999 Hempleman et. al, 2000). Ischemia and the subsequent formation of ROS can also increase intracellular calcium [Ca++]i (Kristian et. al., 1998; Turrens, 2003), which is a known depressant of IPC excitability (Hempleman et al., 2006). The inhibitory effect of 10 min anoxia on IPC CO 2 transduction was entirely reversible.
Notlar:
School code: 0391
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Yer Numarası | Demirbaş Numarası | Shelf Location | Lokasyon / Statüsü / İade Tarihi |
---|---|---|---|
XX(692146.1) | 692146-1001 | Proquest E-Tez Koleksiyonu | Arıyor... |
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