path(MESH:Hypoxia)
By contrast, no or limited increases in renal blood flow are observed during acute hemodilution (15, 42), leading to earlier and more severe renal tissue hypoxia (5, 38), and an increase in the magnitude of hypoxia signaling responses, including stabilization of the transcription factor hypoxia- inducible factor- (HIF-) (42, 43). PubMed:29351418
The absent or relatively small increase in renal blood flow likely contributed to the occurrence of renal tissue hypoxia in both models. PubMed:29351418
The renal blood flow response to anemia is proportionally much smaller than the increase observed in cerebral blood flow (50–100%). This relative difference in organ blood flow likely explains why the kidney becomes profoundly hypoxic, whereas brain oxygenation is largely preserved during anemia (12, 32, 42). PubMed:29351418
Our data provided clear evidence of renal tissue hypoxia, which was in part due to a lack of increase in renal blood flow. PubMed:29351418
However, as reviewed above, several experimental tal studies and our new data have demonstrated that both acute and subacute anemia are associated with renal tissue hypoxia (5, 38, 41, 43). PubMed:29351418
However, as reviewed above, several experimental tal studies and our new data have demonstrated that both acute and subacute anemia are associated with renal tissue hypoxia (5, 38, 41, 43). PubMed:29351418
Depending on the extension of the vaso-occlusion, some tissues may experience hypoxia and damage. PubMed:24904418
Hp and Hpx significantly inhibited stasis in response H/R or LPS (Fig 5). PubMed:29694434
Our experimental data provided clear evidence that moderate subacute anemia resulted in a profound level of renal tissue hypoxia, as characterized by a reduction in kidney PtO2, an increase in regional HIF/luciferase radiance in vivo, and a substantial increase in EPO mRNA level at a Hb concentration consistent with moderate anemia (90 g/l). PubMed:29351418
Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240
Physiological, pathophysiological, and biochemical stimuli known to induce proliferation of NPC via NF-κB activation include cerebral infarction [165], traumatic brain injury [166], reactive oxygen species [167], hypoxia [168-172], sAPPα [147], and sphingosine-1-phosphate [173] PubMed:28745240
Depending on the extension of the vaso-occlusion, some tissues may experience hypoxia and damage. PubMed:24904418
Hp and Hpx significantly inhibited stasis in response H/R or LPS (Fig 5). PubMed:29694434
However, as reviewed above, several experimental tal studies and our new data have demonstrated that both acute and subacute anemia are associated with renal tissue hypoxia (5, 38, 41, 43). PubMed:29351418
However, as reviewed above, several experimental tal studies and our new data have demonstrated that both acute and subacute anemia are associated with renal tissue hypoxia (5, 38, 41, 43). PubMed:29351418
We observed a mild degree of plasma hypoxia could lead to organ injury. PubMed:29351418
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