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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There is general concern that major blood loss during deliberate hypotension could produce severe organ ischemia, but documentation of the magnitude of this response remains obscure. To examine this response, we studied 43 male Sprague-Dawley rats that were divided into seven groups: the control animals received 1 MAC (1.4%) isoflurane only; the hypotensive animals received a 1.4% isoflurane baseline anesthetic and were then rendered hypotensive by either increasing the isoflurane concentration (dISO), or by adding sodium nitroprusside (SNP), or 2-chloroadenosine (2AD) to the baseline anesthetic, decreasing the MAP to 51 mmHg; hemorrhaged animals had hypotension produced in the same manner as for the hypotensive animals, but additionally were bled 20% of estimated blood volume during deliberate hypotension produced with either deep isoflurane (dISOH), sodium nitroprusside (SNPH), or 2-chloroadenosine (2ADH). After a 25-min period of hypotension, or hypotension plus hemorrhage, cardiac output and blood flow to brain, heart, gastrointestinal tract, kidney, and liver were measured with 141Ce-labelled 15-microns microspheres. Hypotension was associated with decreased blood flow to the kidneys in all groups and to the liver in the 2AD group and an increased blood flow to the heart in the SNP and 2AD groups. Hemorrhage decreased blood flow during deliberate hypotension to the brain and the gastrointestinal tract in the dISOH and 2ADH groups and to the liver in the dISOH group. Our results suggest that hemorrhage during deliberate hypotension with dISO or isoflurane plus 2AD may be associated with compromised organ blood flow, whereas blood flow to vital organs is maintained after 20% hemorrhage during isoflurane and superimposed SNP-induced hypotension.
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PMID:The influence of hemorrhage on organ perfusion during deliberate hypotension in rats. 834 11

Mitophagy is the sole mechanism for neurons to eliminate superfluous or damaged mitochondria. Although the critical implications of mitophagy have been emphasized in a variety of neurological disorders, it remains ambiguous how neurons control the quality of axonal mitochondria. By employing an oxygen-glucose-deprivation and reperfusion (OGD-Rep) model in cultured neurons, our recent results clearly documented the prompt recovery of retrograde transport of axonal mitochondria to neuronal soma. Moreover, by selectively labeling axonal mitochondria, we found that these axonal mitochondria appear in neuronal soma and are eliminated via autophagosomes in priority. This mitochondrial movement from axon to soma has a critical contribution to overall neuronal mitophagy under ischemia. Because forced expression of an anchoring protein, SNPH (Syntaphilin), significantly blocks mitophagy, and aggravates mitochondrial dysfunction and neuronal injury. Conversely, promoted retrograde mitochondrial movement facilitates neuronal mitophagy and attenuates ischemic neuronal demise. In conclusion, we propose stimulating the somatic autophagy of axonal mitochondria after ischemic insults. These findings may provide further insight into how neurons control the mitochondrial quality in pathological conditions and offer novel strategies to cure neurological disorders.
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PMID:Come and eat: mitochondrial transport guides mitophagy in ischemic neuronal axons. 3097 99