High colloid osmotic pressure as a proposed mechanism of acute renal injury after pharmacomechanical thrombectomy

Hansen's membrane manometer method for measuring plasma colloid osmotic pressure was used to obtain the osmolality changes of dogs breathing different levels of CO2. Osmotic pressure was converted to osmolality by calibration of the manometer with saline and plasma, using freezing point depression osmometry. The addition of 10 vol% of CO2 to tonometered blood caused about a 2.0 mosmol/kg H2O increase of osmolality, or 1.2% increase of red blood cell volume. The swelling of the red blood cells was probably due to osmosis caused by Cl- exchanged for the HCO3- which was produced rapidly by carbonic anhydrase present in the red blood cells. The change in colloid osmotic pressure accompanying a change in co2 tension was measured on blood obtained from dogs breathing different CO2 mixtures. It was approximately 0.14 mosmol/kg H2O per Torr Pco2. The corresponding change in red cell volume could not be calculated from this because water can exchange between the plasma and tissues.

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The role of E-type prostaglandin receptor EP3 in acute renal injury induced by ischemia-reperfusion

Journal of Molecular and Cellular Cardiology ◽

10.1016/j.yjmcc.2019.11.135 ◽

2020 ◽

Vol 140 ◽

pp. 56

Author(s):

Leng Jing ◽

Zhao Wen ◽

Liu Bin

Keyword(s):

Renal Injury ◽

Ischemia Reperfusion ◽

Acute Renal Injury ◽

Prostaglandin Receptor

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Salvianolic Acid B Prevents Iodinated Contrast Media-Induced Acute Renal Injury in Rats via the PI3K/Akt/Nrf2 Pathway

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/7079487 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 26

Author(s):

Liu Tongqiang ◽

Liu Shaopeng ◽

Yu Xiaofang ◽

Song Nana ◽

Xu Xialian ◽

...

Keyword(s):

Oxidative Stress ◽

Contrast Media ◽

Renal Injury ◽

Salvianolic Acid B ◽

Pi3k Inhibitor ◽

Iodinated Contrast Media ◽

Acute Renal Injury ◽

Nrf2 Pathway ◽

Salvianolic Acid ◽

Iodinated Contrast

Contrast-induced acute renal injury (CI-AKI) has become a common cause of hospital-acquired renal failure. However, the development of prophylaxis strategies and approved therapies for CI-AKI is limited. Salvianolic acid B (SB) can treat cardiovascular-related diseases. The aim of the present study was to assess the effect of SB on prevention of CI-AKI and explore its underlying mechanisms. We examined its effectiveness of preventing renal injury in a novel CI-AKI rat model. Compared with saline, intravenous SB pretreatment significantly attenuated elevations in serum creatinine and the histological changes of renal tubular injuries, reduced the number of apoptosis-positive tubular cells, activated Nrf2, and lowered the levels of renal oxidative stress induced by iodinated contrast media. The above renoprotection of SB was abolished by the PI3K inhibitor (wortmannin). In HK-2 cells, SB activated Nrf2 and decreased the levels of oxidative stress induced by hydrogen peroxide and subsequently improved cell viability. The above cytoprotection of SB was blocked by the PI3K inhibitor (wortmannin) or siNrf2. Thus, our results demonstrate that, due to its antioxidant properties, SB has the potential to effectively prevent CI-AKI via the PI3K/Akt/Nrf2 pathway.

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