Impaired medullary circulation in postischemic acute renal failure

Karlberg, Lars; Norlén, Bo Johan; Öjteg, G.; Wolgast, M.

doi:10.1111/j.1748-1716.1983.tb07234.x

Cited by 78 publications

(53 citation statements)

References 25 publications

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“…This observation could reflect the lower postischemic medullary blood flow, which has been attributed to characteristic dysfunctions in acute renal failure (11). The c-Kitϩ/CM-Dilϩ cells had apparently not significantly incorporated into the walls of small vessels.…”

Section: Discussionmentioning

confidence: 94%

Epac-1 activator 8-O-cAMP augments renoprotective effects of allogeneic murine EPCs in acute ischemic kidney injury

Patschan

Wessels

et al. 2010

American Journal of Physiology-Renal Physiology

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Endothelial progenitor cells (EPCs) protect kidneys from acute ischemic damage. The aim of this study was to identify “treatment parameters” that optimize an EPC-based therapy of acute ischemic renal failure. Male C57BL/6N mice underwent unilateral nephrectomy with simultaneous contralateral renal artery clamping for 30, 35, and 40 min. Tagged murine EPCs were systemically injected at the time of reperfusion. In some experiments, EPCs were pretreated with the Epac (exchange protein directly activated by cAMP-1) activator 8-pCPT-2′- O-Me-cAMP (Epac-1 Ac) and the integrin binding antagonist cyclic Arg-Gly-Asp peptide (cRGD). Injections of 106 EPCs after 30 and 35 min of renal ischemia protected animals from acute renal failure. The same effect occurred with 0.5×106 EPCs after a 35-min period of ischemia. If ischemia lasted for 40 min, 0.5×106 cells mice did not prevent acute renal failure. To analyze whether EPC integrin receptor activation would modify the cells' renoprotective activity, EPCs were pretreated with Epac-1 Ac. Such animals did not develop acute renal failure, even if ischemia lasted for 40 min. This effect was negated if the cells were pretreated with both Epac-1 Ac and cRGD. In kidneys from those animals medullopapillary EPCs were significantly accumulated. In vitro Epac-1 Ac preactivation of EPCs did not increase the overall expression intensity but induced a redistribution of β1-integrins toward the cell membranes. We conclude that EPC pretreatment with the integrin receptor activator 8-pCPT-2′- O-Me-cAMP augments the anti-ischemic potential of the cells.

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Section: Discussionmentioning

confidence: 94%

Epac-1 activator 8-O-cAMP augments renoprotective effects of allogeneic murine EPCs in acute ischemic kidney injury

Patschan

Wessels

et al. 2010

American Journal of Physiology-Renal Physiology

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“…The decrease in GFR after renal ischemia/reperfusion is associated with an increased production of endothelin and reactive oxygen species, which may be responsible for increasing renal vascular resistance after ischemia/reperfusion (34,35). One of the most sensitive regions of the kidney to alterations in blood flow after ischemia is the medullary circulation (36,37). Recent studies have demonstrated that CO is endogenously produced in this region of the kidney and that this locally produced CO plays an important role in the regulation of medullary blood flow (38).…”

Section: Discussionmentioning

confidence: 99%

Protective Effect of Carbon Monoxide–Releasing Compounds in Ischemia-Induced Acute Renal Failure

Vera

Henegar²,

Drummond³

et al. 2005

Journal of the American Society of Nephrology

129

105

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Heme oxygenase (HO) induction has been demonstrated to be beneficial in limiting the extent of cellular damage after ischemia-induced acute renal failure (ARF). Because increased HO activity is associated with the production of carbon monoxide (CO) as well as the potent antioxidant bilirubin, it is unclear which of the two is of greater importance in the protective effects of HO induction. The purpose of this study was to determine the protective role of CO alone in ischemia-induced ARF. Bilateral clamping of the renal pedicle for 40 min was associated with a ninefold increase in the levels of plasma creatinine 24 h after reperfusion as compared with normal plasma creatinine levels; however, administration of CO donor compounds tricarbonyldichlororuthenium(II) dimer, ([Ru(CO) 3 Cl 2 ] 2 , 10 mg/kg) or tricarbonylchloro(glycinato)ruthenium(II) ([Ru(CO) 3 Cl(glycinate)], (CORM-3) 1 h before the onset of ischemia significantly decreased the levels of plasma creatinine 24 h after reperfusion as compared with vehicle-treated mice. Surprising, treatment with the CO donors was associated with an increase in HO activity 24 h after ischemia. For determining whether the protective effects of the CO donors were due to CO or HO-1 induction, experiments were performed in which HO was inhibited before administration of the CO donors. Pretreatment with the HO inhibitor had no effect on the level of plasma creatinine 24 h after reperfusion after treatment with the CO donor compounds. These results suggest that CO itself may be protective and limit renal damage in ischemia induced ARF. 16: 950-958, 2005. J Am Soc Nephrol

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“…Of greater importance are the regional alterations in RBF that occur during AKI (13). Blood flow to the outer medulla is reduced disproportionately to the reduction in total kidney perfusion in animal models of AKI (17,18) and likely in humans following ischemic injury to the kidney. Endothelial cells are important determinants of vascular tone, leukocyte function, and smooth muscle responsiveness (19).…”

Section: Endothelium and Vascular Components Of Injurymentioning

confidence: 99%