In aortic surgery, interruption of spinal cord blood flow might cause irreversible spinal cord injury which is rare and devastating. However, the mechanisms of spinal cord injury remain elusive. Methods A PubMed/Medli...In aortic surgery, interruption of spinal cord blood flow might cause irreversible spinal cord injury which is rare and devastating. However, the mechanisms of spinal cord injury remain elusive. Methods A PubMed/Medline-literature search for spinal cord injury in aortic surgery over the past decade （aortic surgery 2000-2012） was conducted. Results Spinal cord injury generally results from interruption of the blood supply to the spinal cord due to aortic occlusion. Multiple factors are involved in the development of spinal cord injury and the mechanism includes two phases. The immediate spinal cord injury is related to acute ischemia of the spinal cord. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury which is a biochemically mediated event and manifests complex lesion. Conclusions Acute ischemia injury and delayed reperfusion injury are involved in spinal cord injury and multiple factors contribute to its outcome.展开更多
The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (...The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (Isoc) in isolated rat hepatocytes after hepatic ischemia/reperfusion injuries were studied. Hepatic ischemia and reperfusion injury model was established and whole cell patch-clamp techniques were used to investigate the effects of 2-APB on Isoc. The results showed that ischemia/reperfusion injuries could significantly reduce hepatocellular viability and further increase Isoc in hepatocytes and 2-APB (20, 40, 60, 80, 100 μmol/L) produced a concentration-dependent decrease of Isoc with IC 50 value of 64.63±10.56 μmol/L (n=8). It was concluded that ischemia/reperfusion injuries could reduce hepatocellular viability, probably through increased Isoc in hepatocytes and 2-APB had a protective effect on ischemia/reperfusion-induced liver injury, probably though inhibiting Isoc.展开更多
Recently added to the therapeutic arsenal against chronic heart failure as a first intention drug,the antidiabetic drug-class sodium-glucose cotransporter-2 inhibitors(SGLT2i)showed efficacy in decreasing overall mort...Recently added to the therapeutic arsenal against chronic heart failure as a first intention drug,the antidiabetic drug-class sodium-glucose cotransporter-2 inhibitors(SGLT2i)showed efficacy in decreasing overall mortality,hospitalization,and sudden death in patients of this very population,in whom chronic or acute ischemia count among the first cause.Remarkably,this benefit was observed independently from diabetic status,and benefited both preserved and altered ventricular ejection fraction.This feature,observed in several large randomized controlled trials,suggests additional effects from SGLT2i beyond isolated glycemia control.Indeed,both in-vitro and animal models suggest that inhibiting the Na+/H+exchanger(NHE)may be key to preventing ischemia/reperfusion injuries,and by extension may hold a similar role in ischemic damage control and ischemic preconditioning.Yet,several other mechanisms may be explored which may help better target those who may benefit most from SGLT2i molecules.Because of a large therapeutic margin with few adverse events,ease of prescription and potential pharmacological efficacity,SGLT2i could be candidate for wider indications.In this review,we aim to summarize all evidence which link SGLT2i and ischemia/reperfusion injuries modulation,by first listing known mechanisms,including metabolic switch,prevention of lethal arrythmias and others,which portend the latter,and second,hypothesize how the former may interact with these mechanisms.展开更多
基金supported by the Major International (Regional) Joint Research Project of Ministry of Science and Technology of China (No. 2008DFA31140,and2010DFA32260)Guangdong Province Natural Science Fund (No.10151008002000003,No.10251008002000002 and No.S2011010005836)
文摘In aortic surgery, interruption of spinal cord blood flow might cause irreversible spinal cord injury which is rare and devastating. However, the mechanisms of spinal cord injury remain elusive. Methods A PubMed/Medline-literature search for spinal cord injury in aortic surgery over the past decade （aortic surgery 2000-2012） was conducted. Results Spinal cord injury generally results from interruption of the blood supply to the spinal cord due to aortic occlusion. Multiple factors are involved in the development of spinal cord injury and the mechanism includes two phases. The immediate spinal cord injury is related to acute ischemia of the spinal cord. And the delayed spinal cord injury involves both ischemic cellular death and reperfusion injury which is a biochemically mediated event and manifests complex lesion. Conclusions Acute ischemia injury and delayed reperfusion injury are involved in spinal cord injury and multiple factors contribute to its outcome.
基金This project was supported by the National Natural Sci ence Foundation of China (No. 30270532), the Trans Cen tury Excellent Talent Development Plan Fund of Ministry ofEducation of China (Official Letter No. 2002 48) and Shu guang Program Project of Shanghai Educational Committee(No. 02SG20).
文摘The effects of hepatic ischemia/reperfusion (I/R) injuries on hepatocellular viability and store-operated calcium current (Isoc) in isolated rat hepatocytes and the effects of 2-APB on store-operated calcium current (Isoc) in isolated rat hepatocytes after hepatic ischemia/reperfusion injuries were studied. Hepatic ischemia and reperfusion injury model was established and whole cell patch-clamp techniques were used to investigate the effects of 2-APB on Isoc. The results showed that ischemia/reperfusion injuries could significantly reduce hepatocellular viability and further increase Isoc in hepatocytes and 2-APB (20, 40, 60, 80, 100 μmol/L) produced a concentration-dependent decrease of Isoc with IC 50 value of 64.63±10.56 μmol/L (n=8). It was concluded that ischemia/reperfusion injuries could reduce hepatocellular viability, probably through increased Isoc in hepatocytes and 2-APB had a protective effect on ischemia/reperfusion-induced liver injury, probably though inhibiting Isoc.
文摘Recently added to the therapeutic arsenal against chronic heart failure as a first intention drug,the antidiabetic drug-class sodium-glucose cotransporter-2 inhibitors(SGLT2i)showed efficacy in decreasing overall mortality,hospitalization,and sudden death in patients of this very population,in whom chronic or acute ischemia count among the first cause.Remarkably,this benefit was observed independently from diabetic status,and benefited both preserved and altered ventricular ejection fraction.This feature,observed in several large randomized controlled trials,suggests additional effects from SGLT2i beyond isolated glycemia control.Indeed,both in-vitro and animal models suggest that inhibiting the Na+/H+exchanger(NHE)may be key to preventing ischemia/reperfusion injuries,and by extension may hold a similar role in ischemic damage control and ischemic preconditioning.Yet,several other mechanisms may be explored which may help better target those who may benefit most from SGLT2i molecules.Because of a large therapeutic margin with few adverse events,ease of prescription and potential pharmacological efficacity,SGLT2i could be candidate for wider indications.In this review,we aim to summarize all evidence which link SGLT2i and ischemia/reperfusion injuries modulation,by first listing known mechanisms,including metabolic switch,prevention of lethal arrythmias and others,which portend the latter,and second,hypothesize how the former may interact with these mechanisms.
