Objectives: This study tested the hypothesis that early extracorporeal membrane oxygenator offered additional benefits in improving 30-day outcomes in patients with acute ST-segment elevation myocardial infarction complicated with profound cardiogenic shock undergoing primary percutaneous coronary intervention. Methods: Between May 1993 and July 2002, 920 patients with acute ST-segment elevation myocardial infarction underwent primary percutaneous coronary intervention. Of these patients, 12.5% (115) with cardiogenic shock were enrolled in this study (group 1). Between August 2002 and December 2009, 1650 patients with acute ST-segment elevation myocardial infarction underwent primary percutaneous coronary intervention. Of these patients, 13.3% (219) complicated with cardiogenic shock were enrolled (group 2). Results: The incidence of profound shock (defined as systolic blood pressure remaining ≤75 mm Hg after intra-aortic balloon pump and inotropic agent supports) was similar in both groups (21.7% vs. 21.0%, p > .5). Extracorporeal membrane oxygenator support, which was available only for patients in group 2, was performed in the catheterization room. The results demonstrated that final thrombolysis in myocardial infarction grade 3 flow in infarct-related artery was similar between the two groups (p = .678). However, total 30-day mortality and the mortality of patients with profound shock were lower in group 2 than in group 1 (all p < .04). Additionally, the hospital survival time was remarkably longer in patients in group 2 than in patients in group 1 (p = .0005). Furthermore, multivariate analysis demonstrated that unsuccessful reperfusion, presence of advanced congestive heart failure, profound shock, and age were independent predictors of 30-day mortality (all p < .02). Conclusion: Early extracorporeal membrane oxygenator-assisted primary percutaneous coronary intervention improved 30-day outcomes in patients with ST-segment elevation myocardial infarction with complicated with profound cardiogenic shock.

Background: Reactive oxygen species are important mediators exerting toxic effects on various organs during ischemia-reperfusion (IR) injury. We hypothesized that adipose-derived mesenchymal stem cells (ADMSCs) protect the kidney against oxidative stress and inflammatory stimuli in rat during renal IR injury.Methods: Adult male Sprague-Dawley (SD) rats (n = 24) were equally randomized into group 1 (sham control), group 2 (IR plus culture medium only), and group 3 (IR plus immediate intra-renal administration of 1.0 × 10⁶autologous ADMSCs, followed by intravenous ADMSCs at 6 h and 24 h after IR). The duration of ischemia was 1 h, followed by 72 hours of reperfusion before the animals were sacrificed.Results: Serum creatinine and blood urea nitrogen levels and the degree of histological abnormalities were markedly lower in group 3 than in group 2 (all p < 0.03). The mRNA expressions of inflammatory, oxidative stress, and apoptotic biomarkers were lower, whereas the anti-inflammatory, anti-oxidative, and anti-apoptotic biomarkers were higher in group 3 than in group 2 (all p < 0.03). Immunofluorescent staining showed a higher number of CD31+, von Willebrand Factor+, and heme oxygenase (HO)-1+ cells in group 3 than in group 2 (all p < 0.05). Western blot showed notably higher NAD(P)H quinone oxidoreductase 1 and HO-1 activities, two indicators of anti-oxidative capacity, in group 3 than those in group 2 (all p < 0.04). Immunohistochemical staining showed higher glutathione peroxidase and glutathione reductase activities in group 3 than in group 2 (all p < 0.02)Conclusion: ADMSC therapy minimized kidney damage after IR injury through suppressing oxidative stress and inflammatory response.

Intravenous administration of xenogenic adipose-derived mesenchymal stem cells (ADMSC) and ADMSC-derived exosomes markedly reduced brain infarct volume and preserved neurological function in rat after acute ischemic stroke

Background: The therapeutic effect of adipose-derived mesenchymal stem cells (ADMSCs) on brain infarction area (BIA) and neurological status in a rat model of acute ischemic stroke (IS) was investigated. Methods: Adult male Sprague-Dawley (SD) rats (n = 30) were divided into IS plus intra-venous 1 mL saline (at 0, 12 and 24 h after IS induction) (control group) and IS plus intra-venous ADMSCs (2.0 × 10⁶) (treated interval as controls) (treatment group) after occlusion of distal left internal carotid artery. The rats were sacrificed and brain tissues were harvested on day 21 after the procedure. Results: The results showed that BIA was larger in control group than in treatment group (p < 0.001). The sensorimotor functional test (Corner test) identified a higher frequency of turning movement to left in control group than in treatment group (p < 0.05). mRNA expressions of Bax, caspase 3, interleukin (IL)-18, toll-like receptor-4 and plasminogen activator inhibitor-1 were higher, whereas Bcl-2 and IL-8/Gro were lower in control group than in treatment group (all p < 0.05). Western blot demonstrated a lower CXCR4 and stromal-cell derived factor-1 (SDF-1) in control group than in treatment group (all p < 0.01). Immunohistofluorescent staining showed lower expressions of CXCR4, SDF-1, von Willebran factor and doublecortin, whereas the number of apoptotic nuclei on TUNEL assay was higher in control group than in treatment group (all p < 0.001). Immunohistochemical staining showed that cellular proliferation and number of small vessels were lower but glial fibrillary acid protein was higher in control group than in treatment group (all p < 0.01). Conclusions: ADMSC therapy significantly limited BIA and improved sensorimotor dysfunction after acute IS.

This study tested the hypothesis that autologous transplantation of adipose-derived mesenchymal stem cells (ADMSCs) can effectively attenuate acute pulmonary ischemia-reperfusion (IR) injury.