Extracorporeal membrane oxygenation for near fatal asthma with sudden cardiac arrest.

INTRODUCTION: Near fatal asthma is a life-threatening disorder that requires mechanical ventilation. Near fatal asthma and COPD with sudden cardiac arrest can worsen the outcomes. Previous studies demonstrated that ECMO is a live-saving measure for near fatal asthma that does not respond to traditional treatment. CASE STUDY: A patient with near fatal asthma (NFA) and COPD presented with high airway resistance, life-threatening acidemia and severe hypoxemia that failed to respond to conventional therapy. His hospital course was complicated by sudden cardiac arrest when preparing to initiate V-V mode extracorporeal membrane oxygenation (ECMO). The mode immediately changed from V-V to V-A, then to V-AV and finally to V-V mode in order to improve cardiac function and promote recovery of lung function. RESULTS: On the sixth day, ECMO was removed and on the ninth day, he was extubated and transferred to the ward. Finally, the patient was discharged home on the nineteenth day after admission to be followed up in the pulmonary clinic. CONCLUSIONS: The early application of ECMO and mode changing plausibly resulted in dramatic improvement in gas exchange and restoration of cardiac function. This case illustrates the critical role of ECMO mode changing as salvage therapy in NFA and COPD with sudden cardiac arrest.

Cotransplantation of human umbilical cord-derived mesenchymal stem cells and umbilical cord blood-derived CD34⁺ cells in a rabbit model of myocardial infarction.

The objective of the study is to investigate the effect of hypoxic preconditioning on the immunomodulatory properties of human umbilical cord-derived mesenchymal stem cells (hUC-MSCs) and the effect of cotransplantation of hUC-MSCs and human umbilical cord blood (hUCB)-derived CD34(+) cells in a rabbit model of myocardial infarction. hUC-MSCs with or without hypoxic preconditioning by cobalt chloride were plated in a 24-well plate, and then cocultured with hUCB-CD34(+) cells and PBMCs for 96 h at 37 °C in a 5% CO2 incubator. For the negative control, hUC-MSCs were omitted. The groups were divided as follows: A1 = HP-MSCs + hUCB-CD34(+) cells + PBMC, A2 = hUC-MSCs + hUCB-CD34(+) cells + PBMC, Negative Control = hUCB-CD34(+) cells + PBMC. Culture supernatants of each group were collected, and the IL-10 and IFN-γ levels were measured by ELISA. A rabbit model of MI was established using a modified Fujita method. The animals were then randomized into three groups and received intramyocardial injections of 0.4 ml of PBS alone (n = 8, PBS group), hUC-MSCs in PBS (n = 8, hUC-MSCs group), or hUC-MSCs + CD34(+) cells in PBS (n = 8, Cotrans group), at four points in the infarct border zone. Echocardiography was performed at baseline, 4 weeks after MI induction, and 4 weeks after cell transplantation, respectively. Stem cell differentiation and neovascularization in the infracted area were characterized for the presence of cardiac Troponin I (cTnI) and CD31 by immunohistochemical staining, and the extent of myocardial fibrosis was evaluated by hematoxylin and eosin (H&E) and Masson's trichrome. IFN-γ was 27.00 ± 1.11, 14.20 ± 0.81, and 7.22 ± 0.14 pg/ml, and IL-10 was 31.68 ± 3.08, 61.42 ± 1.08, and 85.85 ± 1.80 pg/ml for the Control, A1 and A2 groups, respectively, which indicated that hUCB-CD34(+) cells induced immune reaction of peripheral blood mononuclear cells, whereas both hUC-MSCs and HP-MSCs showed an immunosuppressive effect, which, however, was attenuated by hypoxic preconditioning. The Cotrans group had less collagen deposition in the infarcted myocardium and better heart function than the hUC-MSCs or PBS group. The presence of cTnI-positive cells and CD31-positive tubular structures indicated the differentiation of stem cells into cardiomyocytes and neovascularization. The microvessel density was 12.19 ± 3.05/HP for the hUC-MSCs group and 31.63 ± 2.45/HP for the Cotrans group, respectively (P < 0.01). As a conclusion, both hUC-MSCs and HP-MSCs have an immunosuppressive effect on lymphocytes, which, however, can be attenuated by hypoxic preconditioning. Cotransplantation of hUC-MSCs and hUCB-CD34(+) cells can improve heart function and decrease collagen deposition in post-MI rabbits. Thus, a combined regimen of hUC-MSCs and hUCB-CD34(+) cells would be more desirable than either cells administered alone. This is most likely due to the increase of cardiomyocytes and enhanced angiogenesis in the infarcted myocardium.