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Artigo em Inglês | MEDLINE | ID: mdl-30020223


BACKGROUND: Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) is effective at limiting hemorrhage from non-compressible sources and restoring, yet causes progressive distal ischemia, supraphysiologic pressures and increased cardiac afterload. Endovascular Variable Aortic Control (EVAC) addresses these limitations, while still controlling hemorrhage. Previous work demonstrated improved outcomes following a 90-minute intervention period in an uncontrolled hemorrhage model. The present study compares automated EVAC to REBOA over an occlusion period reflective of contemporary REBOA usage. METHODS: Following instrumentation, 12 Yorkshire-cross swine underwent controlled 25% hemorrhage, a 45-minute intervention period of EVAC or REBOA, and subsequent resuscitation with whole blood and critical care for the remainder of a six-hour experiment. Hemodynamics were acquired continuously and laboratory parameters were assessed at routine intervals. Tissue was collected for histopathologic analysis. RESULTS: No differences were seen in baseline parameters. During intervention, EVAC resulted in more physiologic proximal pressure augmentation compared to REBOA (101 mmHg vs 129 mmHg 95CI 105-151, p=0.04). During critical care, EVAC animals required less than half the amount of crystalloid (3450 ml 95CI 1215-5684 vs 7400 ml 95CI 6148-8642, p<0.01) and vasopressors (21.5 ng/kg 95CI 7.5-35.5 vs 50.5 ng/kg 95CI 40.5-60.5, p=0.05) when compared to REBOA animals. EVAC resulted in lower peak and final lactate levels. EVAC animals had less aortic hyperemia from reperfusion with aortic flow rates closer to baseline (36 ml/kg/min 95CI 30-44 vs 51 mL/kg/min 95CI 41-61, p=0.01). CONCLUSION: For short durations of therapy, EVAC produces superior hemodynamics and less ischemic insult than REBOA in this porcine controlled hemorrhage model, with improved outcomes during critical care. This study suggests EVAC is a viable strategy for in-hospital management of patients with hemorrhagic shock from non-compressible sources. Survival studies are needed to determine if these early differences persist over time. LEVEL OF EVIDENCE: 1 STUDY TYPE: Translational Science.

Stem Cells ; 27(12): 2906-16, 2009 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19725137


Spontaneous calcium (Ca(2+)) transients in the developing nervous system can affect proliferation, migration, neuronal subtype specification, and neurite outgrowth. Here, we show that telencephalic human neuroepithelia (hNE) and postmitotic neurons (PMNs) generated from embryonic stem cells display robust Ca(2+) transients. Unlike previous reports in animal models, transients occurred by a Gd(3+)/La(3+)-sensitive, but thapsigargin- and Cd(2+)-insensitive, mechanism, strongly suggestive of a role for transient receptor potential (Trp) channels. Furthermore, Ca(2+) transients in PMNs exhibited an additional sensitivity to the canonical Trp (TrpC) antagonist SKF96365 and shRNA-mediated knockdown of the TrpC1 subunit. Functionally, inhibition of Ca(2+) transients in dividing hNE cells led to a significant reduction in proliferation, whereas either pharmacological inhibition or shRNA-mediated knockdown of the TrpC1 and TrpC4 subunits significantly reduced neurite extension in PMNs. Primary neurons cultured from fetal human cortex displayed nearly identical Ca(2+) transients and pharmacological sensitivities to Trp channel antagonists. Together these data suggest that Trp channels present a novel mechanism for controlling Ca(2+) transients in human neurons and may offer a target for regulating proliferation and neurite outgrowth when engineering cells for therapeutic transplantation.

Cálcio/metabolismo , Diferenciação Celular , Células-Tronco Embrionárias/metabolismo , Regulação da Expressão Gênica no Desenvolvimento , Neurônios/metabolismo , Canais de Cátion TRPC/metabolismo , Bloqueadores dos Canais de Cálcio/farmacologia , Proliferação de Células , Células Cultivadas , Células-Tronco Embrionárias/citologia , Células-Tronco Embrionárias/efeitos dos fármacos , Humanos , Neurônios/citologia , Neurônios/efeitos dos fármacos , Canais de Cátion TRPC/genética