Objective: Augmentation of left ventricular (LV) contractility and heart rate (HR) by sympathetic nerve stimulation and amelioration of heart failure by vagal nerve stimulation has been reported. However, the effects of concomitant electrical stimulation of both sympathetic and parasympathetic cardiac nerves in tissues such as those of the cardiac plexus remain unclear. This study sought to assess acute changes in cardiac function and hemodynamics in response to endovascular cardiac plexus stimulation (CPS).
Methods: Twelve dogs received endovascular CPS via a bipolar catheter within the right pulmonary artery. Stimulation frequency (20 Hz) and pulse width (4 milliseconds) were fixed; voltage varied (range, 15-60 V).
Results: Results fell into three categories: 1, no response (n = 4); 2, an increase in systemic arterial pressure that was dependent on electrode placement (n = 4); and 3, a very reproducible and stable increase in aortic pressure (n = 4). In the third group, mean systolic aortic pressures, maximum value of the first derivative of LV pressure, and LV stroke work increased with stimulation (P < 0.02 for all parameters) as did cardiac output, end-systolic elastance, and preload recruitable stroke work (P = 0.03). Systemic and pulmonary vascular resistance, central venous pressure, pulmonary arterial pressure, and HR remained unchanged (P > 0.05).
Conclusions: In contrast to conventional inotropic agents, endovascular CPS induced significant and selective increases in LV contractility without increasing HR. Efforts to optimize electrode placement and fixation will improve the reproducibility of endovascular CPS treatment.
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From the Neuroendovascular Program, Massachusetts General Hospital & Brigham and Women's Hospital, Harvard University, Boston, Mass (A.A.D., R.W.R., C.J.S., J.D.R., A.B.P.); Departments of Medical Imaging and Neurosurgery, Neurovascular Centre, St. Michael's Hospital, Toronto, ON, Canada M5B 1W8 (A.A.D., N.M.C., T.R.M., V.M.P.); Departments of Neurologic Surgery & Radiology, Mayo Clinic, Rochester, Minn (S.G., H.K., R.K.); Cooper Neurologic Institute, Cooper University Hospital, Cooper Medical School of Rowen University, Camden, NJ (J.E.S., H.S., J.K., A.J.T., A.G.); Departments of Radiology & Neurology, Boston Medical Center, Boston, Mass (M.A., P. Klein, T.N.N.); Department of Interventional Neuroradiology, Stanford Medical Center, Palo Alto, Calif (J.J.H.); Department of Neurosurgery, Thomas Jefferson University, Philadelphia, Pa (K.E.N., A.A., S.I.T., P.J.); Department of Neurosurgery and Interventional Neuroradiology, Louisiana State University, Shreveport, La (H.A.S., B.M., N.A., H.H.C.S.); Department of Diagnostic and Interventional Neuroradiology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany (L.M., J.F. T.D.F.); Department of Neurology, Hôpital Civil Marie Curie, Charleroi, Belgium (A.D., F.B.); Department of Neuroradiology, University Hospital of Limoges, Université de Limoges, Limoges, France (G.F., A.R., S. 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Lower Extremity Extracorporeal Distal Revascularization in a Swine Model of Prolonged Extremity Ischemia.
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Background: Acute arterial occlusion of the lower extremity is a time-dependent emergency that requires prompt revascularization. Lower extremity extracorporeal distal revascularization (LEEDR) is a technique that can be initiated bedside when definitive therapy is delayed. The aim of this study is to evaluate this technique in a swine model of prolonged extremity ischemia.
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Department of Neurology, The Hague Medical Center, The Hague, Netherlands.
Background: Clinical trials of neuroprotection in acute ischemic stroke (AIS) have provided disappointing results. Reperfusion may be a necessary condition for positive effects of neuroprotective treatments. This systematic review provides an overview of efficacy of neuroprotective agents in combination with reperfusion therapy in AIS.
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Department of Vascular and Internal Diseases, Nicolaus Copernicus University in Toruń, Ludwik Rydygier Collegium Medicum, Bydgoszcz, Poland. Electronic address:
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