Circulation
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We have shown that acadesine (AICAr: 5-amino-4-imidazole carboxamide riboside) improves the early recovery of function of the ischemic and reperfused rat heart. In the present studies we used the transplanted rat heart, with reperfusion for up to 24 hours, to assess whether the beneficial effect of acadesine is a transient or a sustained phenomenon (i.e., to determine whether the drug improves the extent of recovery or only the rate). ⋯ Acadesine can afford sustained functional protection against injury during extended periods of ischemia and reperfusion. We present evidence that the beneficial effect of acadesine may be mediated by two different components, with one operative during ischemia and early reperfusion and the other acting later in the reperfusion period.
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To examine whether an extremely enlarged left atrium (giant left atrium) obstructs the venous return from the inferior vena cava (IVC), the velocity of IVC flow was measured at its junction with the right atrium (IVC orifice) in patients with mitral stenosis by use of color and pulsed-wave Doppler echocardiography from a right parasternal longitudinal plane. ⋯ A giant left atrium in patients with mitral stenosis obstructs venous return at the IVC orifice by marked displacement of the atrial septum toward the right atrium.
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When used to reverse the anticoagulant effect of heparin, protamine sulfate often causes vasodilation that can lead to systemic hypotension. Protamine is rich in the basic amino acid arginine, which is the precursor of endothelial cell synthesis of nitric oxide, and nitric oxide is the active component of endothelium-derived relaxing factor (EDRF). ⋯ This study demonstrates that protamine stimulates the release of EDRF from arterial endothelium, and that endothelium-dependent vasodilation may be an important cause of systemic hypotension during protamine infusion.
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Two sequential biphasic shocks delivered over separate lead configurations markedly improve defibrillation efficacy compared with a single shock alone. We investigated the effect of varying the intershock interval between sequential biphasic shocks on defibrillation. ⋯ The optimal intershock interval between two sequential biphasic shocks is either less than or equal to 10 msec or greater than or equal to 75 and less than or equal to 125 msec. The marked rise in the DFT at a shock separation of 50 msec, requiring more energy than that for the first shock alone, suggests that the second shock at this time delay is likely to reinduce fibrillation after it is halted by the first shock until the second shock is strong enough to defibrillate independently of the first shock.