Key result
EDRF inhibition causes a ~37% drop in cardiac output during massive sympathetic activation in rabbits.
Why the study?
The role of endothelium-derived relaxing factor (EDRF) in modulating pulmonary and systemic hemodynamic responses and left ventricular dysfunction during massive sympathetic nervous system activation was unclear.
Does EDRF inhibition with L-NNA modulate hemodynamic responses, LV dysfunction, and pulmonary edema during massive sympathetic activation in rabbits?
Comparison
EDRF inhibitor (N omega-nitro-L-arginine) pretreatment vs no pretreatment
Design
Preclinical experimental study
Authors
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EDRF inhibition may exacerbate LV dysfunction during sympathetic activation in this model; leaves open relevance to human neurogenic stress or pulmonary edema syndromes.
Does EDRF inhibition with L-NNA modulate hemodynamic responses, LV dysfunction, and pulmonary edema during massive sympathetic activation in rabbits?
Absolute Event Rate: 37% vs 8%
Inhibition of EDRF during massive sympathetic activation exacerbates LV dysfunction and increases pulmonary vascular resistance, leading to right ventricular failure which paradoxically protects against pulmonary edema.
Pilati et al. (1995) studied Massive sympathetic nervous system activation (n=27). N omega-nitro-L-arginine (L-NNA) vs. Untreated was evaluated on Decrease in cardiac output. Inhibition of EDRF with L-NNA during massive sympathetic activation in rabbits led to a 37% decrease in cardiac output compared to an 8% decrease in untreated controls.
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