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1 US Army Institute of Surgical Research, and 2 Brooke Army Medical Center, Fort Sam Houston, Texas 78234; 3 Department of Surgery, University of Florida, Gainesville, Florida 32610; and 4 Department of Surgery, Rhode Island Hospital, Providence, Rhode Island 02903
We evaluated the
effect of long-term inhalation of nitric oxide (NO) on cardiac
contractility after endotoxemia by using the end-systolic
elastance of the left ventricle (LV) as a load-independent contractility index. Chronic instrumentation in 12 pigs included implantation of two pairs of endocardial dimension transducers to
measure LV volume and a micromanometer to measure LV pressure. One week
later, the animals were divided into a control group (n = 6) or a NO group
(n = 6). All animals received
intravenous Escherichia coli
endotoxin (10 µg · kg
1 · h
1)
and equivalent lactated Ringer solution. NO inhalation (20 parts/million) was begun 30 min after the initiation of endotoxemia and
was continued for 24 h. In both groups, tachycardia, pulmonary
hypertension, and systemic hyperdynamic changes were noted. The
end-systolic elastance in the control group was significantly decreased
beyond 7 h. NO inhalation maintained the end-systolic elastance at
baseline levels and prevented its impairment. These findings indicate
that NO exerts a protective effect on LV contractility in this model of endotoxemia.
left ventricular function; cardiac contractility; nitric oxide inhalation; endotoxin; hemodynamics
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