Abstract
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.
Original language | English (US) |
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Pages (from-to) | 2018-2024 |
Number of pages | 7 |
Journal | Journal of applied physiology |
Volume | 85 |
Issue number | 6 |
DOIs | |
State | Published - Dec 1998 |
Keywords
- Cardiac contractility
- Endotoxin
- Hemodynamics
- Left ventricular function
- Nitric oxide inhalation
ASJC Scopus subject areas
- Physiology
- Physiology (medical)