| Measurement of Ventilation-Perfusion Ratio Using Multiple Inert Gas Elimination Technique in the Endotoxin-Induced Septic Rabbit. |
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Yong Bo Jeong, Ji Yeon Sim, Seung Ill Ha, In Cheol Choi |
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Department of Anesthesiology, University of Ulsan, College of Medicine, Seoul, Korea. |
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| Abstract |
BACKGROUND
Endotoxin is a complex lipopolysaccharide molecule situated within the outer membrane of Gram-negative bacteria. Sepsis and acute respiratory failure (ARDS) can be induced by endotoxin. In order to introduce and develop the experimental model of ARDS in sepsis, we induced sepsis with the endotoxin and investigated the change of respiratory pathophysiology during sepsis using a multiple inert gas elimination technique (MIGET).
METHODS
Ten New Zealand white rabbits were anesthetized and ventilated with a Harvard apparatus. In 5 rabbits, 2 mg/kg of lipopolysaccaride from E. coli was infused intravenously for 30 min (Toxin group). At 1, 2, 3, and 4 hours after endotoxin infusion, arterial blood gas, and hemodynamic profiles were checked. To perform the MIGET, six inert gases (SF6, krypton, desflurane, enflurane, diethyl ether, acetone) of widely varying solubility were infused peripherally and the excretion and retention data was determined from measurements of inert gas tensions in pulmonary arterial, systemic arterial blood samples and mixd expiratory gas sampling of pre and post septicemia using gas chromatography. We transformed and analysed the data into a V/Q distribution curve to find out the change of V/Q distribution curve. After the experiments, the animals were dissected and the lungs were extracted for wet/dry weight ratio (WW/DW) and microscopic examination.
RESULTS
In the Toxin group, the pulmonary arterial pressures were increased and arterial oxygen tensions were decreased after the endotoxin infusion. The lung WW/DW were increased and inflammatory findings were seen in microscopic examination. In the MIGET, shunt, deadspace and log SDQ were increased in the toxin group, though there were wide V/Q distributions in the control group.
CONCLUSIONS
We developed a successful endotoxin induced septic animal model, V/Q distribution curve and data using MIGET. The accomplishment of the experiment will not only allow us to better understand pulmonary pathophysiology of endotoxin induced sepsis using MIGET, but it will also contribute to other pulmonary physiology experiments associated with sepsis. |
| Key Words:
Infection: sepsis; Pharmacology: endotoxin; Ventilation: MIGET, V/Q distribution |
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