Little is known of the
endorphins' role in
sepsis-induced respiratory distress and
naloxone's effect as a treatment of it. Thirteen piglets were infused with live Escherichia coli at a rate of 2 to 10 X 10(8) colony-forming units per hour for six hours or until death and were divided into two groups: the septic control group (n = 8), and the
naloxone-treated group (n = 5), which received 8 mg/kg/h of
naloxone by continuous infusion. Hemodynamic parameters, the intrapulmonary shunt fraction (QS/QT), physiologic dead space (VD/VT), minute ventilation, and blood gas levels were measured. Lung lymph flow was obtained by cannulating the right lymphatic duct. The extravascular lung water weight was also measured. The results showed a significant reduction of QS/QT, VD/VT, and arterial
carbon dioxide pressure at one hour and a significant increase of arterial
carbon dioxide pressure and minute ventilation at 1, 3, and 4 hours in the
naloxone-treated group, compared with the untreated septic group. None of the piglets in the
naloxone-treated group developed
ventilatory depression, while 75% of those in the untreated septic group did. Among the latter piglets, three died of
apnea within one hour. These beneficial effects of
naloxone are likely related to its action on the central and peripheral respiratory regulatory mechanisms. A transient protection of the cardiac output and relatively decreased extravascular lung water with
naloxone treatment may also, in part, improve the ventilation-perfusion maldistribution and secondarily reduce QS/QT and VD/VT. We conclude that
endorphins play a role in septic
ventilatory depression and that
naloxone is effective in ameliorating it.