Related Experiment Videos
Mild intraoperative hypothermia reduces production of reactive oxygen intermediates by polymorphonuclear leukocytes
C Wenisch1, E Narzt, D I Sessler
1Department of Infectious Diseases, University of Vienna, Austria.
Abstract:
Mild hypothermia directly impairs numerous immune functions in vitro. However, the in vivo effects of mild hypothermia on neutrophil phagocytosis and oxidative killing remain unknown. We tested the hypothesis that mild intraoperative hypothermia decreases neutrophil phagocytic capacity and generation of reactive oxygen intermediates (a measure of oxidative killing). Additionally, we evaluated the effects of in vitro temperature manipulations on each function. Thermal management was randomly assigned in 10 surgical patients, causing intraoperative core temperatures to range from 33 to 37 degrees C. Production of reactive oxygen intermediates and neutrophil phagocytosis were evaluated using flow cytometry at ambient temperature. Phagocytic capacity was assessed by uptake of fluorescein isothiocyanate-labeled Escherichia coli. Reactive oxygen production was estimated by the intracellular conversion of dihydrorhodamine 123 to rhodamine 123. Blood samples were obtained preoperatively, 1 h after surgery started, and 2 h postoperatively. Blood was also obtained from 10 matched control subjects and tested at 32, 37, and 40 degrees C. Neutrophil oxidative and phagocytic capacities were significantly reduced intraoperatively, compared with preoperative and postoperative values. Intraoperative production of reactive oxygen species was linearly related to core temperature. In contrast, there was no correlation between core temperature and phagocytic activity. In vitro production of reactive oxygen intermediates increased sixfold from 32 to 40 degrees C. In vitro phagocytic capacity increased fourfold in this temperature range. Production of oxidative intermediates was most closely related to intraoperative core temperature, decreasing nearly fourfold over a 4 degree C range. This in vitro temperature dependence was matched in vitro. Impaired neutrophil oxidative killing may contribute to the observed hypothermia-induced reduction in resistance to infection.
Insights
Mild intraoperative hypothermia significantly reduces neutrophil oxidative killing, a key immune function. This impairment, linked to core body temperature, may increase infection risk in surgical patients.
Area of Science:
- Immunology
- Surgical Research
- Physiology
Background:
- Mild hypothermia is known to impair immune functions in laboratory settings.
- The in vivo impact of mild hypothermia on neutrophil phagocytosis and oxidative killing during surgery is not well understood.
Purpose of the Study:
- To investigate the in vivo effects of mild intraoperative hypothermia on neutrophil phagocytic capacity and reactive oxygen intermediate production.
- To evaluate the influence of in vitro temperature changes on these neutrophil functions.
Main Methods:
- Ten surgical patients underwent randomized thermal management, with core temperatures ranging from 33-37°C.
- Neutrophil phagocytosis (E. coli uptake) and reactive oxygen intermediate production (dihydrorhodamine 123 conversion) were assessed via flow cytometry.
- Blood samples from 10 control subjects were tested at 32°C, 37°C, and 40°C in vitro.
Main Results:
- Intraoperative neutrophil oxidative and phagocytic capacities were significantly reduced compared to pre- and post-operative levels.
- Reactive oxygen species production showed a linear relationship with core temperature, decreasing significantly with lower temperatures.
- In vitro studies confirmed a strong temperature dependence for both oxidative killing and phagocytosis, with functions increasing substantially from 32°C to 40°C.
Conclusions:
- Mild intraoperative hypothermia impairs neutrophil oxidative killing in vivo.
- The observed reduction in neutrophil function may contribute to increased susceptibility to infection following surgery.
- Temperature management during surgery is critical for maintaining immune competence.