Susceptibility of human and porcine neutrophils to hypothermia in vitro.

Hypothermia may contribute to serious life-threatening infections. An experimental model has been established in pigs in order to study the effects of hypothermia on host bacterial defenses. The function of blood neutrophils from pigs and humans was examined in vitro at 37 and 29 degrees C. Bacterial killing of Staphylococcus aureus 502A by human neutrophils after 90 and 180 min incubation at 29 degrees C was reduced to 76 +/- 6% and 83 +/- 7% of killing at 37 degrees C. Porcine neutrophil killing was similarly reduced at 90 min (72 +/- 9%) and remained significantly impaired after 180 min (52 +/- 11%). Phagocytosis of ORO-DP-LPS particles by human neutrophils after 5 min at 29 degrees C was 40 +/- 5% of that at 37 degrees C and only 55 +/- 7% after 15 min by which time maximum phagocytosis had occurred at 37 degrees C. Porcine neutrophils ingested significantly less ORO (68 +/- 8%) after 5 min at 29 degrees C and reached normal values by 15 min. Stimulation of hexose monophosphate pathway in human neutrophils for 20 min at 29 degrees C was only 13 +/- 5% of that at 37 degrees C and required 2 h of stimulation to reach normal values. Porcine cells were reduced to 74 +/- 9% after 20 min incubation and reached normal values by 30 min. Directed neutrophil migration as assessed under agarose was impaired for both human (39 +/- 6%) and porcine (20 +/- 4%) neutrophils at 29 degrees C compared to 37 degrees C.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of hypothermia on neutrophil function in vitro.

Hypothermia may be associated with compromised host defenses and serious bacterial infections in man. We have examined the effects of moderate hypothermia (29 degrees C) on neutrophil function in vitro. At 29 degrees C, neutrophil phagocytosis of Staphylococcus aureus was impaired. In contrast, neutrophil killing of Streptococcus faecalis was most affected by hypothermia. Phagocytosis, as measured by neutrophil ingestion of opsonized oil-red-O-particles, was reduced at 29 degrees C over the 15 min of observation. Neutrophil metabolism linked to bactericidal pathways dependent on oxidative metabolism was reduced at 29 degrees C. Hexose monophosphate pathway (HMP) activity in neutrophils early after stimulation with latex particles was reduced. After 2 hr HMP activity was similar at 29 degrees C and 37 degrees C. Neotetrazolium dye reduction was reduced early after latex stimulation of neutrophils and after 30 min it was similar to cells at 37 degrees C. Leukocyte migration under agarose to bacterial-derived and formyl-methionyl-phenylalanine chemotactic factors was reduced by 50% and 70%, respectively. Migration to serum-derived chemotactic factor was reduced by only 20%. When cells were cooled to 29 degrees C for 30 to 90 min and rewarmed, neutrophil function was normal. These effects of hypothermia on neutrophil function may explain, in part, the increased incidence of serious and frequently fatal bacterial infections in man.

Effects of incubation at various 'room' temperatures on the sensitivity and specificity of Microstix-3.

The feasibility of room temperature incubation of Microstix-3 specimens to detect urinary tract infection was studied. This procedure, if successful, would allow home monitoring of patients and eliminate the need for an incubator. Four Microstix-3 strips were dipped into each of 1,241 urine specimens and incubated at 18, 22, 27 or 37 degree C. Results after incubation for 24 h at 27 degree C and after 48 h at 22 degree C were comparable to those after incubation for 18-24 h at 37 degree C. However, even after 72 h, incubation at 18 degree C did not produce results comparable to those obtained at 37 degree C. It appears that the incubator can be successfully eliminated at the higher temperatures tested if the limits of time outlined are observed.