Centrally and locally mediated thermoregulatory responses alter subcutaneous oxygen tension.

Mild perianesthetic hypothermia decreases resistance to infections. Decreased resistance likely results in part from direct immune inhibition. However, decreased tissue oxygen partial pressure also decreases resistance to infection by impairing oxidative killing by neutrophils and collagen deposition. Thermoregulatory vasoconstriction decreases skin blood flow and may also decrease subcutaneous tissue oxygen tension. Accordingly, we determined the influence of centrally and locally mediated thermoregulatory vasomotion on subcutaneous oxygen tension. We also compared subcutaneous oxygen tension to other potential markers of tissue perfusion: laser Doppler flowmetry and transcutaneous oxygen tension. Arterial oxygen tension was maintained near 325 mm Hg in five volunteers. Control subcutaneous oxygen tension values were recorded after 1 hour of euthermia (no sweating or vasoconstriction). Volunteers were then cooled with a circulating-water mattress positioned under the trunk and legs. After 1.5 hours of cooling sufficient to produce shivering, the right upper arm was covered for 1 hour with a small circulating water blanket set to 40 degrees C while systemic cooling continued. The volunteers were then systematically warmed to produce sweating, and the right arm was locally cooled. There was no correlation among laser Doppler flowmetry, transcutaneous oxygen tension, and subcutaneous oxygen tension. Systemic cooling significantly decreased subcutaneous oxygen tension, but subcutaneous oxygen tension in the right arm returned to control values during local heating. Systemic warming significantly increased subcutaneous oxygen tension, and 1 hour of local cooling failed to fully reverse the increase. These data indicate that thermoregulatory vasoconstriction significantly decreases tissue oxygen availability. Decreased subcutaneous oxygen tension may be one mechanism by which mild perianesthetic hypothermia facilitates development of surgical wound infections.

Mild hypothermia during isoflurane anesthesia decreases resistance to E. coli dermal infection in guinea pigs.

Small changes in core temperature profoundly alter cutaneous blood flow, a major factor influencing resistance to wound infection. Furthermore, when measured in vitro, various immune functions are temperature dependent in the physiological range. Accordingly, we tested the hypothesis that mild hypothermia impairs and mild hyperthermia improves resistance to dermal infections. Thirty-two guinea pigs were anesthetized for 6 h using 1.5% (1.25 MAC) inspired isoflurane. Their core temperatures were maintained at either 39 degrees C (normal for guinea pigs, n = 11), 36 degrees C (n = 12), or 41 degrees C (n = 9). One h after induction of anesthesia, 2 x 10(8) E. coli were injected intradermally with a 26-g needle at eight sites on each animal's back. Core temperatures were not controlled after recovery from anesthesia, and animals in each group were maintained in the same environment. Twenty-four h after injection, the area of induration surrounding each injection site was measured. This is a standard test of resistance to wound infection. Values were compared using one-way ANOVA and Scheffé's S tests. Results are presented as means +/- standard deviations; differences were considered significant when P < 0.05. Areas of inflammation on the hypothermic animals were significantly larger (48 +/- 10 mm2) than those on normothermic (36 +/- 10 mm2) or hyperthermic (37 +/- 6 mm2) animals. These data suggest that mild hypothermia during anesthesia significantly impairs resistance to dermal infection. In contrast, mild hyperthermia does not appear to be protective.

Mild hypothermia during halothane-induced anesthesia decreases resistance to Staphylococcus aureus dermal infection in guinea pigs.

Because various immune functions are impaired at temperatures only 1 degrees to 3 degrees C less than normal, we tested the hypothesis that mild hypothermia during anesthesia impairs resistance to dermal infections. Guinea pigs were anesthetized for 6 hours with 1% inspired halothane. Their core temperatures were maintained at either 39 degrees C (normal for guinea pigs, n = 12) or 36 degrees C (n = 12). Two hours after induction of anesthesia, three doses each of Staphylococcus aureus (10(8), 10(7), and 10(6) organisms) were injected intradermally at nine sites on each animal's back. Core temperatures were not controlled after recovery from the anesthetic, and animals in each group were maintained in the same environment. Four days after anesthesia, each injection site was excised to obtain a count of viable bacteria. Subcutaneous oxygen partial pressure values, averaged over time, were 53 +/- 3 mm Hg (mean +/- SEM) in the hypothermic group and 62 +/- 4 mm Hg in the normothermic group (p = 0.06). Capillary perfusion, as assessed by laser Doppler flowmetry, was comparable in the two groups. One day after injection of 10(8) bacteria, the area of induration was 89 +/- 11 mm(2) in the hypothermic group but only 61 +/- 6 mm(2) in the normothermic group (p < 0.05). On postanesthetic day 4, the area of induration was 72 +/- 6 and 59 +/- 6 mm(2) in the hypothermic and normothermic groups, respectively (p > 0.05). After inoculation with 10(8) bacteria, the fraction recovered was 1.0 +/- 0.2 in the hypothermic groups and 0.6 +/- 0.2 in the normothermic group (p < 0.05). After inoculation with 10(7) and 10(6) bacteria, the fraction recovered was less than 0.2, and no difference was found between the hypothermic and normothermic animals. Thus mild hypothermia during halothane-induced anesthesia slightly impairs resistance to dermal infection.