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Biomedical subjects

D I Sessler

Publications and source records attributed to D I Sessler.

At least 145 records · Page 8Linked to original sources
PubMed1997

Meperidine decreases the shivering threshold twice as much as the vasoconstriction threshold.

BACKGROUND: Meperidine administration is a more effective treatment for shivering than equianalgesic doses of other opioids. However, it remains unknown whether meperidine also profoundly impairs other thermoregulatory responses, such as sweating or vasoconstriction. Proportional inhibition of vasoconstriction and shivering suggests that the drug acts much like alfentanil and anesthetics but possesses greater thermoregulatory than analgesic potency. In contrast, disproportionate inhibition would imply a special antishivering mechanism. Accordingly, the authors tested the hypothesis that meperidine administration produces a far greater concentration-dependent reduction in the shivering than vasoconstriction threshold. METHODS: Nine volunteers were each studied on three days: 1) control (no opioid); 2) a target total plasma meperidine concentration of 0.6 microgram/ml (40 mg/h); and 3) a target concentration of 1.8 micrograms/ml (120 mg/h). Each day, skin and core temperatures were increased to provoke sweating and then subsequently reduced to elicit vasoconstriction and shivering. Core-temperature thresholds (at a designated skin temperature of 34 degrees C) were computed using established linear cutaneous contributions to control sweating (10%) and vasoconstriction and shivering (20%). The dose-dependent effects of unbound meperidine on thermoregulatory response thresholds was then determined using linear regression. Results are presented as means +/- SDs. RESULTS: The unbound meperidine fraction was approximately 35%. Meperidine administration slightly increased the sweating threshold (0.5 +/- 0.8 degree C.microgram-1.ml; r2 = 0.51 +/- 0.37) and markedly decreased the vasoconstriction threshold (-3.3 +/- 1.5 degrees C.microgram-1.ml; r2 = 0.92 +/- 0.08). However, meperidine reduced the shivering threshold nearly twice as much as the vasoconstriction threshold (-6.1 +/- 3.0 degrees C.microgram-1.ml; r2 = 0.97 +/- 0.05; P = 0.001). CONCLUSIONS: The special antishivering efficacy of meperidine results at least in part from an uncharacteristically large reduction in the shivering threshold rather than from exaggerated generalized thermoregulatory inhibition. This pattern of thermoregulatory impairment differs from that produced by alfentanil, clonidine, propofol, and the volatile anesthetics, all which reduce the vasoconstriction and shivering thresholds comparably.

Alfentanil↗
PubMed1997

A rapid increase in foot tissue temperature predicts cardiovascular collapse during anaphylactic and anaphylactoid reactions.

BACKGROUND: Cardiovascular collapse during anaphylactic and anaphylactoid reactions results from release of histamine and other vasoactive substances. Intense arteriolar vasodilation associated with severe allergic reactions is likely to increase convective transfer of heat and peripheral tissue temperature, and finally to provoke cardiovascular collapse. Therefore the authors tested the hypothesis that during anaphylactic and anaphylactoid reactions, an acute increase in peripheral tissue temperature precedes cardiovascular collapse and that the magnitude of the increase correlates with the severity of the reaction. METHODS: During a 13-yr period, approximately 120,000 patients were screened for clinical evidence of intraoperative anaphylactic and anaphylactoid reactions. Core temperature was measured in the distal esophagus, and "deep" foot tissue temperature was measured on the sole of one foot in all these patients. Otherwise unexplained cardiovascular collapse accompanied by bronchospasm and/or cutaneous signs such as urticaria, flushing, or angioedema occurred in 32 patients who were entered into a prospective diagnostic protocol. Among these, 15 met laboratory criteria for anaphylactic or anaphylactoid reactions. Anaphylaxis was confirmed in nine of them by a positive skin test to the suspected agent, the in vitro leukocyte histamine-release test, or the Praunitz-Küstner test. Reactions were considered anaphylactoid in six others when laboratory evidence did not support anaphylaxis, but plasma histamine or tryptase concentrations were much greater during episodes than 6 weeks later. RESULTS: Development of anaphylactic and anaphylactoid reactions followed a characteristic pattern: (1) Foot temperature, which was initially 3.3 +/- 1.7 degrees C less than core temperature, increased to within 0.3 degrees C of core temperature 3.2 +/- 1.4 min after drug administration; (2) onset of cardiovascular collapse ensued 1.8 +/- 0.8 min later; and (3) core temperature increased from 34.7 +/- 1.0 degrees C to peak values 37.1 +/- 0.6 degrees C 13 +/- 5 min after drug administration. The most severe reactions were associated with shorter times to comparable core and foot temperatures, faster onset of cardiovascular collapse, and higher maximum core temperatures. CONCLUSIONS: The normal core-to-peripheral tissue temperature gradient was obliterated several minutes before hemodynamic consequences associated with anaphylactic and anaphylactoid reactions. Further, a rapid increase in deep foot temperature and maximum core temperature correlated with clinical severity.

Adolescent↗
PubMed1997

Dexmedetomidine does not alter the sweating threshold, but comparably and linearly decreases the vasoconstriction and shivering thresholds.

BACKGROUND: Clonidine decreases the vasoconstriction and shivering thresholds. It thus seems likely that the alpha2 agonist dexmedetomidine will also impair control of body temperature. Accordingly, the authors evaluated the dose-dependent effects of dexmedetomidine on the sweating, vasoconstriction, and shivering thresholds. They also measured the effects of dexmedetomidine on heart rate, blood pressures, and plasma catecholamine concentrations. METHODS: Nine male volunteers participated in this randomized, double-blind, cross-over protocol. The study drug was administered by computer-controlled infusion, targeting plasma dexmedetomidine concentrations of 0.0, 0.3, and 0.6 ng/ml. Each day, skin and core temperatures were increased to provoke sweating and then subsequently reduced to elicit vasoconstriction and shivering. Core-temperature thresholds were computed using established linear cutaneous contributions to control of sweating, vasoconstriction, and shivering. The dose-dependent effects of dexmedetomidine on thermoregulatory response thresholds were then determined using linear regression. Heart rate, arterial blood pressures, and plasma catecholamine concentrations were determined at baseline and at each threshold. RESULTS: Neither dexmedetomidine concentration increased the sweating threshold from control values. In contrast, dexmedetomidine administration reduced the vasoconstriction threshold by 1.61 +/- 0.80 degrees C x ng(-1) x ml (mean +/- SD) and the shivering threshold by 2.40 +/- 0.90 degrees C x ng(-1) x ml. Hemodynamic responses and catecholamine concentrations were reduced from baseline values, but they did not differ at the two tested dexmedetomidine doses. CONCLUSIONS: Dexmedetomidine markedly increased the range of temperatures not triggering thermoregulatory defenses. The drug is thus likely to promote hypothermia in a typical hospital environment; it is also likely to prove an effective treatment for shivering.

Adrenergic alpha-Agonists↗
PubMed1997

Alfentanil blocks reflex pupillary dilation in response to noxious stimulation but does not diminish the light reflex.

BACKGROUND: Estimation of the mu-agonist opioid effect in anesthetized and paralyzed patients is often imprecise and can be obscured by concomitant administration of drugs that affect the sympathetic nervous system, such as beta-adrenergic blocking agents. As an alternative to hemodynamic measures of opioid effect, the authors tested the hypothesis that the pupillary light reflex or pupillary reflex dilation correlated with alfentanil concentrations during isoflurane anesthesia. METHODS: Six volunteers were anesthetized on 4 days with 0.8% isoflurane. Alfentanil was administered intravenously to target total plasma concentrations of 0, 25, 50, and 100 ng/ml. A 5-s tetanic electrical stimulus was applied to the skin. Pupil size and the pupillary light reflex were recorded before and after alfentanil administration, and before and for 8 min after the stimulus. RESULTS: Alfentanil exponentially impaired reflex pupillary dilation, decreasing the maximum response amplitude from 5 mm at 0 ng/ml, to 2.3 mm at 25 ng/ml, to 1.0 mm at 50 ng/ml, and finally to 0.2 mm at 100 ng/ml. In contrast, only the highest concentration of alfentanil depressed the dilation of the pupil in the first 2 s after the stimulus. Alfentanil administration had no effect on the pupillary light reflex. CONCLUSIONS: Dilation of the pupil in response to a noxious stimulus is a measure of opioid effect in isoflurane-anesthetized volunteers. In contrast, the pupillary light reflex is unaffected by alfentanil during isoflurane anesthesia. These data suggest that stimulus-induced pupillary dilation may be used to evaluate the analgesic component of a combined volatile and opioid anesthetic.

Adult↗
PubMed1997

Spinal anesthesia speeds active postoperative rewarming.

BACKGROUND: Redistribution of body heat decreases core temperature more during general than regional anesthesia. However, the combination of anesthetic- and sedative-induced inhibition may prevent effective upper-body thermoregulatory responses even during regional anesthesia. The extent to which each type of anesthesia promotes hypothermia thus remains controversial. Accordingly, the authors evaluated intraoperative core hypothermia in patients assigned to receive spinal or general anesthesia. They also tested the hypothesis that the efficacy of active postoperative warming is augmented when spinal anesthesia maintains vasodilation. METHODS: Patients undergoing lower abdominal and leg surgery were randomly assigned to receive general anesthesia (isoflurane and nitrous oxide; n = 20) or spinal anesthesia (bupivacaine; n = 20). Fluids were warmed to 37 degrees C and patients were covered with surgical drapes. However, no other active warming was applied during operation. Ambient temperatures were maintained near 20 degrees C. After operation, patients were warmed with a full-length, forced-air cover set to 43 degrees C. Shivering, when observed, was treated with intravenous meperidine. RESULTS: The mean spinal analgesia level, which was at the sixth thoracic level during surgery, remained at the T12 dermatome after 90 min after operation. Core temperatures did not differ significantly during surgery and decreased to 34.4 +/- 0.5 degrees C and 34.1 +/- 0.4 degrees C, respectively, in patients given spinal and general anesthesia. After operation, however, core temperatures increased significantly faster (1.2 +/- 0.1 degrees C/h vs. 0.7 +/- 0.2 degrees C/h, mean +/- SD; P < 0.001) in patients given spinal anesthesia. Consequently, patients given spinal anesthesia required less time to rewarm to 36.5 degrees C (122 +/- 28 min vs. 199 +/- 28 min; P < 0.001). CONCLUSIONS: Comparable intraoperative hypothermia during general and regional anesthesia presumably resulted because the combination of spinal anesthesia and meperidine administration obliterated effective peripheral and central thermoregulatory control. Vasodilation increased the rate of core rewarming in patients after operation with residual lower-body sympathetic blocks, suggesting that vasoconstriction decreased peripheral-to-core heat transfer after general anesthesia.

Adult↗
PubMed1997

Efficacy of intraoperative cooling methods.

BACKGROUND: Patients may require perioperative cooling for a variety of reasons including treatment of a malignant hyperthermia crisis and induction of therapeutic hypothermia for neurosurgery. The authors compared heat transfer and core cooling rates with five cooling methods. METHODS: Six healthy volunteers were anesthetized with desflurane and nitrous oxide. The cooling methods were 1) circulating water (5 degrees C, full-length mattress and cover), 2) forced air (10 degrees C, full-length cover), 3) gastric lavage (500 ml iced water every 10 min), 4) bladder lavage (300 ml iced Ringer's solution every 10 min), and 5) ice-water immersion. Each method was applied for 40 min or until the volunteers' core temperatures approached 34 degrees C. The volunteers were rewarmed to normothermia between treatments. Core cooling rates were evaluated using linear regression. RESULTS: The first volunteer developed abdominal cramping and diarrhea after gastric lavage. Consequently, the technique was not again attempted. Bladder lavage increased heat loss approximately 10 W and decreased core temperature 0.8 +/- 0.3 degrees C/h (r2 = 0.99 +/- 0.002; means +/- SD). Forced-air and circulating-water cooling comparably increased heat flux, approximately 170 W. Consequently, core cooling rates were similar during the two treatments at 1.7 +/- 0.5 degrees C/h (r2 = 0.99 +/- 0.001) and 1.6 +/- 1.1 degrees C/h (r2 = 0.98 +/- 0.02), respectively. Immersion in an ice water slurry increased heat loss approximately 600-800 W and decreased core temperature 9.7 +/- 4.4 degrees C/h (r2 = 0.98 +/- 0.01). Immersion cooling was associated with an afterdrop of approximately 2 degrees C. CONCLUSIONS: Bladder lavage provided only trivial cooling and gastric lavage provoked complications. Forced-air and circulating-water cooling transferred relatively little heat but are noninvasive and easy to implement. Forced-air or circulating-water cooling, perhaps combined with intravenous administration of refrigerated fluids, may be sufficient in some patients. When noninvasive methods prove insufficient for rapid cooling, ice-water immersion or peritoneal lavage probably should be the next lines of defense.

Adult↗
PubMed1997

Mild intraoperative hypothermia prolongs postanesthetic recovery.

BACKGROUND: Intraoperative hypothermia is common and persists for several hours after surgery. Hypothermia may prolong immediate recovery by augmenting anesthetic potency, delaying drug metabolism, producing hemodynamic instability, or depressing cognitive function. Accordingly, the authors tested the hypothesis that intraoperative hypothermia prolongs postoperative recovery. METHODS: Patients undergoing elective major abdominal surgery (n = 150) were anesthetized with isoflurane, nitrous oxide, and fentanyl. They were randomly assigned to routine thermal management (hypothermia) or extra warming (normothermia). Postoperative surgical pain was treated with patient-controlled analgesia. Fitness for discharge from the postanesthesia care unit was evaluated at 20-min intervals by investigators blinded to group assignment and postoperative core temperatures. Scoring was based on a modification of a previously published system that included activity, ventilation, consciousness, and hemodynamic responses. Patients were considered fit for discharge when they sustained a score of 80% (13 points) for at least two consecutive measurement periods. RESULTS: Morphometric characteristics and anesthetic management were similar in each group. Final intraoperative core temperatures differed by approximately 2 degrees C: 34.8 +/- 0.6 versus 36.7 +/- 0.6 degrees C (mean +/- SD, P < 0.001). Postoperative pain scores and postoperative use of patient-controlled opioid were similar. Hypothermic patients required approximately 40 min longer (94 +/- 65 vs. 53 +/- 36 min) to reach fitness for discharge, even when return to normothermia was not a criterion (P < 0.001). Duration of recovery in the two groups differed by approximately 90 min when a core temperature >36 degrees C was also required (P < 0.001). CONCLUSION: Maintaining core normothermia decreases the duration of postanesthetic recovery and may, therefore, reduce costs of care.

Abdomen↗
PubMed1997

Perioperative fever.

Unlike normal thermoregulatory control, which is largely neuronally mediated, fever is activated by circulating pyrogens. Pyrogens are triggered by either infectious or non-infectious etiologies, all of which may be present in patients undergoing ambulatory surgery. Fever is a regulated elevation in the setpoint temperature for all thermoregulatory responses (warm and cold defenses). To increase core temperature according to the newly elevated setpoint, cold defenses such as vasoconstriction and shivering are activated. In contrast, anesthesia widens the interthreshold range, thus resulting in hypothermia. As a result, general anesthesia impairs the febrile response to pyrogenic stimulation. However, the precise nature of the interaction between fever and anesthesia has yet to be determined. Postoperative fever continues to be a major problem. Wound infections are responsible for many such fevers, although numerous other etiologies contribute. Initial diagnosis should thus focus on determining the etiology of fever. Once that is established, treatment can focus on the specific cause.

Ambulatory Surgical Procedures↗
PubMed1996

Perioperative normothermia to reduce the incidence of surgical-wound infection and shorten hospitalization. Study of Wound Infection and Temperature Group.

BACKGROUND: Mild perioperative hypothermia, which is common during major surgery, may promote surgical-wound infection by triggering thermoregulatory vasoconstriction, which decreases subcutaneous oxygen tension. Reduced levels of oxygen in tissue impair oxidative killing by neutrophils and decrease the strength of the healing wound by reducing the deposition of collagen. Hypothermia also directly impairs immune function. We tested the hypothesis that hypothermia both increases susceptibility to surgical-wound infection and lengthens hospitalization. METHODS: Two hundred patients undergoing colorectal surgery were randomly assigned to routine intraoperative thermal care (the hypothermia group) or additional warming (the normothermia group). The patient's anesthetic care was standardized, and they were all given cefamandole and metronidazole. In a double-blind protocol, their wounds were evaluated daily until discharge from the hospital and in the clinic after two weeks; wounds containing culture-positive pus were considered infected. The patients' surgeons remained unaware of the patients' group assignments. RESULTS: The mean (+/- SD) final intraoperative core temperature was 34.7 +/- 0.6 degrees C in the hypothermia group and 36.6 +/- 0.5 degrees C in the normothermia group (P < 0.001) Surgical-wound infections were found in 18 of 96 patients assigned to hypothermia (19 percent) but in only 6 of 104 patients assigned to normothermia (6 percent, P = 0.009). The sutures were removed one day later in the patients assigned to hypothermia than in those assigned to normothermia (P = 0.002), and the duration of hospitalization was prolonged by 2.6 days (approximately 20 percent) in hypothermia group (P = 0.01). CONCLUSIONS: Hypothermia itself may delay healing and predispose patients to wound infections. Maintaining normothermia intraoperatively is likely to decrease the incidence of infectious complications in patients undergoing colorectal resection and to shorten their hospitalizations.

Adult↗
PubMed1996

Mild hypothermia increases blood loss and transfusion requirements during total hip arthroplasty.

BACKGROUND: In-vitro studies indicate that platelet function and the coagulation cascade are impaired by hypothermia. However, the extent to which perioperative hypothermia influences bleeding during surgery remains unknown. Accordingly, we tested the hypothesis that mild hypothermia increases blood loss and allogeneic transfusion requirements during hip arthroplasty. METHODS: Blood loss and transfusion requirements were evaluated in 60 patients undergoing primary, unilateral total hip arthroplasties who were randomly assigned to normothermia (final intraoperative core temperature 36.6 [0.4] degrees C) or mild hypothermia (35.0 [0.5] degrees C). Crystalloid, colloid, scavenged red cells, and allogeneic blood were administered by strict protocol. FINDINGS: Intra- and postoperative blood loss was significantly greater in the hypothermic patients: 2.2 (0.5) L vs 1.7 (0.3) L, p < 0.001). Eight units of allogeneic packed red cells were required in seven of the 30 hypothermic patients, whereas only one normothermic patient required a unit of allogeneic blood (p < 0.05 for administered volume). A typical decrease in core temperature in patients undergoing hip arthroplasty will thus augment blood loss by approximately 500 mL. INTERPRETATION: The maintenance of intraoperative normothermia reduces blood loss and allogeneic blood requirements in patients undergoing total hip arthroplasty.

Adult↗
PubMed1996

Forced air speeds rewarming in accidental hypothermia.

STUDY OBJECTIVE: To compare the rates of rewarming of forced-air and passive insulation as a treatment for accidental hypothermia. METHODS: We carried out a prospective, randomized clinical trial in two urban, university-affiliated emergency departments. Our subjects were 16 adult hypothermia victims with core temperatures less than 32 degrees C. A convective cover inflated with air at about 43 degrees C (forced-air group) or cotton blankets (control group) were applied until the patient's core temperature reached 35 degrees C. Members of both groups were given IV fluids warmed to 38 degrees C and warmed, humidified oxygen at 40 degrees C by inhalation. RESULTS: The mean +/- SD initial temperature was 28.8 degrees +/- 2.5 degrees C (range, 25.5 degrees C to 31.9 degrees C) in the patients who underwent forced-air rewarming and 29.8 degrees +/- 1.5 degrees C (range, 28.2 degrees C to 31.9 degrees C) in those given blankets. Core temperature increased about 1 degree C/hour faster in patients treated with forced-air rewarming (about 2.4 degrees C/hour) than in patients given only cotton blankets (about 1.4 degrees C/hour, P = .01). Core-temperature afterdrop was detected in neither group. CONCLUSION: Forced air accelerated the rate of rewarming without producing apparent complications in hypothermic patients.

Adult↗
PubMed1996

Thermoregulation and heart rate variability.

1. Heart rate variability is modulated by multiple control systems, including autonomic and hormonal systems. Long-term variability, i.e. the very low-frequency band of the power spectra, has been postulated to reflect thermoregulatory vasomotor control, based upon thermal entrainment experiments. However, the relationship between thermoregulatory responses (vasoconstriction and shivering) and heart rate variability has not been studied. 2. We performed two distinct protocols in a series of human subjects. In the first protocol, core temperature was reduced by intravenous infusion of cold saline, while skin temperature was unchanged. The second protocol involved skin-surface warming and cooling until shivering developed. Power spectral analysis was performed using a fast Fourier transformation, and the area in three distinct band-widths was determined. 3. Very low-frequency power (0.0039-0.04 Hz) increased significantly in response to core cooling, peripheral vasoconstriction and shivering, while both very low- and low- (0.04-0.15 Hz) frequency power increased in response to skin-surface cooling. Heart rate decreased during core cooling-induced vasoconstriction, suggesting a direct thermal response, and increased in relation to the metabolic demands associated with shivering. 4. Our results suggest that very low-frequency power is modulated by thermal stimuli which result in core hypothermia and thermoregulatory activity, while skin-surface cooling without core hypothermia does not selectively modulate this frequency band.

Adult↗
PubMed1996

Thermal response in acute porcine malignant hyperthermia.

This study was designed to evaluate how vital organ and skin-surface temperatures correlate with other clinical signs of a malignant hyperthermia (MH) episode. Six susceptible swine were anesthetized with thiopental and nitrous oxide and kept normothermic (approximately equal to 38 degrees C). After a 30-min control period, halothane (1 minimum alveolar anesthetic concentration) was administered, followed in 5 min by a bolus of succinylcholine (2 mg/kg intravenously). Monitoring included: 1) ETCO2; 2)PaO2, PaCO2, pHa; 3) cardiovascular function; 4) core temperatures (esophagus, pulmonary artery, and rectum); 5) organ temperatures (brain, kidney, liver, and four skeletal muscles); and 6) skin temperatures (forehead, neck, and axilla). Within 10 min after exposure to halothane and succinylcholine, all animals developed fulminant MH. Kidney, liver, and brain temperatures increased more rapidly than pulmonary artery temperature with the onset of MH. Temperatures significantly increased in the visceral organs prior to the detection of contractures within skeletal muscles. The masseter, longissimus dorsi, quadriceps, deltoid, and extensor digiti II intramuscular temperatures were 1-2 degrees C less than pulmonary artery and esophageal temperatures during the episodes, whereas those of the kidney, liver, and brain were the same or slightly greater. When it occurs, core hyperthermia during acute MH results largely from heat produced in central organs, not in skeletal muscle per se. In these swine, changes in axilla skin surface temperatures correlated well with core temperature trends, whereas those of the neck and forehead did not. Unless a skin-surface probe can be placed in close proximity to a major vessel, cutaneous temperatures should not be substituted for measurements at an appropriate core site.

Acute Disease↗
PubMed1996

Prior hypothermia attenuates malignant hyperthermia in susceptible swine.

This study was designed to determine the extent by which mild or moderate hyperthermia attenuates the triggering of malignant hypothermia (MH) induced by the combined administration of halothane and succinylcholine. Sixteen susceptible swine were initially anesthetized with nontriggering drugs and then either kept normothermic (approximately equal to 38 degrees C, n = 6) or cooled to induce mild (approximately equal to 35 degrees C, n = 6), or moderate (approximately equal to 33 degrees C, n = 4) hypothermia. Next, after a 30-min control period, the normothermic and mildly hypothermic animals were administered 1 minimum alveolar anesthetic concentration (MAC) halothane followed by a bolus dose of succinylcholine (2 mg/kg). Within 10 min all normothermic animals developed fulminant MH, whereas the onset of MH was slowed or was absent in the mildly hypothermic group. To test whether moderate hypothermia could more effectively minimize the signs of a MH episode, this group of animals was exposed to 1.5 MAC halothane followed 10 min later by a 3-mg/kg bolus of succinylcholine. MH was not induced and anesthesia was then changed to nontriggering drugs (ketamine and pancuronium). The animals were then aggressively rewarmed to 38 degrees C: a slight increase in the ETCO2 was detected, but MH episodes did not spontaneously occur. Subsequently, the readministration of halothane and succinylcholine rapidly provoked fulminant MH. We concluded that the induction of mild hypothermia impairs triggering and reduces the progression of MH induced by the combined administration of halothane and succinylcholine, whereas moderate hypothermia was completely protective and thus could be considered for prophylaxis.

Animals↗
PubMed1996

Mild intraoperative hypothermia reduces production of reactive oxygen intermediates by polymorphonuclear leukocytes.

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.

Acute-Phase Proteins↗