Biomedical subjects

D J Loegering

Publications and source records attributed to D J Loegering.

At least 37 records · Page 2Linked to original sources

PubMed1990

Effect of phagocytosis of erythrocytes and erythrocyte ghosts on macrophage phagocytic function and hydrogen peroxide production.

Our previous studies have shown that an in vivo phagocytic challenge with IgG-coated erythrocytes can depress Kupffer cell complement and Fc receptor function, as well as decrease the survival rate following endotoxemia and bacteremia. In an effort to better understand the mechanism underlying these in vivo findings, the present study evaluated the in vitro effects of a phagocytic challenge with either IgG-coated erythrocytes (EIgG) or erythrocyte ghosts (GIgG) on macrophage phagocytic and respiratory burst activity. Elicited rat peritoneal macrophage (PM) monolayers were challenged with varying doses of EIgG, then the noninternalized EIgG were lysed hypotonically and the monolayers incubated for an additional hour prior to determining phagocytic function and PMA-stimulated hydrogen peroxide production. Challenge of PM with 1 x 10(6) EIgG per well had no effect, but challenge with 1 x 10(7) or 1 x 10(8) EIgG per well caused a dose-dependent depression of phagocytic function or hydrogen peroxide production. GIgG were formed by hypotonically lysing EIgG bound to PM at 4 degrees C. The bound GIgG were phagocytized during a subsequent incubation at 37 degrees C. Challenge with GIgG depressed phagocytic function only with the highest challenge dose tested (1 x 10(8) per well) and did not depress hydrogen peroxide production. The observation that prior phagocytic challenge with EIgG depressed macrophage function to a greater extent than challenge with GIgG supports our previous in vivo observations. Furthermore, these studies suggest that the internalization of erythrocyte contents, and not phagocytosis per se, plays an important role in determining macrophage host defense function.

Animals↗

PubMed1989

Determination of Kupffer cell Fc receptor function in vivo following injury.

This study was carried out to determine whether Kupffer cell Fc receptor function is depressed after injury. Three approaches to the determination of Fc receptor function were evaluated: IgG-coated erythrocytes (EIgG) were used as the receptor probe with a perfused liver system, EIgG were used as the receptor probe in vivo, and small aggregates of IgG (AIgG) were used as the receptor probe in vivo. Nearly half of the injected dose of EIgG was taken up by the perfused liver (nonrecirculating, serum-free system). In contrast, only 2.6% of erythrocytes not coated with IgG were taken up, and only 5.6% of erythrocytes coated with IgM were taken up by the perfused liver. Thus, there was little nonspecific or complement-dependent uptake of EIgG by the liver. The uptake of EIgG by the perfused liver was depressed following thermal injury, endotoxemia, and the phagocytosis of EIgG. These results were interpreted as indicating that Kupffer cell Fc receptor function was depressed under these conditions. The results obtained with the hepatic uptake of EIgG in vivo were very similar to those with EIgG in the perfused liver. However, since it was found that complement receptors as well as Fc receptors were probably involved in the in vivo clearance of EIgG, these results could be due to a depression of one or both of these receptors. The hepatic uptake of AIgG was not depressed by complement depletion, but was decreased by the injection of large aggregates of IgG. However, the hepatic uptake of AIgG was not depressed following thermal injury, endotoxemia, or the phagocytosis of EIgG. Thus, AIgG was not sensitive to the effects of injury on Kupffer cell function, whereas the uptake of EIgG by the perfused liver may provide an indication of Kupffer cell Fc receptor function. The depression of Kupffer cell Fc receptor function following injury may contribute to the impairment of host defense caused by injury.

Animals↗

PubMed1989

Effect of ibuprofen and dexamethasone on Kupffer cell complement receptor function after endotoxemia and the phagocytosis of erythrocytes.

Depression of Kupffer cell complement receptor (CR) function is associated with several states of depressed host defense. This study was carried out to determine if ibuprofen and dexamethasone, which decrease the mortality rate following endotoxemia, could prevent the depression of CR function caused by endotoxemia and the phagocytosis of antibody-coated erythrocytes (EIgG). The depression of CR function caused by endotoxin was completely prevented by the administration of ibuprofen or dexamethasone. Thus, the ability of these drugs to prevent the depression of macrophage function may contribute to their salutory effects during endotoxin shock. In contrast to the effect with endotoxemia, the depression of CR function caused by the phagocytosis of EIgG was not modified by pretreatment with ibuprofen or dexamethasone. Additional studies demonstrated that the depression of CR function caused by EIgG was probably not due to EIgG in the blood or bound to Kupffer cells, interfering with the receptor probe for access to the CR. This study has shown that ibuprofen and dexamethasone can prevent the depression of CR function caused by endotoxin but not the depression caused by the phagocytosis of EIgG. These results suggest that different mechanisms mediate the depression of CR function caused by endotoxin and the phagocytosis of EIgG.

Animals↗

PubMed1988

Effect of beta-receptor stimulation on Kupffer cell complement receptor clearance function.

The clearance function of complement receptors on Kupffer cells is depressed after several forms of experimental injury. In vitro studies have shown that stimulation of beta-receptors on macrophages causes a depression of several aspects of macrophage function. The present study evaluated the possibility that the increase in sympathetic activity associated with injury contributes to the depression of Kupffer cell complement receptor function. Complement receptor function was assessed in rats from the hepatic uptake of rat erythrocytes coated with IgM. Isoproterenol caused a depression of receptor function when infused at a rate of 5.0 and 0.5 micrograms/kg/min for 15 min but not after infusion of 0.05 micrograms/kg/min. Infusion of isoproterenol, norepinephrine, and epinephrine at 0.5 micrograms/kg/min depressed receptor function by 41%, 38%, and 29%, respectively. Beta-receptor blockade with propranolol prevented the depression of receptor function caused by isoproterenol and norepinephrine. Thermal injury depressed receptor function by 65%, and this depression was reduced to 35% by beta-receptor blockade. Therefore, stimulation of beta-receptors on macrophages by increased circulating levels of catecholamines after injury could contribute to the depression of Kupffer cell function caused by injury.

Animals↗

PubMed1988

Kupffer cell complement receptor clearance function after surgical injury and phagocytosis of immune complexes: effect of changes in plasma fibronectin.

The present study evaluated the effect of changes in plasma fibronectin levels on the degree of depression of in vivo clearance function of Kupffer cell complement receptors after injury and the phagocytosis of immune complexes. In vitro studies have suggested that fibronectin may act as an opsonin for the clearance of immune complexes from the blood by binding to C1q and may influence the expression and activation of immune receptors on macrophages. Complement receptor clearance function was assessed in rats from the hepatic uptake of rat erythrocytes coated with antierythrocyte IgM. Increasing plasma fibronectin by the injection of purified fibronectin or decreasing fibronectin by the injection of gelatin had no effect on complement receptor function in otherwise normal animals. Surgical injury depressed both plasma fibronectin levels and complement receptor function. Injection of fibronectin at the time of injury prevented the depression of receptor function; however, when fibronectin was given 1 hour after injury, receptor function remained depressed even though fibronectin levels were increased. The phagocytosis of immune complexes (IgG-coated rat erythrocytes [EIgGs]) depressed complement receptor function but did not depress plasma fibronectin levels. The depression of receptor function caused by the phagocytosis of EIgGs was prevented by administering fibronectin and was potentiated by administering gelatin, which decreased plasma fibronectin levels. Therefore, plasma fibronectin concentrations can influence in vivo Kupffer cell complement receptor function under certain conditions that lead to the depression of complement receptor function.

Animals↗

PubMed1987

Effect of Kupffer cell phagocytosis of erythrocytes and erythrocyte ghosts on susceptibility to endotoxemia and bacteremia.

The phagocytosis of erythrocytes by macrophages has previously been shown to depress macrophage function. In this study we compared the effect of the phagocytosis of erythrocytes and erythrocyte ghosts by Kupffer cells on the duration of the depression of complement receptor clearance function and host defense against endotoxemia and bacteremia. Phagocytosis of erythrocytes and erythrocyte ghosts was induced in rats by the injection of rat erythrocytes or erythrocyte ghosts coated with anti-rat erythrocyte immunoglobulin G (EIgG and GIgG, respectively). The hepatic uptake of EIgG and GIgG (17.4 X 10(8)/100 g) occurred during the first 30 min after injection. The digestion of phagocytized EIgG and GIgG, as assessed by electron microscopy, was complete at 24 and 3 h after injection, respectively. The depression of Kupffer cell complement receptor clearance function caused by EIgG and GIgG returned to normal by 6 h after injection of EIgG and by 3 h after injection of GIgG. Phagocytosis of EIgG depressed the survival rate after endotoxemia and bacteremia when endotoxin or bacteria were injected at 30 min after EIgG. The survival rate returned to normal when the endotoxin and bacteria were injected at 12 and 6 h after the EIgG, respectively. Phagocytosis of GIgG did not depress the survival rate after endotoxemia and bacteremia. Thus, compared with erythrocytes, erythrocyte ghosts are more rapidly digested after phagocytosis, depress complement receptor function for a shorter period of time, and cause less depression of host defense. These findings indicate that the contents of erythrocytes play an important role in the impairment of host defense caused by the phagocytosis of erythrocytes by Kupffer cells.

Animals↗

PubMed1986

Hepatic macrophage complement receptor clearance function following injury.

Previous work has demonstrated that in vivo hepatic macrophage complement receptor clearance function is depressed following thermal injury. The present study was carried out to determine if complement receptor function depression is associated with other states of depressed host defense. Hepatic complement receptor clearance function was determined from the hepatic uptake of rat erythrocytes coated with antierythrocyte IgM (EIgM) in rats. Receptor function was determined following cannulation of a carotid artery, laparotomy plus enterotomy, hemorrhagic shock, trauma, thermal injury, acute bacteremia, acute endotoxemia, and injection of erythrocyte stroma, gelatinized lipid emulsion, or colloidal carbon. Hepatic uptake of EIgM was depressed following each of these experimental interventions except arterial cannulation. This effect was shown not to be due to a decrease in hepatic blood flow or depletion of complement and was therefore due to a depression in hepatic macrophage complement receptor clearance function. Thus, impairment of hepatic macrophage complement receptor function is associated with several states of depressed host defense.

Animals↗

PubMed1986

Left ventricular function during lethal and sublethal endotoxemia in swine.

Our previous studies suggested that after a median lethal dose (LD50) of endotoxin, cardiac contractility was depressed in nonsurviving dogs. The canine cardiovascular system is unlike humans in that dogs have a hepatic vein sphincter that is susceptible to adrenergic stimulation capable of raising hepatic and splanchnic venous pressures. We retested the hypothesis that lethality after endotoxin administration is associated with cardiac contractile depression in pigs, because the hepatic circulation in this species is similar to that of humans. We compared cardiac mechanical function of pigs administered a high dose (250 micrograms/kg) or a low dose (100 micrograms/kg) endotoxin by use of the slope of the end-systolic pressure-diameter relationship (ESPDR) as well as other measurements of cardiac performance. In all the pigs administered a high dose, ESPDR demonstrated a marked, time-dependent depression, whereas we observed no significant ESPDR changes after low endotoxin doses. The other cardiodynamic variables were uninterpretable, due to the significant changes in heart rate, end-diastolic diameter (preload), and aortic diastolic pressure (afterload). Plasma myocardial depressant factor activity accumulated in all endotoxin-administered animals, tending to be greater in the high-dose group. In this group, both subendocardial blood flow and global function were depressed, whereas pigs administered the low dose of endotoxin demonstrated slight, but nonsignificant, increases in flow and function. These observations indicate that myocardial contractile depression is associated with a lethal outcome to high doses of endotoxin. One possible mechanism for this loss of contractile function may be a relative hypoperfusion of the subendocardium.

Animals↗

PubMed1986

Kupffer cell complement receptor clearance function and host defense.

Kupffer cells are well known to be important for normal host defense function. The development of methods to evaluate the in vivo function of specific receptors on Kupffer cells has made it possible to assess the role of these receptors in host defense. The rationale for studying complement receptors is based on the proposed important role of these receptors in host defense and on the observation that the hereditary deficiency of a complement receptor is associated with recurrent severe bacterial infections. The studies reviewed here demonstrate that forms of injury that are associated with depressed host defense including thermal injury, hemorrhagic shock, trauma, and surgery also cause a decrease in complement receptor clearance function. This decrease in Kupffer cell receptor clearance function was shown not to be the result of depressed hepatic blood flow or depletion of complement components. Complement receptor function was also depressed following the phagocytosis of particulates that are known to depress Kupffer cell host defense function. Endotoxemia and bacteremia also were associated with a depression of complement receptor function. Complement receptor function was experimentally depressed in uninjured animals by the phagocytosis of IgG-coated erythrocytes. There was a close association between the depression of complement receptor clearance function and increased susceptibility to the lethal effects of endotoxin and bacterial infection. These studies support the hypotheses that complement receptors on Kupffer cells are important for normal host defense and that depression of the function of these receptors impairs host defense.

Animals↗

PubMed1985

Prostaglandin E2 and muscle protein turnover in Pseudomonas aeruginosa sepsis.

Rats were injected intraperitoneally with Pseudomonas aeruginosa (septic group) or sterile 0.9% NaCl (controls). Soleus muscles were excised 7 h later, and muscle prostaglandin E2 release and tyrosine release were measured in vitro. Muscles of septic rats exhibited 226-326% higher release of prostaglandin E2 and 54-84% higher net proteolysis than muscles of controls. Inclusion of aspirin or indomethacin in the incubation medium almost completely inhibited prostaglandin E2 production, but had no effect on net proteolysis in muscles from either group. Inclusion of cycloheximide, a protein synthesis inhibitor, increased tyrosine release of control muscles by 42%, whereas no statistically significant increase was observed in muscles from infected rats. However, total proteolytic rate, indexed by tyrosine release in the presence of cycloheximide, was 22% higher in muscles of septic rats compared to that of control animals. Concomitantly, inclusion of cycloheximide inhibited prostaglandin E2 release by muscles of infected rats by 91% and that of controls by 65%. It is concluded that muscles of septic animals exhibit a pronounced stimulation of prostaglandin E2 release and net proteolysis, combined with a small increase in total proteolytic rate, the stimulation of net proteolysis is mainly due to inhibition of protein synthesis, the increases in net and total proteolysis appear to be independent of prostaglandin E2 production, cycloheximide has a previously unrecognized inhibitory effect on muscle prostaglandin E2 production.

Animals↗

PubMed1985

Reticuloendothelial-depressing substance: studies on the mechanism of action.

This study was carried out to evaluate the mechanism of action of a reticuloendothelial (RE)-depressing substance. This RE-depressing substance was obtained from the plasma of dogs subjected to 3 hr of intestinal ischemia. RE-depressing substance was partially purified by dialysis and reverse-phase column chromatography. The assay of RE-depressing activity was based on the depression of the rate of clearance of colloidal carbon from the blood of rats or mice. The effect of RE-depressing substance on three other RE system (RES) test particles (gelatinized lipid emulsion, formalinized sheep erythrocytes, and IgM-coated erythrocytes) was determined. RE-depressing substance did not affect the clearance rate or the organ localization of these three test particles. Therefore, RE-depressing substance affected only the clearance of colloidal carbon. Since platelet aggregation has been shown to contribute to the clearance of colloidal carbon, the effect of RE-depressing substance on platelet aggregation was evaluated. RE-depressing substance depressed in vitro platelet aggregation induced by ADP or collagen. It was concluded that the effect of RE-depressing substance on the clearance of colloidal carbon was due to a depression of platelet aggregation rather than to a depression of hepatic macrophage phagocytic function.

Animals↗

PubMed1985

Canine left ventricular function during experimental pancreatitis.

Left ventricular contractility following induction of experimental pancreatitis (EP) was studied. Contractility was evaluated by analyzing the left ventricular end systolic pressure-diameter relationship (sigma ES). Sigma ES is independent of large changes in preload, afterload, and heart rate, but sensitive to changes in ventricular contractility. Following injection of 100,000 IU trypsin in 4% taurocholate into the pancreas to induce EP, seven of eight dogs survived 5 hr. These dogs exhibited an initial significant reduction in mean arterial pressure (MABP) which stabilized at 90% of control at 3-5 hr post-EP. Cardiac output (CO) dropped slowly after EP induction (from 3.08 +/- 0.43 to 2.22 +/- 0.22 liters/min) associated with no significant change in peripheral resistance. Stroke work and stroke volume were markedly depressed reflecting the changes in MABP and CO. No consistent changes in +dP/dt or -dP/dt were observed. The ratio of endo/epicardial blood flow was unchanged as was blood Ca2+ levels throughout the experiment. Ventricular contractility as reflected by sigma ES tended to improve (from 49.7 to 69.6 mm Hg/mm at 4 hr following EP). Therefore, it was concluded that these animals exhibited no loss of ventricular contractility during EP.

Acute Disease↗

PubMed1985

Depressing hepatic macrophage complement receptor function causes increased susceptibility to endotoxemia and infection.

Previous work has demonstrated that in vivo hepatic macrophage complement receptor clearance function is depressed after thermal injury. To determine whether impairment of complement receptor function is important in host defense, the present study evaluated the effect of the depression of complement receptor function in uninjured animals on susceptibility to endotoxin shock and bacterial infection. Hepatic complement receptor clearance function was evaluated by measuring the hepatic uptake of a test dose (2.9 X 10(8)/100 g) of rat erythrocytes coated with anti-erythrocyte immunoglobulin M (EIgM) or EIgG in rats. Depression of hepatic complement receptor function was induced by the injection of EIgG. The hepatic uptake of the test dose of EIgM or EIgG was depressed after the injection of 8.7 X 10(8) EIgG per 100 g and 17.4 X 10(8) EIgG per 100 g but not after the injection of 2.9 X 10(8) EIgG per 100 g. This effect was shown not to be due to a decrease in hepatic blood flow or a depletion of serum C3 and was, therefore, due to a depression in hepatic macrophage complement receptor clearance function. Susceptibility to endotoxin shock was increased with the dose of 8.7 X 10(8) EIgG per 100 g, and susceptibility to infection with Pseudomonas aeruginosa was increased with the dose of 17.4 X 10(8) EIgG per 100 g. Therefore, depression of hepatic macrophage complement receptor clearance function with EIgG is associated with depressed host defense.

Animals↗

PubMed1984

Effect of red blood cells and red blood cell ghosts on reticuloendothelial system function.

Previous studies have shown that hepatic phagocytosis of red blood cell (RBC) stroma can depress reticuloendothelial system (RES) phagocytic function and increase susceptibility to shock. Since the RBC stroma used in these experiments contained substantial amounts of adherent hemoglobin, the present study was carried out to evaluate the role of the hepatic uptake of RBC membrane material on RES phagocytic function and susceptibility to endotoxin shock in rats. Neuraminidase-treated RBC which contained normal amounts of hemoglobin and RBC ghosts which were hemoglobin-free were used. Both preparations were removed from the circulation primarily by the liver. RES phagocytic function was depressed following the hepatic uptake of 29 X 10(8) neuraminidase-treated RBC and 26 X 10(8) RBC ghosts. RES uptake of neuraminidase-treated RBC was associated with an increase in susceptibility to endotoxin shock, but RBC ghosts did not affect shock susceptibility. Thus, RBC ghosts and intact RBC are equally effective in depressing RES phagocytic function, but RBC ghosts did not affect susceptibility to endotoxin shock.

Animals↗

PubMed1984

Effect of extravascular hemolysis on the RES depression following thermal injury.

This study was carried out to determine if the reticuloendothelial system (RES) uptake of damaged red blood cells (RBC) following thermal injury is sufficient to depress hepatic and splenic clearance function or to increase susceptibility to endotoxin shock. This was approached by determining the extent of the RES uptake of intact RBC (extravascular hemolysis) following thermal injury in rats, and by determining the effect on RES function of a similar degree of extravascular hemolysis induced in uninjured animals by the injection of heat damaged RBC. The RES uptake of three doses of heated RBC was characterized and the second largest dose caused a degree of extravascular hemolysis which was comparable to that associated with thermal injury. This latter dose of heated RBC depressed splenic clearance function but did not depress hepatic clearance function as determined using the smallest dose of heated RBC or formalinized sheep red blood cells at the test particles. Susceptibility to endotoxin shock was increased following the injection of the dose of heated RBC which stimulated the degree of extravascular hemolysis associated with thermal injury. Thus, the extravascular hemolysis associated with thermal injury is sufficient to depress splenic clearance function but not hepatic clearance function, and may contribute to the increased susceptibility to endotoxin shock following thermal injury. These findings further support the hypothesis that the hemolysis induced by thermal injury contributes to the depression of host defense associated with this form of injury.

Animals↗

PubMed1984

Role of the liver in host defense to pneumococcus following splenectomy.

Splenectomy is associated with increased susceptibility to bacterial infection, and this is thought to be primarily due to a decrease in clearance of bacteria from the blood. The purpose of the present study was to determine if splenectomy could increase susceptibility to pneumococcus type 3, which is cleared primarily by the liver in rats, and if hepatic function is altered by splenectomy. Splenectomy increased the mortality of rats challenged iv with pneumococcus. Heat-killed, 51Cr-labeled pneumococci were rapidly cleared by the liver and splenectomy did not alter the initial clearance rate or the initial hepatic uptake of bacteria. Injection of viable pneumococci showed that blood levels were unchanged at 30 min but were much greater 5 hr after challenge in splenectomized animals. Hepatic uptake of viable pneumococcus was also not changed at 30 min after injection but at 5 hr the number of bacteria in the liver was greater in the splenectomized animals. This suggests an impairment in hepatic bactericidal function. Another contributing factor may have been that the hepatic bactericidal capacity was overwhelmed by the pneumococci which would normally have been killed by the spleen. Lung localization of viable bacteria was increased initially but there was no decrease in pulmonary bactericidal function. Thus, splenectomy increased susceptibility to a bacteria cleared primarily by the liver which was attributed to an impairment of hepatic bactericidal function and/or an inability of the liver to compensate for the loss of splenic function due to a saturation of the bactericidal system.

Animals↗

PubMed1984

Depression of in vivo clearance function of hepatic macrophage complement receptors following thermal injury.

Previous studies have implicated a role for impaired hepatic macrophage blood clearance function in the increased susceptibility to infection caused by experimental thermal injury. The present study evaluated in vivo hepatic macrophage complement receptor clearance function as a possible factor contributing to impaired hepatic clearance after thermal injury. Rat erythrocytes treated with anti-erythrocyte serum (EA) were used as the test particle in rats. EA were rapidly removed from the circulation primarily by the liver and hepatic uptake of EA was greatly depressed in animals rendered C3 deficient by treatment with cobra venom factor. Thermal injury caused a large depression in the hepatic uptake of EA. It was shown that the depression in the binding of EA to hepatic macrophages was not due to decreased hepatic blood flow, decreased serum complement levels, or increased fluid phase C3b. Also, the depression of the hepatic uptake of EA incubated with serum prior to injection (EAC) was not different from that of EA after thermal injury. On this basis it was concluded that the impairment in binding of EA to the macrophages was at the cellular level and represented a depression in complement receptor clearance function. Additional studies showed that the injection of erythrocyte stroma, as a model of intravascular hemolysis, also depressed in vivo hepatic macrophage complement receptor clearance function. This latter finding suggests that the intravascular hemolysis caused by thermal injury may contribute to the depression of macrophage receptor function. The depression of hepatic macrophage complement receptor clearance function may contribute to the impaired bacterial clearance and increased susceptibility to infection following experimental thermal injury.

Animals↗

PubMed1984

Effect of red blood cell stroma on the reticuloendothelial system clearance and killing of Streptococcus pneumoniae.

Previous studies from this laboratory have shown that thermal injury can cause sufficient intravascular hemolysis to depress reticuloendothelial system (RES) phagocytic function and that the injection of red blood cell (RBC) stroma depresses RES function and increases susceptibility to experimental shock. The present study evaluated the effect of thermal injury and RBC stroma on susceptibility to infection with Streptococcus pneumoniae as well as the effect of RBC stroma on the RES clearance and killing of the bacteria. The mortality rate following pneumococcal infection was increased after thermal injury from 0% to 100% (P less than .01), and with the injection of RBC stroma (0.5 ml/100 g) mortality increased from 20% to 80% (P less than .01). Hepatic uptake of heat-killed S. pneumoniae was depressed from 64% to 44% of the injected dose following the injection of RBC stroma. RBC stroma depressed complement CH50 levels by 31%. The reduction in the number of viable S. pneumoniae present in the liver between 30 min and 4 hr following bacterial challenge was decreased in animals receiving RBC stroma. This was interpreted as an indication of impaired hepatic bactericidal function and was associated with an increase in the number of circulating viable S. pneumoniae. It is concluded that the increased susceptibility to pneumococcal infection induced by RBC stroma was probably due to an impairment in hepatic clearance and killing of the bacteria. The depressed bacterial clearance could have been contributed to by the stroma-induced decrease in complement levels. This study further supports the hypothesis that the intravascular hemolysis caused by thermal injury contributes to the increased susceptibility to infection following this form of injury.

Animals↗