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D J Loegering

Publications and source records attributed to D J Loegering.

At least 55 records · Page 3Linked to original sources
PubMed1983

Reticuloendothelial depressing substance and burn injury in animals and patients.

This study was carried out to investigate the relative time courses of the presence of a reticuloendothelial (RE) depressing substance and reticuloendothelial system (RES) phagocytic function following thermal injury in animals: additionally, RE depressing activity was determined in burned patients. Following thermal injury in dogs, RE depressing activity was first detected 2 hr after injury and persisted for 12 hr. RE depressing activity was present in the circulation of burned rats at 3 and 24 hr but not 48 hr after injury. RES phagocytic function was also depressed at 3 and 24 hr but not at 48 hr after thermal injury in rats, showing that there was a close association between the presence of RE depressing activity and RES depression. Injection of RE depressing substance into normal animals depressed the RES for less than 60 min. Five of six burned patients studied within 5 days after injury had detectable RE depressing activity in their circulation. These findings further support the concept that a RE depressing substance contributes to the depression of RES phagocytic function and impairment of host defense following thermal injury.

Adult↗
PubMed1983

Intravascular hemolysis and RES phagocytic and host defense functions.

Depression of the reticuloendothelial system (RES) is thought to contribute to the pathogenesis of circulatory shock and to the increased susceptibility to infection following injury. An important aspect of the data supporting this concept is the observation that the phagocytosis of foreign particulates induces a period of RES depression and increased susceptibility to shock and infection. Since the RES normally removes altered autologous material from the circulation, the possibility exists that the phagocytosis of autologous material may induce an RES depression in the same way as the experimental RES uptake of foreign particulates. Thermal injury causes hemolysis with the generation of disrupted and damaged red blood cells (RBC), and this form of injury is followed by marked depression of host defense. Recent studies have demonstrated that simulation of intravascular hemolysis by the injection of hemolyzed blood causes a depression of RES phagocytic function. This effect was due to the particulate stroma component of the hemolyzed blood. RBC stroma was found to be rapidly removed from the circulation by the phagocytic cells of the liver. The RES depression induced by hemolyzed blood or RBC stroma was associated with an increased susceptibility to hemorrhagic shock, endotoxin shock, and septic shock. Additionally, the dose of hemolyzed blood required to depress the RES represented about 2.8% of the blood volume and thermal injury was found to cause acute intravascular lysis of 3.1% of the RBC mass, indicating that sufficient RBC debris can be generated to depress the RES by thermal injury. Thus, the generation and subsequent phagocytosis of altered autologous material, particularly RBC, may play an important role in the depression of RES phagocytic and host-defense functions following thermal injury.

Animals↗
PubMed1983

RES uptake of red blood cell stroma: time course of effects on phagocytic function and susceptibility to endotoxin shock.

Previous studies have demonstrated that the injection of red blood cell (RBC) stroma to simulate the reticuloendothelial system (RES) uptake of RBC debris following intravascular hemolysis causes an acute depression in RES phagocytic function and an increase in shock susceptibility. The present study evaluated the time course of these changes. Initial studies demonstrated that the uptake of iodinated RBC stroma was followed by a decrease in the amount of radioactivity present in the liver between 30 and 60 min after injection. This was associated with an increase in free label in the circulation, indicating an active deiodination of the stroma. Phagocytic function was depressed at 30 min after injection of RBC stroma, but had returned to control by 60 min. Susceptibility to endotoxin shock was increased when endotoxin was injected 30 min, 1 hr, 3 hr, or 6 hr but not 24 hr after the RBC stroma. The increased mortality with endotoxin shock was shown not to be due to depletion of complement by the RBC stroma. This study demonstrated that over the period of recovery of RES phagocytic function following the ingestion of RBC stroma there is metabolism (deiodination) of the particulate material. Additionally, susceptibility to endotoxin shock is increased for a longer period of time than the depression of phagocytic function.

Animals↗
PubMed1983

Effect of erythrocyte stroma on reticuloendothelial system phagocytic function.

Previous studies have demonstrated that intravenous administration of erythrocyte stroma is followed by a depression of RES phagocytic function. The present study evaluated the possibility that depression of hepatic blood flow, activation of the coagulation system, or depletion of opsonic factors mediates the RES depression induced by erythrocyte stroma. Stroma was prepared from washed rat erythrocytes and injected into rats at doses of 0.3, 0.5, 0.75, and 1.0 ml/100 gm. RES depression increased progressively after stroma doses greater than 0.3 ml/100 gm. Hepatic blood flow was decreased only after the 1.0 ml/100 gm dose. Fibrinogen levels were decreased with the 1.0 ml/100 gm dose but were unchanged with the 0.5 ml/100 gm dose of stroma, and the RES depression induced by the 0.5 ml/100 gm dose was not modified by the administration of heparin. Circulating fibronectin levels were not consistently depressed after stroma injection, and in vitro incubation of stroma with serum did not affect fibronectin levels. Erythrocyte stroma decreased hemolytic complement levels but depletion of complement with purified cobra venom factor did not depress RES phagocytic function. Preopsonization of the RES test particle did not modify the stroma-induced RES depression. These results indicate that decreased hepatic blood flow, activation of the coagulation system, or depletion of opsonins did not contribute to the RES depression induced by the 0.5 ml/100 gm dose of stroma. These results suggest that impairment of phagocytic cell function may mediate the effect of erythrocyte debris on RES phagocytic function.

Animals↗
PubMed1982

Effect of splenic sequestration of erythrocytes on splenic clearance function and susceptibility to septic peritonitis.

The effect of splenic sequestration of erythrocytes (RBC) on splenic clearance function and susceptibility to septic peritonitis was studied. Homologous RBC were treated with 20 mM phenylhydrazine hydrochloride in vitro and injected into rats at doses of 5, 15, 75, and 150 mg of hemoglobin per 100 g. Splenic 93, 23, and 13% of the injected dose, respectively, whereas less than 2.1% of the same doses of washed RBC were localized in the spleen. The total quantity of phenylhydrazine-treated RBC sequestered by the spleen was similar for the three larger doses (40 to 45 mg of hemoglobin per g of tissue), indicating that this is the capacity of the spleen to take up this type of RBC in 234 h. The phenylhydrazine-treated RBC in doses of 15, 75, and 150 mg of hemoglobin per 100 g depressed the clearance rate and splenic localization of a test dose of phenylhydrazine-treated RBC, whereas splenic clearance function was unchanged after a dose of 5 mg of hemoglobin per 100 g. Splenectomy or injection of doses of phenylhydrazine-treated RBC which depressed splenic clearance function increased the susceptibility to septic peritonitis induced by cecal ligation and puncture. After thermal injury, splenic clearance function was found to be depressed. Also, splenic localization of RBC 24 h after thermal injury was found to be approximately equal to that after injection of the doses of phenylhydrazine-treated RBC which depressed splenic clearance function. It is concluded that splenic sequestration of RBC can depress splenic clearance function and increase susceptibility to peritonitis, and that this may be one mechanism for the increased susceptibility to infection seen after thermal injury.

Animals↗
PubMed1981

Reticuloendothelial system depression with hemolyzed blood and susceptibility to endotoxin shock and thermal injury.

The present study was carried out to determine if the reticuloendothelial system (RES) depression induced by the injection of hemolyzed blood and components of hemolyzed blood was associated with an increase in susceptibility to endotoxin shock and thermal injury. Hemolyzed blood and the particulate stroma fraction, but not the soluble supernatant fraction of hemolyzed blood, depressed RES phagocytic function at a dose of 0.3 ml/100g in rats. Hemolyzed washed red blood cells (RBC) and hemolyzed RBC stroma also depressed RES function. Susceptibility to endotoxin shock was increased by hemolyzed blood and the fractions of hemolyzed blood that depressed RES function. However, susceptibility to thermal injury was increased only by large doses of hemolyzed RBC stroma. These findings suggest that the hemolysis associated with thermal injury may induce RES depression and increase susceptibility to endotoxin shock.

Animals↗
PubMed1981

Hemolysis following thermal injury and depression of reticuloendothelial system phagocytic function.

Previous studies have demonstrated that the injection of homologous hemolyzed blood, and reticuloendothelial system (RES) clearance of the erythrocyte membrane debris, depress RES phagocytic function and increase shock susceptibility. This study was carried out to determine if the degree of intravascular hemolysis following experimental thermal injury was comparable to the dose of hemolyzed blood required to depress RES function. The IV injection of graded doses of hemolyzed blood into rats demonstrated that 0.2 mg/100 gm of hemolyzed blood was the minimum dose of hemolyzed blood which would cause an RES depression. This volume of hemolyzed was equivalent to 2.8% of the blood volume of the animals studied. Hemolysis was assessed from the plasma hemoglobin and blood volume following graded thermal injury in anesthetized animals. Thermal injury which caused an 80% mortality rate was associated with the acute hemolysis of 3.1% of the blood sufficient erythrocyte membrane debris to induce RES depression and therapy impair host defense.

Animals↗
PubMed1981

Local effect of thermal injury on skeletal muscle blood flow and nucleotide levels.

We have previously shown that 3 days following a 3-sec scald of one hind limb, in vitro glucose utilization was markedly increased in soleus muscle from the burned limb but not in soleus from the contralateral unburned limb. The aim of the present study was to evaluate factors that might contribute to this local metabolic alteration. Three days following a 3-sec scald of one hind limb of the rat, blood flow through soleus and gastrocnemius muscles of the burned limb as measured with labeled microspheres was increased 167% (P less than 0.01) and 58% (P less than 0.04), respectively. Calf muscles of the burned limb, frozen in situ, showed a 48% decrease in ATP (P less than 0.001), 37% decrease in ADP (P less than 0.001), 192% increase in AMP (P less than 0.01), 45% decrease in total adenine nucleotides (P less than 0.001), 132% increase in pyruvate (P less than 0.001), and 377% increase in lactate (P less than 0.001). Blood flow and ATP, ADP, total nucleotides, and pyruvate levels of calf muscles of unburned limb of burned rats did not differ from controls, but AMP and lactate were increased 115% (P less than 0.05) and 144% (P less than 0.001), respectively. The decrease in ATP and increase in AMP and lactate in muscles of the burned limb suggest an increased rate of glycolysis in vivo which may be due, in part, to the stimulation of phosphofructokinase. Furthermore, the increased AMP and lactate may contribute to the increase in blood flow in muscles of the burned limb. It is proposed that thermal injury alters local adenine nucleotide levels, which results in elevated glucose utilization and blood flow in muscles of the burned region.

Adenosine Triphosphate↗
PubMed1981

Presence of a reticuloendothelial depressing substance in portal vein blood following intestinal ischemia and thermal injury.

This study was carried out to determine if an RE depressing substance is present following intestinal ischemia or thermal injury. Intestinal ischemia consisted of occluding the celiac and mesenteric arteries for 3 hr, and thermal injury was a 30% body-surface-area scald (30 sec in 90 degrees C water) in dogs anesthetized with sodium pentobarbital. Immediately following release of the arterial occlusions or 3 hr after thermal injury, portal vein blood was collected and plasma extracts prepared. RE depressing substance activity was assayed by measuring the colloidal carbon clearance rate in rats following the IV injection of the plasma extracts or saline. Plasma extracts from control animals never had detectable RE depressing substance activity. Following intestinal ischemia RE depressing activity was consistently detected in 6 assays on plasma extracts from 12 animals. Thermal injury was associated with the presence of RE depressing activity in each of the 4 animals studied. Neither intestinal ischemia or thermal injury was associated with a significant decrease in mean arterial blood pressure. These results indicate that RE depressing substance may contribute to the RES depression and impaired host-defense seen following intestinal ischemia and thermal injury.

Animals↗
PubMed1980

Reticuloendothelial system depression with hemolyzed blood.

This study was carried out to evaluate the effects of hemolyzed blood and components of hemolyzed blood on RES function. Phagocytic index, determined using four different test particles in rats, was depressed 30 minutes following the injection of 0.3 ml/100 gm hemolyzed blood. Fractionation of hemolyzed blood into particulate and soluble fractions revealed that only the particulate material caused an RES depression. A decrease in phagocytic index was seen after the injection of hemoglobin-free erythrocyte ghosts, further indicating that the membrane components of hemolyzed blood are capable of depressing RES function. Injection of hemolyzed blood, as well as RES blockade, increased the mortality rate following endotoxin administration. Injection of hemoglobin had no effect on RES function or endotoxin shock susceptibility. It is concluded that hemolyzed blood causes a nonspecific depression in RES phagocytic function, as well as probably impairing endotoxin detoxification. These findings indicate that the hemolysis that accompanies burn injury may induce RES depression and increase susceptibility to shock states.

Animals↗