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Biomedical subjects

E J Schiffrin

Publications and source records attributed to E J Schiffrin.

14 recordsLinked to original sources
PubMed1992

Effect of acute and chronic lipopolysaccharide (LPS) administration on reticuloendothelial system (RES) phagocytic activity in vivo.

The effect of injection or chronic infusion of lipopolysaccharide (LPS) into unanaesthetized rats on the distribution of [99Tcm-]SC has been determined. At a dose of 2.5 mg/kg, LPS injection caused a marked alteration in the distribution of the radiolabelled material, with more uptake being achieved in the lung while less was taken up by the spleen. Kidney and liver uptake were also changed. Chronic infusion of LPS at a similar dose (3 mg/kg in 24 h) caused a marked increase in the uptake of the radioactive material by the lung only. These data are consistent with a working hypothesis that the alterations in RES phagocytic activity of the lung observed in rats subjected to burn trauma could be related in part to LPS, either coming as a bolus, or being continuously presented.

Animals↗
PubMed1992

Effect of chronic interleukin-2 treatment on RES phagocytic activity in the rat.

The effect of chronic interleukin-2 (IL-2) injection upon reticuloendothelial system (RES) function in the rat has been determined. Seven-day treatments with two doses of human recombinant IL-2 resulted in a dramatic reduction in the phagocytic uptake of the liver and spleen, while increasing the weight of both organs. There were dramatic histological changes in the intestine, liver and spleen as well. These results suggest that the chronic use of IL-2 can result in hepatic dysfunction, which is associated with altered RES phagocytic function.

Animals↗
PubMed1992

Effect of heta-starch colloidal solutions on reticuloendothelial phagocytic system (RES) function in burned and infected rats.

The biodistribution of the plasma expander colloidal solution, heta-starch (HES), has been examined in rats, subjected to thermal injury or sepsis. The ability of these solutions to alter RES phagocytic function of [99mTc]-sulphur colloid ([99mTc]SC) uptake in vivo has been examined. The biodistribution of radiolabelled HES has been determined in normal rats. The HES colloidal solution has no deleterious effect upon RES function in vivo in the thermally injured animals or the septic animals as compared to sham controls. In addition, the HES colloidal solution seemed to be distributed primarily within the liver, spleen and kidney, with a small amount residing in the lung. Thermal injury did not increase the uptake of this material by the lung. These results suggest that the use of HES in thermally injured and septic individuals has no deleterious effects on RES function, nor does it accumulate in the lungs, and hence, should be advocated for use in these situations.

Animals↗
PubMed1991

Platelet-activating factor induces intestinal necrosis, but not septic shock, in germ-free and specific-pathogen-free rodents.

Platelet-activating factor (PAF) was injected into conventional mice, endotoxin-resistant mice (C3H/HEJ), conventional rats, germ-free rats and specific-pathogen-free (SPF) mice. The PAF resulted in significant necrosis and damage to the small intestines of all the animals tested. In general, the frequency and severity of the lesions were similar in all groups. All the conventional rats and mice, as well as the endotoxin-resistant HEJ mice, were dead 18 h after the injection of the PAF, while all the germ-free rats and the SPF mice survived. These data demonstrate that development of massive intestinal lesions, in the absence of aerobic bacteria, is not sufficient to cause the death of the host from septic shock and endotoxaemia.

Animals↗
PubMed1991

Effect of platelet activating factor on reticuloendothelial system function.

The effect of platelet activating factor (PAF) injections on the uptake of 99mTc-SC (99mTc-SC (99mTc-sulphur colloid) was determined in vivo. PAF (2 micrograms) injected intravenously into unanaesthetized, unrestrained rats was associated with the development of lesions in the small intestine and alteration of 99mTc-SC uptake in vivo. 99mTc-SC uptake into the lung was increased while spleen uptake was decreased. Pretreatment of the animals with a PAF antagonist, SRI-64-441, prevented the intestinal lesions and alterations of 99mTc-SC uptake. Macrophages, isolated from lung lavage of the PAF-treated rats, demonstrated a decreased generation of hydrogen peroxide in vitro. The present results suggest that, in addition to its other effects on the immune system, PAF can also alter the in vivo phagocytic activity of the reticuloendothelial system in the rat.

Animals↗
PubMed1990

Prevention of necrotizing enterocolitis in the rat with prenatal cortisone.

Cortisone acetate is known to accelerate maturation of the immature intestine. The effect of prenatal administration of cortisone acetate on the morbidity and mortality of necrotizing enterocolitis was examined in a rat pup model. Pregnant rats were administered cortisone acetate, 20 mg/100 g of body weight, or normal saline by daily IP injection from day 18-21 of gestation. Rat pups were taken from the mothers before suckling was initiated, fed a simulated rat milk formula, and subjected to daily ischemic insults to produce an animal model of necrotizing enterocolitis. Both morbidity and the mortality rates were significantly improved with prenatal cortisone treatment. Maturation of the intestinal mucosal barrier was accelerated with the cortisone treatment as measured by decreased serum concentrations of a fed antigen, ovalbumin. Aerobic bacterial colonization of the small intestine and translocation of bacteria to the liver were decreased in the pups pretreated with steroids. These changes observed in a rat model of necrotizing enterocolitis may explain the decreased incidence of necrotizing enterocolitis in human infants born to mothers who received corticosteroids late in gestation.

Animals↗
PubMed1990

Role of neutrophils in the intestinal alterations associated with thermal injury.

We have examined the role of neutrophils in the alterations observed in the intestines of rats subjected to 40 per cent surface area scald injury. Histologically, there was no evidence of neutrophilia in the intestinal tissue, and myeloperoxidase activity in mucosal scrapings was not elevated. The distribution of labelled human neutrophils injected into the burned rats showed no enhancement of uptake in the intestines, although there was increased uptake by the lung. The present data suggest that neutrophil migration may not play a role in the alterations in small intestinal function and morphology seen in burn trauma in the rat, but may be a factor in lung damage associated with thermal injury.

Acute Disease↗
PubMed1990

Effect of acute burn trauma on reticuloendothelial system phagocytic activity in rats. II: Comparison of uptake of radiolabelled colloid and bacteria.

The uptake of radiolabelled colloid or bacteria was compared in normal rats and animals subjected to acute burn trauma. The uptake of colloid by the liver was unaffected by burn trauma, but uptake of the labelled bacteria was reduced. Spleen uptake of both colloid and bacteria was reduced by burn trauma while lung uptake was increased. These data are consistent with the hypothesis that acute burn trauma alters reticuloendothelial system phagocytic activity in the rat towards both inert particles and live bacteria.

Acute Disease↗
PubMed1990

Role of skin in the burn-induced reduction of reticuloendothelial phagocytic activity in rats.

Acute burn trauma has been demonstrated to depress reticuloendothelial system (RES) phagocytic activity, which could partially explain the development of septicaemia in burn patients. In the present study we have attempted to determine the role that skin plays in the depression of the RES. One group of Lewis rats was subjected to a 100 degrees C scald burn for 10 s. Eschar was then removed and implanted onto the backs of a second group of normal controls. A third group of Lewis rats were subjected to sham treatment; the eschar of these animals was removed and implanted onto the back of a fourth group of normal rats. The excision sites of the donor animals were immediately covered with Biobrane. Twenty-four hours later the technetium-99m sulphur colloid [( 99mTS]SC) method described earlier (Trop et al., 1989) was used to determine phagocytosis in these four groups of animals. Acute burn trauma produced a marked reduction in colloid uptake by the spleen and a marked increase in the uptake of colloid material by the lung, although no effect was observed on liver or kidney uptake. Implantation of the burn eschar into normal control rats had no statistically significant effect upon colloid uptake. These data suggest that alterations in phagocytic activity of the spleen and lung occur within minutes after burn injury and may be unrelated to the presence of the burn eschar itself.

Acute Disease↗
PubMedDate not supplied

Effect of acute burn trauma on phagocytic activity of the reticuloendothelial system in rats.

The effect of acute burn trauma on phagocytic activity of the reticuloendothelial system measured in vivo with technetium 99m sulfur colloid was examined in rats subjected to acute burn trauma. After the scald injuries (10-second, full-thickness burns) were induced, a reduction in phagocytic activity by the spleen took place with an accompanying increase in the uptake of colloid material by the lungs. Uptake of colloid material by the liver was essentially unchanged. These uptake changes, observed within hours after the inducement of acute burn trauma and apparently continuing for 7 days after burn injury, may explain, in part, the development of septicemia in patients with burns because altered phagocytic activity of the reticuloendothelial system can result in subsequent overabundance of microorganisms and bacteria in the blood.

Animals↗
PubMedDate not supplied

Effect of irreversible dermal necrosis on phagocytic activity of reticuloendothelial system.

A model of full-thickness dermal necrosis was produced in rats by the application of liquid nitrogen to a 20% total body surface area of the dorsal skin surface. In this model there was an alteration of reticuloendothelial system phagocytic activity of the lung and spleen as measured by the uptake of technetium 99m-labeled sulfur colloid in vivo. The present results suggest that marked alterations in reticuloendothelial system phagocytic activity can be produced by full-thickness dermal necrosis in the absence of heat.

Animals↗
PubMedDate not supplied

Core body temperature responses immediately after cutaneous thermal injury in rats.

Internal temperatures were continuously measured in rats that received 20% or 40% body surface area cutaneous scald injuries in 25 degrees C and 38.5 degrees C environments. In animals that received thermal injuries in the 25 degrees C environment, intraperitoneal, intraesophageal, and intrarectal temperatures rapidly rose to 40 degrees C within 5 minutes but returned to normal values within 15 minutes after injury. When 20% body surface area injuries were induced in a 25 degrees C environment, all of the animals survived. In the 25 degrees C environment, neither acute core body temperature elevations nor use of fluid resuscitation predicted survival. In contrast, in a 38.5 degrees C environment core body temperatures rapidly exceeded 41 degrees C with the 20% injury, and all of the animals died within minutes in spite of fluid resuscitation. These studies suggest that the ambient environmental temperature may significantly influence a thermally injured animal's ability to rapidly eliminate absorbed heat of injury and result in an elevated core body temperature, which may contribute to the immediate lethality of the injury.

Animals↗