Intraperitoneal sodium carboxymethylcellulose administration prevents reformation of peritoneal adhesions following surgical lysis.

Although intraperitoneal administration of sodium carboxymethylcellulose (SCMC) prevents the formation of adhesions following laparotomy in rats, it remains unknown whether SCMC treatment prevents the recurrence of preformed peritoneal adhesions following surgical lysis. Additionally, the optimal amount of SCMC required for adhesion prevention, as well as the effects of SCMC upon the healing of bowel anastomoses, has yet to be determined. To study this, 114 male rats underwent laparotomy and adhesion induction via peeling of the cecal serosa with a gauze sponge.

A novel nonanticoagulant heparin improves splenocyte and peritoneal macrophage immune function after trauma-hemorrhage and resuscitation.

Recent studies have shown that heparinization of animals prior to or even after hemorrhagic shock improves tissue perfusion and organ function. However, the anticoagulant properties of conventional heparin preclude its clinical use in trauma care. The aim of our study, therefore, was to determine whether chemically modified heparin, i.

Hemorrhage affects the ability of murine peritoneal macrophages to alkanize intracellular pH in acidic environments.

Although departures from the normal physiologic pH range, associated with states of shock, injury, and/or infection are thought to impair phagocytic function and chemotaxis, it remains unknown if the ability of the peritoneal macrophage (pMø) to gate H+ is affected following hemorrhagic shock. To study this, male C3H/HeN mice were bled to a BP of 40 mm Hg and maintained at that level for 1 hr. Following resuscitation with the shed blood plus 2x that volume as Ringer's lactate, pMø was harvested via lavage in bicarbonate-free RPMI 1640 and enumerated to 2 million cells/ml.

Downregulation of hepatic beta-adrenergic receptors after trauma and hemorrhagic shock.

Although it is well known that sympathoadrenal activity increases under various adverse circulatory conditions, it is not known whether there are any alterations in hepatic plasma membrane beta-adrenergic receptors after trauma-hemorrhage and crystalloid resuscitation. To study this, rats underwent a 5-cm midline laparotomy (i.e.

Effects of hydroxyethyl starch after trauma-hemorrhagic shock: restoration of macrophage integrity and prevention of increased circulating interleukin-6 levels.

Objectives: To determine the effects of resuscitation with the colloidal solution (hydroxyethyl starch) vs. crystalloid solution on cell-mediated immune functions after trauma-hemorrhage.

Design: Prospective, multiexperimental, randomized, controlled study.

ATP-MgCl2 restores depressed endothelial cell function after hemorrhagic shock and resuscitation.

Although ATP-MgCl2 produces beneficial effects following various adverse circulatory conditions, it remains unknown whether this agent restores the depressed endothelial cell function [i.e., the reduced release of endothelium-derived nitric oxide (EDNO) and endothelium-derived contracting factors (EDCF)] in a model of trauma-hemorrhage and resuscitation.

The induction of accelerated thymic programmed cell death during polymicrobial sepsis: control by corticosteroids but not tumor necrosis factor.

Thymic programmed cell death (PCD) or apoptosis (Ao) is elevated during inflammation by a variety of stressors in vitro (i.e., glucocorticoids, tumor necrosis factor (TNF), prostanoids, etc.

The role of bacterial translocation on Kupffer cell immune function following hemorrhage.

Studies have shown that Kupffer cell and splenic macrophage, as well as peritoneal macrophage antigen presentation function, was significantly depressed following hemorrhage and remained so for at least 96 hours after resuscitation. Although macrophage antigen presentation was depressed, in all the cell populations studied, it was only the Kupffer cells which were upregulated to produce increased inflammatory cytokines. Furthermore, Kupffer cells from hemorrhaged animals exhibited enhanced, as opposed to reduced toxicity by peritoneal and splenic macrophages.

Hepatocellular dysfunction occurs earlier than the onset of hyperdynamic circulation during sepsis.

Studies indicate that hepatocellular dysfunction occurs at 2 h after cecal ligation and puncture (CLP, i.e., sepsis model) despite the increased cardiac output (CO) and hepatic perfusion.

Dietary n-3 polyunsaturated fatty acid modulation of immune cell function before or after trauma.

We describe the role of increased eicosanoid production in inducing immunodepression associated with shock and trauma and the potential mechanisms by which prostaglandins produce immunosuppression. The effects of prefeeding with a diet high in n-3 polyunsaturated fatty acids (PUFAs) in preventing trauma-induced immunosuppression, and of such a diet on cellular immunity in patients after trauma are described. The potential mechanisms by which enteral diets containing n-3 PUFAs produce beneficial effects are also discussed.

Cytokine gene expression in splenic macrophages and Kupffer cells following haemorrhage.

TNF-alpha, IL-1, IL-6 and TGF-beta are important macrophage-derived mediators which play the pleiotropic role in inflammatory, metabolic, hematopoietic and immunologic processes. Studies have shown that haemorrhagic shock without significant tissue trauma induces profound immunosuppression which is associated with elevated plasma levels of TNF-alpha IL-1, IL-6 as well as TGF-beta. Furthermore, Kupffer cells but not the splenic M phi isolated from post-haemorrhaged animals showed an increased capacity to release inflammatory cytokines in response to LPS stimulation in vitro.

Dextran 70 administration after trauma-hemorrhagic shock does not impair cellular immune functions.

Purpose: Although the effects of the colloid dextran 70 on induction of anaphylactoid reactions or reticuloendothelial phagocytosis have been examined previously, its effects on specific cell-mediated immunity after trauma-hemorrhage shock remain unknown.

Methods: Nonheparinized C3H/HeN mice underwent a laparotomy, were bled, and then maintained at a blood pressure of 35 mm Hg for 60 minutes. Then they were resuscitated with either 4 x the shed blood volume as lactated Ringer's solution (LRS) or 2 x LRS + 1 x dextran 70.

Mechanism of enhanced susceptibility to sepsis following hemorrhage. Interleukin-10 suppression of T-cell response is mediated by eicosanoid-induced interleukin-4 release.

Objectives: To determine (1) whether interleukin-10 (IL-10) contributes to depressed T-cell responses observed following hemorrhage and (2) what effect other immunosuppressive agents known to play a role in hemorrhage have on IL-10 release.

Design: Hemorrhage was induced in C3H/HeN mice. The mice were resuscitated and then killed 2 hours after hemorrhage to obtain plasma, splenocytes, splenic macrophages, and splenic T cells.

Nitric oxide. To block or enhance its production during sepsis?

Background: Although it has been suggested that over-production of nitric oxide (NO) is responsible for death during endotoxic shock or sepsis, recent studies indicate that NO inhibition under such conditions is detrimental. The reason for these seemingly controversial findings may be because most studies were not standardized, ie, they were conducted at different stages of sepsis.

Objective: To determine whether differential alterations in endothelium-derived NO occur at different stages of sepsis.

Methods to prevent colonic injury in pelvic radiation.

Purpose: Radiation has become an adjunct in the treatment of pelvic malignancies. Attempts to prevent adjacent tissue injury have met with varying degrees of success, and the purpose of this study was to investigate potential radioprotective effects of an elemental diet, sodium meclofenamate, and vitamin A in an animal model of acute and chronic pelvic radiation previously described.

Methods: Female Sprague-Dawley rats, 200-250 grams, were anesthetized and then received 900 rads of pelvic radiation once per week for five weeks for a total of 4500 rads.

Biological significance of elevated TNF levels: in vivo administration of monoclonal antibody against tnf following haemorrhage shock increases the capacity of macrophages to release TNF while restoring immunoresponsiveness.

Haemorrhagic shock results in a severe depression of the cellular and humoral immunity, thus rendering the host increasingly susceptible to sepsis. To study the effect of elevated TNF release following haemorrhagic shock on depressed macrophage and splenocyte functions, C3H/HeN mice were pretreated intraperitoneally with either anti-murine TNF-Ab or saline. Twenty hrs later, mice were bled to and maintained at a mean BP of 35 mmHg for 60 min followed by adequate fluid resuscitation.

Peritoneal macrophages show increased cytokine gene expression following haemorrhagic shock.

Tumour necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), IL-1 and transforming growth factor-beta (TGF-beta) have been recognized as important mediators of pathophysiological and immunological events associated with shock. Previous studies have indicated that although peritoneal macrophage (PM phi) antigen presentation was depressed following haemorrhage, the cytokine release capacity in response to lipopolysaccharide (LPS) was not affected in vitro. To determine the effect of haemorrhagic shock on PM phi cytokine mRNA transcription, C3H/HeN male mice were bled to and maintained at a mean arterial blood pressure of 35 mmHg for 60 min, and then adequately resuscitated.

Chemically modified heparin improves hepatocellular function, cardiac output, and microcirculation after trauma-hemorrhage and resuscitation.

Background: Although heparinization before hemorrhagic shock improves tissue perfusion and organ function, the anticoagulant properties of conventional heparin preclude its clinical use. The purpose of this study was to determine whether chemically modified heparin (CMH), which does not have any significant anticoagulant activity, produces any beneficial effects on hepatocellular and cardiovascular function and microcirculation after trauma-hemorrhage and resuscitation.

Methods: After induction of tissue trauma (that is, laparotomy), rats were bled to and maintained at a mean arterial pressure of 40 mm Hg until 40% of maximum bleedout volume was returned in the form of Ringer's lactate (RL).

ATP-MgCl2 administration normalizes macrophage cAMP and beta-adrenergic receptors after hemorrhage and resuscitation.

Although ATP-MgCl2 attenuates the release of inflammatory cytokines and restores the defective macrophage (M phi) antigen presentation function after hemorrhage and resuscitation, it is not known whether administration of this agent after hemorrhage affects M phi adenosine 3',5'-cyclic monophosphate (cAMP) levels and beta-adrenergic receptors. To determine this, rats underwent a midline laparotomy (i.e.

Effects of trauma, duration of hypotension, and resuscitation regimen on cellular immunity after hemorrhagic shock.

Objective: To determine the effects of: a) surgical trauma, b) crystalloid resuscitation, and c) different durations of hypotension on cellular immunity after hemorrhagic shock.

Design: Prospective, multiexperimental, randomized, controlled studies.

Setting: University research laboratory.

ATP-MgCl2 treatment after trauma-hemorrhage/resuscitation increases hepatocyte P2-purinoceptor binding capacity.

Although our studies indicate that P2-purinoceptor binding capacity decreases after hemorrhage and resuscitation, it is not known whether ATP-MgCl2 administration after hemorrhage has any beneficial effects on the receptor dynamics. To study this, we performed laparotomy (i.e.

Downregulation of hepatocyte P2-purinoceptor binding capacity after trauma-hemorrhage/resuscitation.

Although P2-purinoceptors play an important role in the regulation of liver metabolism under normal conditions, it is not known if trauma-hemorrhage and resuscitation have any effects on such receptors. To study this, we performed a 5-cm midline laparotomy (i.e.

Administration of tumor necrosis factor-alpha in vivo depresses endothelium-dependent relaxation.

Although depressed endothelium-dependent relaxation occurs during early sepsis, the precise mechanism responsible for this remains unknown. Because the elevated levels of plasma tumor necrosis factor (TNF) play a major role in the pathophysiology of sepsis, we investigated whether TNF-alpha administration alters endothelium-dependent relaxation. To study this, recombinant TNF-alpha (1.