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1.
Immunobiology ; 223(3): 310-318, 2018 03.
Article in English | MEDLINE | ID: mdl-29102048

ABSTRACT

OBJECTIVE: After blunt thoracic trauma (TxT) and hemorrhagic shock with resuscitation (H/R) intense local inflammatory response and cell loss frequently impair the pulmonary function. Ethyl pyruvate (EP) has been reported to improve the pathophysiologic derangements in models of acute inflammation. Here, we studied the effects of EP on inflammation and lung damage after TxT+H/R. METHODS: Twenty four female Lewis rats (180-240g) were randomly divided into 3 groups: two groups underwent TxT followed by hemorrhagic shock (35±3mmHg) for 60min and resuscitation with either Ringers-Lactat (RL) alone or RL supplemented with EP (EP, 50mg/kg). Sham operated animals underwent surgical procedures. Two hours later bronchoalveolar lavage fluid (BAL), lung tissue and blood were collected for analyses. RESULTS: EP significantly improved pO2 levels compared to RL after TxT+H/R. TxT+H/R induced elevated levels of lactate dehydrogenase, total protein concentration in BAL and lung damage as evidenced by lung histology; these effects were significantly reduced by EP. Local inflammatory markers, lung TNF-alpha protein levels and infiltration with polymorphonuclear leukocytes (PMNL) significantly decreased in EP vs. RL group after TxT+H/R. Indicators of apoptosis as reduced BCL-2 and increased FAS gene expression after TxT+H/R were significantly increased or decreased, respectively, by EP after TxT+H/R. EP reduced TxT+H/R-induced p65 phosphorylation, which was concomitant with reduced HMGB1 levels in lung sections. CONCLUSIONS: Taken together, TxT+H/R induced strong inflammatory response and apoptotic changes as well as lung injury which were markedly diminished by EP. Our results suggest that this might be mediated via NF-κB and/or HMGB1 dependent mechanism.


Subject(s)
Acute Lung Injury/drug therapy , Anti-Inflammatory Agents/therapeutic use , Lung/drug effects , Pyruvates/therapeutic use , Shock, Hemorrhagic/diet therapy , Thoracic Injuries/drug therapy , Animals , Disease Models, Animal , Gene Expression Regulation , HMGB1 Protein/metabolism , Humans , Lung/physiology , NF-kappa B/metabolism , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , Rats , Rats, Inbred Lew , Signal Transduction/drug effects , Tumor Necrosis Factor-alpha/metabolism
2.
Shock ; 26(1): 77-86, 2006 Jul.
Article in English | MEDLINE | ID: mdl-16783202

ABSTRACT

The i.v. infusion of hypertonic NaCl solutions, as in small volume hypertonic NaCl resuscitation, improves cardiovascular function in hypovolemic shock. The mechanism(s) of action of this treatment is(are) not fully elucidated. In this study, we investigate the possible importance of fully functional neurocardiovascular regulation for the effect of intracerebroventricular (i.c.v.) and i.v. administration of hypertonic NaCl on the hemodynamic responses to hemorrhage. Six groups (each n = 6) of adult ewes were subjected to hypotensive hemorrhage during treatment with i.c.v. infusion (20 microL/min) of either artificial cerebrospinal fluid (controls) or 0.5 mol/L NaCl, or i.v. infusion of 1.2 mol/L NaCl (4 mL/kg) when conscious, respectively anesthetized with isoflurane. Thirty minutes into infusion, treatment blood was withdrawn at 0.7 mL/kg per minute from a jugular vein until the mean arterial pressure dropped to a value just below 50 mmHg. In conscious animals, the amount of blood loss needed to lower the mean arterial pressure to less than 50 mmHg was increased by the i.c.v. and i.v. infusions of hypertonic NaCl (24.0 +/- 4.6 and 22.4 +/- 3.3 mL/kg, respectively), compared with controls receiving i.c.v. infusion of artificial cerebrospinal fluid (14.2 +/- 1.4 mL/kg). Isoflurane anesthesia, as such, severely compromised the cardiovascular compensatory mechanisms activated by hemorrhage and reduced the blood loss necessary to cause hypotension (10.2 +/- 2.5 mL/kg). Furthermore, anesthesia totally abolished the effect of i.c.v. hypertonic NaCl (10.4 +/- 2.2 mL/kg) and blunted the response to i.v. hypertonic NaCl (15.9 +/- 2.1 mL/kg) seen in conscious animals. The results show that an intact autonomic cardiovascular control is crucial for the effect of i.c.v. hypertonic saline and indicate that i.v. hypertonic saline exerts some of its action through the central nervous system.


Subject(s)
Anesthetics, Inhalation/administration & dosage , Hemodynamics/drug effects , Isoflurane/administration & dosage , Saline Solution, Hypertonic/administration & dosage , Shock, Hemorrhagic/physiopathology , Anesthetics, Inhalation/adverse effects , Animals , Blood Pressure/drug effects , Central Nervous System/physiopathology , Female , Injections, Intravenous , Injections, Intraventricular , Isoflurane/adverse effects , Sheep , Shock, Hemorrhagic/diet therapy
3.
J Hepatol ; 41(3): 377-83, 2004 Sep.
Article in English | MEDLINE | ID: mdl-15336439

ABSTRACT

BACKGROUND/AIMS: Cholestatic patients are prone to septic complications after major surgery due to an increased susceptibility to endotoxin and hypotension. High-fat enteral nutrition reduces endotoxin after hemorrhagic shock. However, it is unknown whether this nutritional intervention is protective in biliary obstruction. We investigated the effect of high-fat enteral nutrition on endotoxin, tumor necrosis factor-alpha (TNF-alpha) and intestinal permeability in cholestatic rats subjected to hemorrhagic shock. METHODS: Bile duct-ligated (BDL) rats were fasted or fed with low-fat or high-fat enteral nutrition before hemorrhagic shock. Blood and tissue samples were taken after 90 min. RESULTS: Plasma endotoxin decreased after hemorrhagic shock in BDL-rats fed with high-fat nutrition compared to fasted (P<0.01) and low-fat treated rats (P<0.05). Additionally, circulating TNF-alpha was reduced in BDL-rats pretreated with high-fat nutrition compared to fasted rats (P<0.01). The increased intestinal permeability to macromolecules was reduced by high-fat enteral nutrition, whereas bacterial translocation did not significantly change. Simultaneously, tight junction distribution in ileum and colon was disrupted in non-treated BDL-rats but remained unchanged in high-fat pretreated BDL-rats. CONCLUSIONS: High-fat enteral nutrition protects against endotoxin-mediated complications independently of intraluminal bile. These results provide a potential new strategy to prevent endotoxin-mediated complications in cholestatic patients undergoing major surgery.


Subject(s)
Dietary Fats/administration & dosage , Enteral Nutrition , Shock, Hemorrhagic/diet therapy , Animals , Endotoxins/blood , Gastrointestinal Tract/physiopathology , Humans , Intestinal Absorption , Jaundice, Obstructive/complications , Jaundice, Obstructive/diet therapy , Jaundice, Obstructive/surgery , Male , Permeability , Postoperative Complications/prevention & control , Rats , Rats, Sprague-Dawley , Shock, Hemorrhagic/complications , Shock, Hemorrhagic/physiopathology , Triglycerides/blood , Tumor Necrosis Factor-alpha/metabolism
4.
Free Radic Biol Med ; 31(10): 1236-44, 2001 Nov 15.
Article in English | MEDLINE | ID: mdl-11705702

ABSTRACT

We investigated the effects of a glycine-containing diet (5%) on liver injury caused by hemorrhagic shock and resuscitation in rats. Anesthetized rats were bled to a mean arterial blood pressure of 35-40 mm Hg for 1 h and then resuscitated with 60% of shed blood and lactated Ringer's solution. Feeding the rats glycine significantly reduced mortality, the elevation of plasma transaminase levels and hepatic necrosis. The increase in plasma TNFalpha and nitric oxide (NO) was also blunted by glycine feeding. Hemorrhagic shock resulted in oxidative stress (significant elevations in TBARS and in the oxidized/reduced glutathione ratio) and was accompanied by a reduced activity of the antioxidant enzymes Mn- and Cu,Zn-superoxide dismutase, glutathione peroxidase and catalase, overexpression of inducible NO synthase (iNOS), and activation of nuclear factor kappa B (NF-kappaB). Glycine ameliorated oxidative stress and the impairment in antioxidant enzyme activities, inhibited NF-kappaB activation, and prevented expression of iNOS. Dietary glycine blocks activation of different mediators involved in the pathophysiology of liver injury after shock.


Subject(s)
Glycine/therapeutic use , Liver Diseases/prevention & control , NF-kappa B/antagonists & inhibitors , Shock, Hemorrhagic/diet therapy , Animals , Body Weight/drug effects , Catalase/blood , Dietary Supplements , Glutathione/blood , Glutathione Peroxidase/blood , Liver/pathology , Liver Diseases/blood , Liver Diseases/etiology , Liver Diseases/pathology , Male , NF-kappa B/blood , Nitric Oxide/blood , Nitric Oxide Synthase/blood , Nitric Oxide Synthase Type II , Oxidative Stress/drug effects , Rats , Rats, Wistar , Shock, Hemorrhagic/complications , Shock, Hemorrhagic/pathology , Superoxide Dismutase/blood , Transaminases/blood , Tumor Necrosis Factor-alpha/metabolism
5.
Rev. Fac. Med. (Caracas) ; 16(1): 34-8, ene.-jun. 1993. tab
Article in English | LILACS | ID: lil-127215

ABSTRACT

Following hemorrhagic shock, severe deragements of hemodynamic and inmune responses occur wich may lead to increased mortality and infectious complications. We utilized a murine model of hemorrhagic shock, and tested the effects of pre-feeding animals for 7 days with 3 different diets. Two consecutive acute hemorrhages were induced by cutting the tail under light anesthesia 30 min apart, with each bleeding depleting the animal of approximately 20// of the blood volume. At 24 hrs after hemorrhage, a period of maximal immunosuppresionand susceptibility to srpsis, animals underwent septic challenge, using cecal ligation. Pre-feeding the animals with a defined diet which contains high protein, arginine, nucleic acids, and structured lipids including fish oil (ImpactTM) improved survival after subsequent abdominal sepsis, compared to animals receiving standard rodent chow does not contain supplemental arginine, nucleic acids or structured lipids (TraumacalTM). Although special diets may improve survival in the face of subsequent septic challenge, the mechanisms involved are not clear, and factors other than immune simulation may account for this effect


Subject(s)
Rats , Animals , Shock, Hemorrhagic/diet therapy , Hemorrhagic Septicemia/diet therapy , Parenteral Nutrition
6.
Arch Surg ; 128(1): 15-20; discussion 20-1, 1993 Jan.
Article in English | MEDLINE | ID: mdl-8418775

ABSTRACT

Studies have suggested that the significant suppression of cellular immunity following hemorrhage may be due to an increased release of prostaglandin E2 (PGE2) by macrophages. Since diets high in n-3 polyunsaturated fatty acids decrease PGE2 synthesis, we assessed whether hemorrhage-induced immunosuppression could be prevented by dietary manipulation. C3H/HeN mice were fed for 3 weeks with fat sources derived from corn oil, safflower oil, or fish oil, then bled to a mean blood pressure of 35 mm Hg maintained for 60 minutes. Following this, the animals were adequately resuscitated with fluids and killed 24 hours later. In the corn oil and safflower oil groups, hemorrhage resulted in a significant increase in PGE2 release by peritoneal macrophages, a marked suppression of peritoneal macrophage antigen presentation capacity, interleukin 1 release, splenocyte proliferation, and interleukin 2 secretion compared with shams. However, feeding mice with fish oil for 3 weeks prior to hemorrhage prevented the rise in PGE2 release and maintained normal macrophage and splenocyte functions following hemorrhage. Thus, the elevated release of PGE2 by peritoneal macrophages plays a pivotal role in hemorrhage-induced immunosuppression. Moreover, diets high in n-3 polyunsaturated fatty acids may offer a new therapeutic approach for preventing posthemorrhage immunosuppression and increased mortality from sepsis.


Subject(s)
Dinoprostone/chemistry , Fatty Acids, Omega-3/therapeutic use , Immune Tolerance/drug effects , Immunity, Cellular/drug effects , Interleukin-1/chemistry , Macrophages/chemistry , Shock, Hemorrhagic/diet therapy , Animals , Dinoprostone/immunology , Disease Models, Animal , Drug Evaluation, Preclinical , Fatty Acids, Omega-3/administration & dosage , Fatty Acids, Omega-3/pharmacology , Humans , Immune Tolerance/immunology , Immunity, Cellular/immunology , Interleukin-2/chemistry , Macrophages/immunology , Male , Mice , Mice, Inbred C3H , Peritoneum/cytology , Shock, Hemorrhagic/immunology , Spleen/cytology
7.
Arch Surg ; 122(1): 78-81, 1987 Jan.
Article in English | MEDLINE | ID: mdl-3800653

ABSTRACT

Previous studies showed that dopamine and norepinephrine levels in rat brain are reduced following stress and that rats fed supplemental tyrosine do not exhibit these reductions. We hypothesized that dietary supplementation with tyrosine would enhance resistance to acute hemorrhagic shock and sepsis by increasing substrate (tyrosine) availability for catecholamine synthesis. Rats were fed either a standard rat chow (6.8 g of tyrosine per kilogram of chow), which supports normal growth, fertility, and longevity, or the same chow supplemented with 10 g of tyrosine per kilogram of chow. Seven days later, the rats underwent cecal ligation and perforation while under intraperitoneal pentobarbital anesthesia. There was a significant increase in survival in the tyrosine-supplemented group. Similarly, in another experiment, tyrosine-supplemented rats were able to tolerate acute fulminant hemorrhagic shock better than were nonsupplemented control animals.


Subject(s)
Infections/diet therapy , Shock, Hemorrhagic/diet therapy , Tyrosine/administration & dosage , Acute Disease , Animals , Catecholamines/biosynthesis , Male , Peritonitis/diet therapy , Rats , Rats, Inbred Strains
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