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Biomedical subjects

O Zamir

Publications and source records attributed to O Zamir.

At least 55 records · Page 3Linked to original sources
PubMed1992

Muscle protein breakdown during endotoxemia in rats and after treatment with interleukin-1 receptor antagonist (IL-1ra).

The purpose of this study was to examine the effect of endotoxemia on muscle protein degradation and to test the hypothesis that muscle proteolysis during endotoxemia is regulated by interleukin-1 (IL-1). Both total and myofibrillar protein breakdown rates in incubated extensor digitorum longus muscles were increased after the subcutaneous injection of 0.1 or 1.0 mg/kg endotoxin in rats. The endotoxin-induced increase in muscle protein breakdown was blunted by IL-1 receptor antagonist, administered intraperitoneally at a total dose of 45 or 105 mg/kg. Results suggest that endotoxemia in rats gives rise to sepsislike changes in muscle protein breakdown. Increased muscle protein breakdown during endotoxemia may be regulated, at least in part, by IL-1.

Animals↗
PubMed1991

Lipid-free total parenteral nutrition and macrophage function in rats.

Certain lipids are immunosuppressive when used for nutritional support, while other lipids and nutritional additives may enhance immunologic function. We hypothesized that total parenteral nutrition (TPN) may be immunosuppressive irrespective of lipids. Twenty-four rats underwent central vein catheterization and received either intravenous saline solution and oral chow or TPN alone. At 7 or 14 days, the animals were killed. Splenic and bone marrow macrophages were isolated and cultured in either M199 medium alone or were stimulated with Escherichia coli lipopolysaccharide. The supernatants were tested for prostaglandin E2 and C3. The splenic prostaglandin E2 levels were significantly higher in the TPN group following lipopolysaccharide stimulation at 7 days but not at 14 days. Administration of TPN to rats, even without lipids, may be immunosuppressive through the release of prostaglandin E2 from splenic macrophages following a septic challenge. This effect appears to be abolished after 14 days of TPN infusion.

Animals↗
PubMed1991

The effect of interleukin-1 alpha and the glucocorticoid receptor blocker RU 38486 on total and myofibrillar protein breakdown in skeletal muscle.

The purpose of the present study was to test the hypothesis that muscle proteolysis induced by interleukin-1 alpha (IL-1 alpha) is mediated by glucocorticoids. Male Sprague-Dawley rats, weighing 40-60 g, were treated with recombinant IL-1 alpha (rIL-1 alpha), 300 micrograms/kg in three divided intraperitoneal doses over 16 hr, or corresponding control injections. Groups of rats received the glucocorticoid receptor blocker RU 38486 by gavage (15 mg/kg in three divided doses over 16 hr) or were subjected to sham-gavage. In other experiments we tested the effectiveness of the same dose of RU 38486 to block muscle proteolysis in rats treated with corticosterone (200 mg/kg in two divided doses over 16 hr). Total and myofibrillar protein breakdown rates in incubated extensor digitorum longus muscles were determined by measuring release of tyrosine and 3-methylhistidine, respectively. Administration of rIL-1 alpha increased total and myofibrillar protein breakdown by 49 and 134%, respectively. This effect of the cytokine was not affected by RU 38486. The same dose of RU 38486, however, completely blocked the increase in total and myofibrillar protein breakdown induced by corticosterone. The results suggest that muscle proteolysis induced by the administration of rIL-1 alpha is not mediated by glucocorticoids.

Animals↗
PubMed1991

Influence of sepsis in rats on muscle protein turnover in vivo and in tissue incubated under different in vitro conditions.

We studied the influence of sepsis on muscle protein synthesis and degradation in vivo and in muscles, incubated flaccid or at resting length. Sepsis was induced in rats by cecal ligation and puncture (CLP). Control rats were sham-operated. A flooding dose of 14C-phenylalanine was used to determine muscle protein synthesis rate in vivo, and protein breakdown was calculated from the difference between protein synthesis and growth rates. Protein synthesis rate in vitro was assessed by determining incorporation of 14C-phenylalanine into protein in incubated extensor digitorum longus (EDL) and soleus (SOL) muscles. Total and myofibrillar protein breakdown rates were determined from release into incubation medium of tyrosine and 3-methylhistidine (3-MH), respectively. Muscle protein synthesis rate in vivo was reduced by 35%, similar to the reduction observed in muscles incubated flaccid or at resting length. The calculated protein breakdown rate in vivo was increased by 31% in septic rats. In incubated muscles, the increase in total protein breakdown (ie, tyrosine release) during sepsis was almost identical in muscles incubated flaccid or at resting length, ie, 83% to 88% in EDL and 47% to 49% in SOL. Myofibrillar protein degradation in vitro (ie, 3-MH release) was increased approximately 10-fold in EDL muscles incubated flaccid or at resting length, but was not significantly affected by sepsis in SOL. Results suggest that sepsis-induced changes in protein synthesis observed in muscles incubated either flaccid or at resting length reflect changes in vivo. Changes in protein breakdown were qualitatively similar in vivo and in vitro, but results in incubated muscles may overestimate the increase in muscle proteolysis caused by sepsis.

Adenosine Triphosphate↗
PubMed1991

Effect of the glucocorticoid receptor antagonist RU 38486 on muscle protein breakdown in sepsis.

The role of glucocorticoids in muscle catabolism during sepsis was tested with the glucocorticoid receptor antagonist RU 38486. Sepsis was induced in male Sprague-Dawley rats (40 to 60 gm) by cecal ligation and puncture (CLP). Other animals underwent sham operation. Two hours before CLP or sham operation, rats received RU 38486 (5 mg/kg) or a corresponding volume of vehicle by gavage. Sixteen hours after CLP or sham operation, protein synthesis rate was determined by measuring incorporation of 14C-phenylalanine into protein in incubated extensor digitorum longus muscles. Total and myofibrillar protein breakdown rates were determined by measuring net release of tyrosine and 3-methylhistidine, respectively. The protein synthesis rate was approximately 30% lower in rats with sepsis than in sham operated rats and was not affected by treatment with RU 38486. The total protein breakdown rate was increased by approximately 70% and myofibrillar protein degradation was increased more than fivefold in muscle from rats with sepsis. Treatment with RU 38486 resulted in a 28% reduction of total and a 44% reduction of myofibrillar protein breakdown in rats with sepsis but did not affect proteolysis in muscle from sham-operated animals. The results support a role of glucocorticoids in accelerated muscle proteolysis during sepsis. It is not clear whether glucocorticoids are the only required mediator or they interact with other substances to induce muscle protein breakdown during sepsis.

Animals↗
PubMed1990

Intercellular dye-coupling in intestinal smooth muscle. Are gap junctions required for intercellular coupling?

The dye Lucifer Yellow was injected into single smooth muscle cells in the guinea pig small intestine in order to study intercellular coupling. Dye-coupling was observed in both the circular and longitudinal muscle layers and was markedly reduced when the intercellular pH was lowered. These results suggest the presence of gap junctions among intestinal muscle cells, but are inconsistent with previous ultrastructural studies that failed to demonstrate such junctions in the longitudinal muscle.

Animals↗
PubMed1990

Prostaglandin E2 does not regulate total or myofibrillar protein breakdown in incubated skeletal muscle from normal or septic rats.

The role of prostaglandins in the regulation of muscle protein breakdown is controversial. We examined the influence of arachidonic acid (5 microM), prostaglandin E2 (PGE2) (2.8 microM) and the prostaglandin-synthesis inhibitor indomethacin (3 microM) on total and myofibrillar protein breakdown in rat extensor digitorum longus and soleus muscles incubated under different conditions in vitro. In other experiments, the effects of indomethacin, administered in vivo to septic rats (3 mg/kg, injected subcutaneously twice after induction of sepsis by caecal ligation and puncture) on plasma levels and muscle release of PGE2 and on total and myofibrillar protein breakdown rates were determined. Total and myofibrillar proteolysis was assessed by measuring production by incubated muscles of tyrosine and 3-methylhistidine respectively. Arachidonic acid or PGE2 added during incubation of muscles from normal rats did not affect total or myofibrillar protein degradation under a variety of different conditions in vitro. Indomethacin inhibited muscle PGE2 production by incubated muscles from septic rats, but did not lower proteolytic rates. Administration in vivo of indomethacin did not affect total or myofibrillar muscle protein breakdown, despite effective plasma levels of indomethacin with decreased plasma PGE2 levels and inhibition of muscle PGE2 release. The present results suggest that protein breakdown in skeletal muscle of normal or septic rats is not regulated by PGE2 or other prostaglandins.

Animals↗
PubMed1990

[Congenital diaphragmatic hernia presenting after the neonatal period].

Congenital diaphragmatic hernia (Bochdalek) is a congenital malformation usually presenting early after birth with a mortality of 50-70%. It is rarely diagnosed after the neonatal period, when the prognosis is considered favorable. We operated on 11 children past the neonatal period, ranging from 6 months to 5.5 years of age. 9 had presented with respiratory symptoms and were operated on semi-electively with excellent results. 2, operated on for strangulation of bowel incarcerated in the hernia, eventually died (aged 7 months and 1 year, respectively). Early diagnosis is important, as early surgery is recommended, even in those without symptoms.

Child, Preschool↗
PubMed1990

Interaction between corticosterone and tumor necrosis factor stimulated protein breakdown in rat skeletal muscle, similar to sepsis.

Protein synthesis and breakdown rates were determined in incubated extensor digitorum longus muscles of rats treated with tumor necrosis factor (TNF; 20 micrograms/100 gm body weight), corticosterone (20 mg/100 gm body weight), or a combination of the two substances. Protein synthesis was measured as incorporation of carbon 14-labeled phenylalanine into protein. Total and myofibrillar protein breakdown rates were assessed as release of tyrosine and 3-methylhistidine, respectively. Administration of TNF alone did not affect muscle protein turnover rates. Corticosterone inhibited muscle protein synthesis and stimulated total and myofibrillar protein breakdown. When TNF was administered together with corticosterone, total and myofibrillar protein breakdown rates were increased further compared with rats treated with corticosterone alone. Because plasma corticosterone levels in rats treated with both TNF and the glucocorticoid were higher than in animals treated with corticosterone alone, it is possible that muscle proteolysis noted after TNF, injected together with costicosterone, was caused by the high glucocorticoid levels. To test that hypothesis, corticosterone alone or in combination with TNF was injected in rats that had undergone adrenalectomy. In these experiments, TNF did not increase plasma corticosterone levels or muscle protein breakdown rates. The results suggest that muscle catabolism induced by administration of TNF is mediated by glucocorticoids.

Adrenalectomy↗
PubMed1989

Glial cells in the guinea pig myenteric plexus are dye coupled.

Glial cells in the myenteric plexus of the guinea pig small intestine were stained intracellularly with Lucifer yellow and horseradish peroxidase. The cells were identified by both their electrophysiological characteristics and by their morphology. Injection of Lucifer yellow, which is known to cross gap junctions, resulted in the staining of many (up to about 100) glial cells. The staining pattern was comparable to the immunostaining of glia with an antiserum for S-100 protein. In contrast to Lucifer yellow, horseradish peroxidase (which does not cross these junctions), was confined to the injected cell. It is concluded that enteric glia are coupled, presumably by gap junctions. This finding indicates that in addition to structural and biochemical similarities, enteric glia may share certain physiological characteristics with central nervous system astrocytes.

Action Potentials↗
PubMed1989

Peritonitis and empyema following the use of dextran in tubal operations.

Two patients developed severe bacterial sepsis with peritonitis and pleural empyema following tubal surgery. Intraperitoneal low-molecular dextran was used in both patients and hydrocortisone was administered perioperatively. The use of dextran in tubal surgery probably increases the risk of severe postoperative infection and should be avoided in susceptible patients. Prophylactic antibiotics may be indicated when dextran is administered.

Adult↗
PubMed1989

Gallbladder distention in premature neonates receiving parenteral nutrition.

Contraction of the gallbladder is mediated through the release of cholecystokinin from duodenal cells secondary to enteral feedings. Premature infants are often nourished by parenteral hyperalimentation leading to prolonged inactivation of the gallbladder. Such inactivation probably accounts for the increased incidence of gallbladder distention observed in premature neonates. Two cases of premature infants are described in whom distention of the gallbladder occurred during parenteral hyperalimentation. The distention resolved spontaneously secondary to the introduction of enteral feedings. A trial period of oral or tube feeding is recommended in such cases prior to any attempt to release the distention by a surgical intervention.

Gallbladder↗
PubMed1988

Idiopathic gastrointestinal perforation in the neonate.

Spontaneous localized perforation of the gastrointestinal tract, unrelated to mechanical intestinal obstruction and with no evidence of necrotizing entrocolitis (NEC), occurred in 20 neonates. Three perforations were located in the stomach, 11 in the small intestine, and six in the colon. Maternal obstetric complications as well as prematurity and postnatal distress were common in these patients. The overall survival rate was 80%. There was no late gastrointestinal symptoms in the survivors. Whether idiopathic perforation of the gastrointestinal tract results from a localized form of NEC or from a distinct lesion of unknown etiology has not yet been ascertained. Some ideas concerning the etiology of this entity, as well as some diagnostic aspects are discussed.

Colon↗
PubMed1988

Gastrointestinal perforations in the neonatal period.

Forty-eight neonates were treated for gastrointestinal perforation during a 9-year period. In 30, perforation occurred within the first week of life. Thirty-six were preterm infants and many had a history of obstetric and postnatal complications. Perforation resulted from necrotizing enterocolitis in 26 patients, whereas in 14 neonates spontaneous perforation occurred in an apparently normal bowel, with no evident cause (idiopathic perforation). In 6 patients perforation was associated with meconium ileus. Primary closure was carried out for perforations of the duodenum and stomach. Intestinal perforations were usually treated by resection and enterostomies. The overall mortality rate in this series was 46%. The highest mortality rate was associated with necrotizing enterocolitis (62%). The mortality rate was only 14% in patients with idiopathic perforation. Despite improvement in the prognosis of neonatal gastrointestinal perforations in recent years, it is still discouraging, reflecting the difficulty in preventing and treating necrotizing enterocolitis.

Enterocolitis, Pseudomembranous↗