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Biomedical subjects

E Vara

Publications and source records attributed to E Vara.

At least 19 recordsLinked to original sources
PubMed2007

Effect of exogenous administration of melatonin and growth hormone on pro-antioxidant functions of the liver in aging male rats.

Aging is accompanied by changes in the morphology and physiology of organs and tissues, such as the liver. This process might be due to the accumulation of oxidative damage induced by reactive oxygen (ROS) and reactive nitrogen species (RNS). Hepatocytes are very rich in mitochondria and have a high respiratory rate, so they are exposed to large amounts of ROS and permanent oxidative stress. Twenty-four male Wistar rats of 22 months of age were divided into three groups. One group remained untreated and acted as the control group. The second was treated with growth hormone (GH) (2 mg/kg/d sc) and the third was submitted to treatment wit 1 mg/kg/d of melatonin in the drinking water. A group of 2-months-old male rats was used as young controls. After 10 wk of treatment the rats were killed by decapitation, and the liver was dissected and homogenized. Mitochondrial, cytosolic and microsomal fractions were obtained and cytochrome C, glutathione peroxidase, s-transferase and nitric oxide (NO) were measured. Aging induced a significant increase in mitochondrial nitric oxide. An increase in cytochrome C in the cytosolic fraction and a reduction in the mitochondrial fraction with age was also observed. Both GH and melatonin treatments significantly reduced the enhanced measures and increased the reduced values. A reduction in glutathione peroxidase and glutathione S-transferase was found in old control rats when compared with the group of young animals. Treatment for 2.5 months of old rats with GH and melatonin were able to increase the enzymes reaching values similar to those found in young animals. In conclusion, GH and melatonin treatment seems to have beneficial effects against age-induced damage in the liver.

Aging↗
PubMed2005

Effect of isoflavone administration on age-related hepatocyte changes in old ovariectomized femal Wistar rats.

Aging seems to be due to the accumulation of oxidative damage in cells and molecules. On the other hand, menopause and ovariectomy induce deleterious effects on different organs and systems that have been shown to be counteracted by estrogens and in a not so evident form also with phytoestrogens. The present study has investigated whether the administration of a commercial soy extract that contains approximately 10% isoflavones was able to modify some parameters related to oxidative stress and inflammation in hepatocytes isolated from old ovariectomized female Wistar rats. Eighteen 22-month-old animals that had been previously ovariectomized at 12 months of age were divided into four groups: ovariectomized control rats, estradiol-treated ovariectomized females and ovariectomized rats treated with isoflavones. Six intact female rats of 2 months of age were used as reference group. Hepatocytes were isolated and cultured, and carbon monoxide (CO) and nitric oxide (NO) release, as well as adenosyl triphosphate (ATP), cyclic guanosyl monophosphate (cGMP), phosphatidylcholine (PC) and lipid peroxide (LPO) content of cells were evaluated. Uterus was also removed and weighed. Hepatocytes isolated from old ovariectomized rats showed a decrease in ATP content as compared to young animals. Age also induced an increase in LPO cell content. NO, CO and cGMP were augmented with age, and PC synthesis showed a dramatic reduction. Treatment with either estradiol or isoflavones were able to improve all the mentioned parameters altered in hepatocytes isolated from old ovariectomized rats, and the magnitude of the improvement was similar for both treatments. Ovariectomy induced a significant reduction in uterine weight, which was significantly counteracted by estradiol treatment but not by isoflavone administration. In conclusion, the administration of a soy extract containing isoflavones seems to prevent oxidative changes in hepatocytes isolated from old ovariectomized female rats, without modifying uterus weight.

Aging↗
PubMed2005

Efficacy of albendazole against Anisakis simplex larvae in vitro.

BACKGROUND: The growing popularity in western countries of eating uncooked seafood has resulted in an increased incidence of anisakidosis. AIM: To study the in vitro activity of different concentrations of albendazole against Anisakis simplex larvae under different media pH. METHODS: A. simplex larvae were obtained from fresh hakes acquired from the fish market of Madrid. They were divided into groups and placed in culture dishes (15 larvae each) containing RPMI-1640, in the presence or absence of different concentrations of albendazole (300, 400 and 500 microg/mL). RESULTS: Albendazole dose-dependently reduced the survival of the larvae, its maximum activity being at 500 microg/mL when it killed almost all larvae at 48 h. Acidic medium pH significantly reduced the efficacy of albendazole. CONCLUSION: Albendazole is effective in killing A. simplex larvae at different pH in vitro, suggesting that this molecule could be useful in treating clinical manifestations of human anisakidosis.

Albendazole↗
PubMed2005

Effect of insulin and growth hormone on rat heart and liver oxidative stress in control and caloric restricted animals.

In order to know if insulin-like signalling is involved in the control of oxidative stress in mammalian tissues in relation to aging, ad libitum-fed and caloric restricted Wistar rats were treated during 2 weeks with GH and insulin. The most consistent effect of the hormonal treatments was an increase in plasma IGF-1 levels. Caloric restriction during 6 weeks decreased ROS generation and oxidative DNA damage in heart mitochondria and this was reversed by insulin treatment. The decrease in oxidative damage to liver nuclear DNA induced by caloric restriction was also reversed by GH and insulin. In the liver, however, insulin and GH decreased mitochondrial ROS generation while they increased oxidative damage to mitochondrial DNA. GH and insulin decreased three different markers of oxidative modification of liver proteins, while they increased lipoxidation-dependent markers. This last result is related to the increase in phospholipid unsaturation induced in the liver by both hormones. The results suggest that the idea that insulin-like signalling controls oxidative stress in mammals cannot be generalized since both prooxidant and protective effects of GH and insulin are observed depending on the particular parameter and tissue selected.

Age Factors↗
PubMed2001

Cyclosporin a treatment is able to revert the decrease in circulating GH and IGF-I and the increase in IGFBPs induced by adjuvant arthritis.

The aim of this study was to find out whether cyclosporin A administration is able to revert the decrease in circulating growth hormone (GH) and insulin-like growth factor-I (IGF-I) and the increase in IGF-binding proteins (IGFBPs) levels caused by adjuvant-induced arthritis in rats. Male Sprague-Dawley rats were intradermically injected with Freund's adjuvant or vehicle. Fourteen days later, rats were randomly divided into two groups - one injected with cyclosporin (15 mg/kg) and the other with vehicle from day 16 to 23 after adjuvant injection. Arthritis decreased body weight gain and serum concentrations of GH. Cyclosporin administration to arthritic rats prevented both effects, whereas cyclosporin had no effect in control rats. Arthritis decreased serum concentrations of IGF-I (p < 0.01), but increased IGFBPs. Cyclosporin administration increased circulating IGF-I, and there was a negative correlation between circulating IGF-I and arthritis index scores in arthritic rats injected with cyclosporin (p < 0.05). Cyclosporin treatment did not alter serum IGFBPs levels in control rats, whereas cyclosporin administration normalised IGFBPs in arthritic rats. These results indicate that the effects of cyclosporin administration on the GH-IGF-IGFBPs system may partly mediate its beneficial effect on body weight in arthritic rats.

Animals↗
PubMed2001

Glucagon-like peptide-1(7-36) amide stimulates surfactant secretion in human type II pneumocytes.

To determine the influence of glucagon-like peptides on the secretion of human pulmonary surfactant, we used human type II pneumocytes. In these cells, GLP-1(7-36) amide and exendin-4 stimulated phosphatidylcholine secretion (PC) and cAMP formation in a concentration-dependent manner; these effects were reversed by exendin(9-39). No changes were observed with other related peptides. The mechanism by which GLP-1(7-36) amide exerts its stimulatory effect was investigated with various agents that are well known to be stimulators or inhibitors of PC secretion. Thus, 8-bromo-cAMP increased and both Rp-cAMPS and H-89, the latter an inhibitor of protein kinase A (PKA), reduced pulmonary surfactant secretion in type II pneumocytes. Also, GLP-1(7-36) amide and TPA exerted additive effects in stimulating PC secretion, and Calph C, a potent inhibitor of protein kinase C (PKC), blocked most of the effect of GLP-1(7-36) amide. By contrast, both the calcium ionophore A23187 and GLP-1(7-36) amide had additive effects in increasing PC secretion, and the specific inhibitor of Ca(2+)-calmodulin-dependent protein kinase (Ca-CM-PK), KN-62, inhibited the effect of A23187 but did not alter the stimulatory action of GLP-1(7-36) amide. Our findings suggest that both PKA and PKC are involved in the stimulatory effects of GLP-1(7-36) amide on PC secretion, whereas this peptide has no effect on PC secretion through a Ca-CM-PK mechanism.

Adult↗
PubMed2000

Growth hormone response to long-term GH-RH administration in lambs.

The pattern of long-term GHRH administration capable of stimulating GH release without depleting pituitary GH content has been investigated using two experimental approaches. In experiment 1, recently weaned male lambs were treated for 3 weeks as follows: Group A) control; B) subcutaneous (sc) continuous infusion of GHRH (1200 mg/day) using a slow release pellet; C) the same as B plus 1 daily sc injection of long acting somatostatin (SS) (octreotide, 20 mg) ; D) 3 daily sc GHRH (250 mg) injections ; E) 2 daily sc injections of GHRH (250 mg) and 2 of natural SS (250 mg). In experiment 2, recently weaned male lambs were continuously GHRH-treated using sc osmotic minipumps (900 mg/day) alone or combined with a daily sc injection of octreotide (20 mg) for 4 weeks. Basal plasma GH levels were increased after chronic pulsatile GHRH treatment but not after any kind of continuous GHRH administration. This increment was maintained during the 3 weeks of experimentation and appeared accompanied by a pituitary GH content similar to controls. A marked GH response to the iv GHRH challenge was observed in controls and in lambs receiving both types of continuous sc GHRH infusions, whereas pulsatile sc GHRH-treated animals did not respond to the iv GHRH challenge in the first and second weeks of the study but did so in the third week of treatment. These data demonstrate that long-term pulsatile GHRH administration is capable of stimulating GH release in growing male lambs, without producing pituitary desensitization.

Analysis of Variance↗
PubMed2000

Increased plasma levels of corticosterone and prolactin and decreased T3 and T4 levels in short-term prehepatic portal hypertension in rats.

Corticosterone, T3, T4, and prolactin serum concentrations at 24 hr (N = 10), 15 days (N = 10), and 45 days (N = 10) of postoperative (postop) evolution were assayed to study the neuroendocrine response to portal hypertension. A triple stenosing ligature of the portal vein was used as the surgical technique of portal hypertension. This technique does not produce mortality and causes a decrease in the serum concentrations of T3 (0.043 +/- 0.009 vs 0.55 +/- 0.08 ng/ml) and T4 (3.93 +/- 0.55 vs 4.65 +/- 0.67 microg/ml) and an increase in those of prolactin (28.61 +/- 20.20 vs 12.84 +/- 3.96 ng/ml) and corticosterone (397.50 +/- 64.17 vs 311.53 +/- 57.41 ng/ml) at 45 days postop. The T3, T4, prolactin, and corticosterone alterations are associated with a persistent increase of TNF-alpha and NO, whose serum concentrations at 45 days postop are, respectively, 1838.33 +/- 247.07 vs 48.89 +/- 8.75 pg/ml and 0.43 +/- 0.13 vs 0.19 +/- 0.01 mmol/ml. TNF-alpha and NO could mediate these hormonal alterations in the evolution of short-term portal hypertension in the rat; thus they are involved in the systemic neuroendocrine response that is induced by this injury.

Animals↗
PubMed2000

Effect of surfactant protein A (SP-A) on the production of cytokines by human pulmonary macrophages.

Surfactant protein A (SP-A) is thought to play a role in the modulation of lung inflammation during acute respiratory distress syndrome (ARDS). However, SP-A has been reported both to stimulate and to inhibit the proinflammatory activity of pulmonary macrophages (Mphi). Because of the interspecies differences and heterogeneity of Mphi subpopulations used may have influenced previous controversial results, in this study, we investigated the effect of human SP-A on the production of cytokines and other inflammatory mediators by two well-defined subpopulations of human pulmonary Mphi. Surfactant and both alveolar (aMphi) and interstitial (iMphi) macrophages were obtained from multiple organ donor lungs by bronchoalveolar lavage and enzymatic digestion. Donors with either recent history of tobacco smoking, more than 72 h on mechanical ventilation, or any radiological pulmonary infiltrate were discarded. SP-A was purified from isolated surfactant using sequential butanol and octyl glucoside extractions. After 24-h preculture, purified Mphi were cultured for 24 h in the presence or absence of LPS (10 microg/mL), SP-A (50 microg/mL), and combinations. Nitric oxide and carbon monoxide (CO) generation (pmol/microg protein), cell cGMP content (pmol/microg protein), and tumor necrosis factor alpha (TNFalpha), interleukin (IL)-1, and IL-6 release to the medium (pg/microg protein) were determined. SP-A inhibited the lipopolysaccharide (LPS)-induced TNFalpha response of both interstitial and alveolar human Mphi, as well as the IL-1 response in iMphi. The SP-A effect on TNFalpha production could be mediated by a suppression in the LPS-induced increase in intracellular cGMP. In iMphi but not in aMphi, SP-A also inhibited the LPS-induced IL-1 secretion and CO generation. These data lend further credit to a physiological function of SP-A in regulating alveolar host defense and inflammation by suggesting a fundamental role of this apoprotein in limiting excessive proinflammatory cytokine release in pulmonary Mphi during ARDS.

Adult↗
PubMed2000

Intervention study for smoking cessation in diabetic patients: a randomized controlled trial in both clinical and primary care settings.

OBJECTIVE: To evaluate the effectiveness of a nurse-managed smoking cessation intervention in diabetic patients. RESEARCH DESIGN AND METHODS: This randomized controlled clinical trial involved 280 diabetic smokers (age range 17-84 years) who were randomized either into control (n = 133) or intervention (n = 147) groups at 12 primary care centers and 2 hospitals located in Navarre, Spain. The intervention consisted of a 40-min nurse visit that included counseling, education, and contracting information (a negotiated cessation date). The follow-up consisted of telephone calls, letters, and visits. The control group received the usual care for diabetic smokers. Baseline and 6-month follow-up measurements included smoking status (self-reported cessation was verified by urine cotinine concentrations), mean number of cigarettes smoked per day, and stage of change. RESULTS: At the 6-month follow-up, the smoking cessation incidence was 17.0% in the intervention group compared with 2.3% in the usual care group, which was a 14.7% difference (95% CI 8.2-21.3%). Among participants who continued smoking, a significant reduction was evident in the average cigarette consumption at the 6-month follow-up. The mean number of cigarettes per day decreased from 20.0 at baseline to 15.5 at 6 months for the experimental group versus from 19.7 to 18.1 for the control group (P < 0.01). CONCLUSIONS: A structured intervention managed by a single nurse was shown to be effective in changing the smoking behavior of diabetic patients.

Adolescent↗
PubMed1999

Effect of melatonin treatment on 24-hour rhythms of serum ACTH, growth hormone, prolactin, luteinizing hormone and insulin in rats injected with Freund's adjuvant.

The effect of melatonin injection on Freund's adjuvant-induced changes in levels and 24-hr rhythms of circulating ACTH, growth hormone (GH), prolactin (PRL), luteinizing hormone (LH), and insulin was assessed in rats. Animals received subcutaneous (s.c.) injections of melatonin (30 microg) or vehicle, 1 hr before lights off for 12 days. Ten days after melatonin treatment, they were injected with Freund's complete adjuvant or its vehicle s.c., and after 3 days, rats were killed at six different time intervals throughout a 24-hr cycle to measure the different hormones by radioimmunoassay (RIA). Following Freund's adjuvant injection, an increase in serum ACTH, with maintenance of ACTH diurnal rhythm was found. Acrophases of the ACTH rhythm varied from 13:39 to 17:12 hr and the amplitude of rhythm was augmented after immunization. In immunized rats, melatonin treatment increased the amplitude of serum ACTH rhythm. For GH, a depressive effect of immunization on circulating levels, together with absence of diurnal rhythmicity were found. Immunization augmented circulating PRL, while conserving its diurnal rhythmicity. Melatonin-injected rats showed significant diurnal variations of serum PRL after immunization only. Acrophases of the serum PRL rhythm varied from 19:37 to 22:04 hr. Immunization decreased circulating LH and suppressed its 24-hr rhythmicity pattern. The effect of immunization on LH was counteracted by melatonin injection. Acrophases of serum LH rhythm varied from 00:44 to 03:53 hr. Significant effects of immunization and time of day on circulating insulin were detected; immunization increased serum insulin levels with a shift in acrophase from early afternoon to midnight. The data indicate that several early changes in levels and 24-hr rhythms of circulating ACTH, PRL, and LH in Freund's adjuvant-injected rats were sensitive to treatment with pharmacological amounts of melatonin.

Adrenocorticotropic Hormone↗
PubMed1998

Effects of endotoxin lipopolysaccharide administration on the somatotropic axis.

The aim of this work was to study the effect of chronic activation of the immune system on the somatotropic axis. Accordingly, the changes in growth hormone (GH) secretion, circulating insulin-like growth factor-I (IGF-I) and IGF binding proteins (IGFBPs) in response to endotoxin lipopolysaccharide (LPS) administration were examined in adult male Wistar rats. Acute LPS injection (2.5, 25 or 250 microg/kg) increased serum corticosterone in a dose-dependent manner and decreased serum levels of insulin and IGF-I, serum GH concentration declined linearly as the LPS dose increased. Western ligand blot showed an increase in the 33 kDa band (corresponding to IGFBP-1 and IGFBP-2) in the rats that received the highest dose of LPS (250 microg/kg). Chronic LPS administration (250 microg/kg daily for 8 days) significantly decreased body weight, serum levels of IGF-I and pituitary GH content, whereas it increased circulating IGFBP-3 (47 kDa band), IGFBP-1 and IGFBP-2 (33 kDa band) and the 24 kDa band (which possibly corresponds to IGFBP-4). Serum concentration of corticosterone and hypothalamic somatostatin content were also increased by chronic LPS treatment. These data suggest that the decrease in GH and IGF-I secretion and the increase in circulating IGFBPs are important mechanisms in body weight loss during chronic inflammation.

Animals↗
PubMed1997

Carbon monoxide contributes to the cytokine-induced inhibition of surfactant synthesis by human type II pneumocytes.

BACKGROUND: An increase in cyclic guanosine 3',5'-monophosphate (cGMP) due to nitric oxide generation is known to participate in the mediation of the tumor necrosis factor alpha (TNF-alpha) effect in type II cells. Because guanylyl cyclase can be activated also by carbon monoxide (CO), in this study we examined the ability of human type II pneumocytes to produce CO in the presence of cytokines and the relative contribution of this molecule to the TNF-alpha and interleukin 1 effects. DESIGN: Type II pneumocytes were isolated from cadaveric multiple-organ donors by enzymatic digestion, adherence separation of macrophages, and gradient purification. After preculture for 24 hours, cells were cultured for 24 hours in the presence or absence of TNF-alpha, interleukin 1, sodium nitroprusside, N(omega)-nitro-1-arginine, CO, hemin, zinc-protoporphyrin type IX, deferoxamine mesylate, S-adenosyl-L-methionine, alpha-tocopherol, methylene blue (a guanylyl cyclase inhibitor), 8-bromine-cGMP, and combinations of these reagents. Both CO (picomole per microgram of protein) and nitric oxide release to the medium and the cGMP (picomole per microgram of protein) content of the cells were measured. In a different set of experiments, D-glucose labeled with radioactive carbon (14C) was added to the medium, and the labeling of several lipid fractions was determined (picomole per microgram of protein). RESULTS: D-[14C]glucose incorporation into phosphatidylcholine, the main surfactant component, was selectively inhibited in the presence of cytokines, CO, sodium nitroprusside, or 8-bromine-cGMP. The inhibitory effect of TNF-alpha was partially reversed by N(omega)-nitro-L-arginine, deferoxamine, or alpha-tocopherol and totally reversed by methylene blue. Tumor necrosis factor alpha induced an increase in cGMP cell content and in the CO and nitric oxide release to the medium. Hemin increased CO and cGMP production and decreased phosphatidylcholine synthesis. Zinc-protoporphyrin type IX, an inhibitor of heme oxygenase, and all 3 antioxidants, which inhibited CO production, also antagonized the TNF-alpha effect on cGMP and phosphatidylcholine synthesis. CONCLUSIONS: Intracellular cGMP increase due to an endogenous generation of both CO and nitric oxide mediates the cytokine-induced inhibition of surfactant synthesis by type II pneumocytes. Both lipid peroxidation and heme oxygenase activity are sources for the observed CO production.

Adolescent↗
PubMed1997

Local production of oxygen free radicals and nitric oxide in rat diaphragm during sepsis: effects of pentoxifylline and somatostatin.

OBJECTIVE: To investigate the effect of giving lipopolysaccharide (LPS) on lipid peroxidation, and myeloperoxidase (MPO), nitric oxide (NO) synthase, and phospholipase A2 (PLA2) activities in rat diaphragm, and see whether they could be modified by giving pentoxifylline (PTXF) or somatostatin. DESIGN: Randomised experimental study. SETTING: Teaching hospital, Spain. MATERIAL: 76 Wistar rats divided into 4 groups of 19: control (saline/saline), LPS/saline, LPS/PTXF and LPS/somatostatin. INTERVENTIONS: The LPS was given intraperitoneally either 30 minutes (early, n = 10 in each group) or 120 minutes (late, n = 9 in each group) before treatment with saline, PTXF (45 mg/kg) or somatostatin (200 microg/kg) given intraperitoneally. Rats were killed 120 minutes after treatment. MAIN OUTCOME MEASURES: Malondialdehyde (MDA) and conjugated dienes content, and MPO, NO synthase, and PLA2 activities in diaphragmatic tissue. RESULTS: Conjugated dienes and MDA content, as well as MPO, NO synthase, and PLA2 activities were significantly increased in the rats given LPS. Independently of the timing of treatment, both PTXF and somatostatin completely prevented these increases. CONCLUSION: It is possible that treatment with PTXF or somatostatin may reduce the risk of ventilatory failure and speed recovery in septic patients.

Analysis of Variance↗
PubMed1996

S-adenosylmethionine protects hepatocytes against the effects of cytokines.

Cytokines are thought to play an important role in the hepatocellular dysfunction that occurs during sepsis. Some cytokines have been shown to increase lipogenesis and to induce toxicity in isolated hepatocytes. Oxygen free radicals have been implicated as mediators of some cytokine effects. In this study we investigate a possible protection action of S-adenosyl-L-methionine against the toxic effects of cytokines on isolated hepatocytes. Isolated rat hepatocytes were precultured for 24 hr and then cultured for 1, 2, 3, 6, 12, or 24 hr in the presence or absence of S-adenosyl-L-methionine (12 micromol/l0) and/or either tumor necrosis factor (100, 200, or 500 ng/ml) or interleukin-1 (30, 60, or 120 IU/ml). Lactate dehydrogenase (media), and malondialdehyde, reduced glutathione, and the incorporation of D-[U- 14 C] glucose into different lipid fractions (cells) were determined. Both cytokines significantly increased hepatocyte malondialdehyde content, lactate dehydrogenase release, and triacylglycerol synthesis. None of these effects were observed in the presence of S-adenosyl--L-methionine. In addition, S-adenosyl-L-methionine was able to attenuate the decrease in phosphatidylcholine labeling also induced by both cytokines, and to prevent the increase in free fatty acid synthesis induced by tumor necrosis factor. Incubation in the presence of S-adenosyl-L-methionine also increased hepatocyte glutathione content (7.1 +/- 0.7, after 24 hr, vs 3.6 +/- 0.3 nmole/mg protein, P < 0.01), and prevented the decrease in glutathione induced by tumor necrosis factor (5.4 +/- 0.2 vs 2.1 +/- 0.1 nmole/mg protein, 100 ng/ml TNF alpha at 24 hr, P < 0.01). Our results show that S-adenosyl-L-methionine has a protective effect on hepatocytes against the in vitro effect of cytokines.

Animals↗
PubMed1996

NO2/NO3 and cytokine plasma profiles under different postoperative parenteral nutrition regimens.

Both nitric oxide and cytokines are considered mediators of the acute-phase response in humans, and their early postoperative period plasma levels have been found to be of prognostic value. On the other hand, it has been suggested that the fatty emulsions used in total parenteral nutrition (TPN) may induce changes in macrophage function. In the present study we investigated the postoperative evolution of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), interleukin-6 (IL-6), and nitrate/nitrite plasma levels under three different TPN regimens. Twenty-one patients diagnosed with upper digestive tract neoplasm, without preoperative TPN, and having undergone radical surgery, were randomly assigned to three groups: Group I, all nonprotein calories supplied by hypertonic glucose solution: Group II, 55% of the nonprotein calories supplied by glucose and 45% by 20% long-chain triacylglycerides emulsion (LCT) (Intralipid 20%, Kabi-Pharmacia); Group III, same as Group II, but a 20% emulsion of a mixture of medium-chain and long-chain triacylglycerides (MCT/LCT) (Lipofundina MCT/LCT 20%, B. Braun) was used instead of LCT. Blood samples were obtained on postoperative Days 1-5 and 10, 3 h after ending the lipid infusion. In all the three groups IL-1, IL-6, and TNF-alpha levels rose after surgery, peaking at Day 2, whereas NO2/NO3 levels had their peak at Day 3. Day-to-day comparison of plasma levels of cytokines and NO2/NO3 between the investigated groups did not show any statistical significance. Differences between group means were not found when the areas under the curve over the first 5 postoperative days were compared (1.72 +/- 0.25, Group I; 1.88 +/- 0.34, Group II; and 2.52 +/- 0.50, Group III, for TNF-alpha; 1.79 +/- 0.12, Group I; 1.92 +/- 0.18, Group II; and 1.50 +/- 0.12, Group III, for NO2/NO3). We conclude that the different parenteral nutrition regimens studied do not evoke alterations in cytokine and NO2 + NO3 levels in the patient groups investigated in this study.

Cytokines↗