Biomedical subjects

M Jeevanandam

Publications and source records attributed to M Jeevanandam.

At least 19 recordsLinked to original sources

PubMed2006

Hydrogeochemistry and groundwater quality assessment of lower part of the Ponnaiyar River Basin, Cuddalore district, South India.

The Lower Ponnaiyar River Basin forms an important groundwater province in South India constituted by Tertiary formations dominated by sandstones and overlain by alluvium. The region enjoyed artesian conditions 50 years back but at present frequent failure of monsoon and over exploitation is threatening the aquifer. Further, extensive agricultural and industrial activities and urbanization has resulted in the increase in demand and contamination of the aquifer. To identify the sources and quality of groundwater, water samples from 47 bore wells were collected in an area of 154 km2 and were analysed for major ions and trace metals. The results reveal that the groundwater in many places is contaminated by higher concentrations of NO3, Cl, PO4 and Fe. Four major hydrochemical facies Ca-Mg-Cl, Na-Cl, Ca-HCO3 and Na-HCO3 were identified using Piper trilinear diagram. Salinity, sodium adsorption ratio, and sodium percentage indicate that most of the groundwater samples are not suitable for irrigation as well as for domestic purposes and far from drinking water standards. The most serious pollution threat to groundwater is from nitrate ions, which are associated with sewage and fertilizers application. The present state of the quality of the lower part of Ponnaiyar River Basin is of great concern and the higher concentration of toxic metals (Fe and Ni) may entail various health hazards.

Hazardous Substances↗

PubMed2001

Clinical role of polyamine analysis: problem and promise.

Polyamines are ubiquitous cell components for growth. They play an important role in cell proliferation, cell growth and synthesis of protein and nucleic acids. Cells that are stimulated to reproduce demonstrated early increases in biosynthetic enzymes involved in polyamine synthesis and subsequent elevations in polyamine levels. Extracellular fluid polyamine concentrations that reflect the intracellular events may be useful as rapid indicators of therapy in disorders which involve altered cell growth. More complex analytical approaches are required to isolate, identify and quantitate these polyamines. Most of the methods require an extraction procedure to remove interfering amino acid derivatives. Daily monitoring of plasma and urine polyamine levels in many pathological states may provide a non-invasive biochemical marker of the existing disease activity or response to therapy or to screen for drug efficacy. Automated high-performance liquid chromatography, with post or pre-column derivatization and fluorescence or electrochemical detection is frequently used for the simultaneous quantitation of picomolar quantities of polyamines. Recently, a new immuno-cytochemical model system incorporating an enzyme-linked immunosorbent assay for specific polyamines has been developed. The increasing momentum of basic science information in the polyamine discipline may lead clinicians to regard polyamines, their metabolites and antimetabolites as sources of effective treatment.

Biomarkers↗

PubMed2000

Altered plasma cytokines and total glutathione levels in parenterally fed critically ill trauma patients with adjuvant recombinant human growth hormone (rhGH) therapy.

OBJECTIVES: Glutathione (GSH) is a potent endogenous antioxidant that serves as one of the body's most important defenses against oxygen metabolites. Plasma levels of GSH are maintained primarily by a balance between secretion from the liver and degradation in the kidney. The ability to maintain and enhance tissue GSH may be of particular importance in controlling cytokine production in response to a stimulus like injury. The interaction after severe trauma between GSH and cytokines, tumor necrosis factor (TNF) -alpha, and interleukin (IL)-6, are not known. The purpose of the study was to investigate the levels of plasma GSH and cytokines TNF-alpha and IL-6 in adult patients admitted to the intensive care unit of our level I trauma center who were treated with recombinant human growth hormone (rhGH) for > or =7 days. DESIGN: Prospective, randomized, controlled trial. SETTING: Trauma intensive care unit. PATIENTS: Twenty-eight patients with multiple injuries and 14 normal postabsorptive controls. INTERVENTIONS: From 48-60 hrs after injury, when resuscitation was complete, a stable hemodynamic status was achieved and the patients were receiving maintenance fluid without nitrogen or calories, a blood sample was drawn for basal, plasma GSH, TNF-alpha, and IL-6 measurement. Intravenous feeding was then started and continued for 7 days. The patients were randomized to receive or not to receive daily intramuscular doses of recombinant human growth hormone (0.15 mg rhGH/kg/day). Daily morning plasma was obtained for analysis of GSH, TNF-alpha, and IL-6 levels. RESULTS: In the early catabolic "flow phase" of severe injury, the plasma levels of GSH were not altered but plasma TNF-alpha and IL-6 levels were increased significantly, compared with uninjured controls. Seven days of total parenteral nutrition alone enhanced plasma GSH levels (76%), but no change in TNF-alpha was observed. Supplementation with rhGH enhanced GSH (180%), and TNF (65%) with no changes in IL-6 levels. There is a significant linear relationship between plasma GSH and TNF-alpha levels in our rhGH-supplemented trauma patients. CONCLUSION: Modification of plasma GSH and TNF-alpha levels by adequate nutritional support with adjuvant rhGH during the postinjury period demonstrates the beneficial role of GSH in enhancing antioxidant defenses.

Adolescent↗

PubMed1999

Release of proinflammatory cytokines by mitogen-stimulated peripheral blood mononuclear cells from critically ill multiple-trauma victims.

This study investigated the alterations in circulating proinflammatory cytokines and cytokine production by peripheral blood mononuclear cells (PBMCs) in response to lipopolysaccharide (LPS) or phytohemagglutinin (PHA) after severe trauma. Plasma and PBMCs were collected from 17 severely injured trauma patients and 10 healthy subjects. Plasma was stored at -80 degrees C and analyzed for cytokines. Isolated PBMCs from each subject were stimulated with LPS or PHA and incubated at 5% CO2 for 24 hours. Supernatants were collected and analyzed for cytokines. There was no significant change in the plasma concentration of free TNF-alpha and IL-1beta between healthy subjects and trauma patients. Plasma IL-6, total TNF-alpha, and total IL-1beta were significantly increased in severely traumatized patients compared with healthy control subjects. PBMCs from trauma patients produced higher levels of TNF-alpha in response to LPS but it showed no significant change in IL-1beta and IL-6 production in response to PHA or LPS in comparison to PBMCs from control subjects. We conclude that severe trauma results in a significant increase in plasma proinflammatory cytokine IL-6. Free TNF-alpha and IL-1beta in plasma remain at levels comparable to those in uninjured controls, while plasma free IL-6 levels in trauma patients remain high. Serious injury is associated with an enhanced production of TNF-alpha by PBMCs stimulated with LPS.

Adult↗

PubMed1999

Substrate fuel kinetics in enterally fed trauma patients supplemented with ornithine alpha ketoglutarate.

BACKGROUND: Ornithine-alpha-ketoglutarate (OKG) is a promising anticatabolic agent and the mechanisms of its potential use in trauma patients are not clearly understood. AIM: To determine the altered whole-body protein, lipid and glucose substrate kinetics in trauma victims in the early flow-phase of injury when they were fed enterally with or without OKG. METHODS: Fourteen adult, multiple trauma patients who were highly catabolic and hypermetabolic were studied. Whole-body protein ((15)N glycine), fat (2 stage glycerol infusion) and glucose ((3H)glucose) kinetics (t/o) and plasma parameters were measured (A) within 48-60 h after injury before starting nutritional support and then (B) after 4 days of enteral feeding. Group A (n=7, control) received a defined enteral formula (Two Cal HN, 1.4 times BEE calories) and Group B (n=7, OKG) received same isonitrogenous diet replacing 2.62gN/d from the enteral diet by OKG-N (20g OKG/d). RESULTS (Mean+/-SEM): Protein turnover is significantly (P<==0.05) increased in OKG treated patients (4.68+/-0. 15 vs 3.90+/-0.23, gP/kg/day) and glycerol turnover is decreased (0. 87+/-0.16 vs 1.46+/-0.16, micro mole/kg/min). Glucose turnover is not changed. Significant (P<== 0.05) increases in circulating plasma levels of hormones (insulin, 44.2+/-8.4 vs 15.7+/-5.0 ulU/ml, growth hormone 1.68+/-0.33 vs 0.92+/-0.16, ng/ml and IGF-1, 106+/-13 vs 75+/-18, ng/ml) and free amino acids (glutamine, 383+/-20 vs 306+/-25, Proline, 203+/-18 vs 146+/-13 and ornithine, 164+/-27 vs 49+/-5 micro mole/l) are found in OKG treated patients, compared to non OKG patients. CONCLUSION: Increased hormone secretion due to OKG and the rapid interaction between the metabolites of OKG at the intermediary metabolism level may be responsible for altered substrate fuel kinetics.

Adult↗

PubMed1998

Amelioration of the protein metabolic response in spermidine-supplemented trauma rats.

Polyamines are biologically active, small, positively charged ubiquitous compounds that play an important role in initiating adaptive changes in cell proliferation, cell growth, and synthesis of proteins and nucleic acids. The potential for exogenous dietary polyamine to significantly contribute to whole-body growth and health has not been explored. This study evaluates the efficacy of feeding a liquid diet supplemented with 0.05% spermidine in injured rats. Rats traumatized by bilateral femur fracture (n = 12) and pair-fed uninjured controls (n = 12) were starved for 2 days and then refed for 4 days with a liquid diet containing 0.05% spermidine or an isonitrogenous control diet. Daily urine and body weight data were collected. At the end of refeeding, the rats were killed, and blood, cerebrospinal fluid (CSF), muscle, and brain tissue were collected. Spermidine supplementation (0.05%) was found to be tolerated well by the rats and (1) did not affect voluntary food intake by traumatized rats, (2) did not alter the growth rate, (3) increased protein utilization efficiency, and (4) decreased leucine, isoleucine, and valine levels in plasma and muscle. The profound effect of trauma on plasma amino acid metabolism seen in rats fed the basal diet was absent in spermidine-supplemented rats. Depletion of plasma glutamine (GLN) levels due to trauma was significantly less in rats with spermidine supplementation (11% v 33%), indicating a beneficial effect to counteract trauma responses. The results suggest that spermidine supplementation improves protein utilization efficiency and ameliorates trauma effects on amino acid levels.

Amino Acids↗

PubMed1997

Nutritional and metabolic effects and significance of mild orotic aciduria during dietary supplementation with arginine or its organic salts after trauma injury in rats.

The effects of acute food deprivation and subsequent refeeding with isonitrogenous oral liquid diets supplemented with arginine (ARG), ARG alpha-ketoglutarate (AKG), or ARG alpha-ketoisocaproate (AKIC) were examined in a Sprague-Dawley rat trauma model (bilateral femur fracture). Both control and trauma rats were starved for 2 days and then pair-fed for 4 days with one of four liquid isonitrogenous diets: diet 1 was a basal casein-based diet, and diets 2, 3, and 4 were the basal diet in which 10% of the nitrogen was replaced by ARG, AKG, or AKIC nitrogen. Two days of starvation resulted in a 13% loss of body weight and also a 27% decrease in the excretion of orotic acid (OA) in control and trauma rats. Although the ARG content of diets 2, 3, and 4 was the same, ARG- and AKIC-supplemented rats excreted significantly (P < .05) more OA than AKG-fed rats. The low level of OA excretion in AKG-fed rats indicates greater use of ARG for metabolic purposes, including efficient urea cycle operation. The metabolic adaptation and nutritional efficacy, i.e., Increased nitrogen retention, larger weight gain, and altered amino acid (AA) metabolism, of AKIC rats seem to be better than in ARG- or AKG-fed rats.

Amino Acids↗

PubMed1997

Reprioritization of liver protein synthesis resulting from recombinant human growth hormone supplementation in parenterally fed trauma patients: the effect of growth hormone on the acute-phase response.

BACKGROUND: One of the major components of the metabolic response to severe trauma is the alteration in concentrations of a large number of plasma proteins referred to as acute-phase proteins (APP). The principle mediators of these liver-synthesized APP are mainly the cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha). METHODS: We have measured the plasma levels of IL-6, TNF alpha, and 20 APP in 24 adult, severely injured, hypermetabolic and highly catabolic patients with multiple injuries within 48-60 hours after injury, when they were receiving maintenance fluids without calories or nitrogen, and subsequently during 7 days of total parenteral nutrition with (n = 12) or without (n = 12) recombinant human growth hormone supplementation (rhGH, 0.15 mg/kg/d). RESULTS: Baseline positive APP due to severe trauma include C-reactive protein (CRP), alpha-1 antichymotrypsin, alpha-1 acid glycoprotein, alpha-1 antitrypsin, fibronectin, and factor B. Negative APP include IgG, IgM, complement-3, prealbumin, transferrin, ceruloplasmin, and albumin. Except for CRP, alpha-1 antichymotrypsin, and albumin, all the APP levels increase during 7 days of nutritional support. Plasma levels of cytokines IL-6 and TNF-alpha, although initially markedly increased after injury, decrease with parenteral refeeding. There is a linear correlation between CRP and IL-6 levels and also between the transport proteins prealbumin and transferrin. Trauma-induced increases in CRP and IL-6 levels decreased with nutrition alone, but did not change with rhGH supplementation. An immunosuppressed state of injury is evident from the decreased immunoglobulin levels (IgG, IgM, IgA) in the trauma patients. Total parenteral nutrition alone increases the immunoglobulin levels to normal. However, with adjuvant rhGH, only IgA levels are normalized. CONCLUSIONS: Adjuvant rhGH therapy does not attenuate the reprioritization of acute liver protein synthesis and results in only limited restoration of host defenses. The clinical implications of these findings await further study.

Acute-Phase Proteins↗

PubMed1996

Adjuvant recombinant human growth hormone does not augment endogenous glucose production in total parenteral nutrition-fed multiple trauma patients.

Hyperglycemia and insulin resistance are well-known, consistent responses to severe injury. The purpose of this study was to investigate the mechanism for the further exaggerated hyperglycemia due to adjuvant recombinant human growth hormone (rhGH) treatment in multiple trauma patients. We have measured in 20 adult severely injured, highly catabolic, hypermetabolic multiple trauma patients, the glucose kinetics (appearance, clearance, oxidation, and recycling) once in the basal state (study I), 48 to 60 hours after injury but before starting nutritional therapy, and again (study II) after 7 days of intravenous nutrition (1.1 times resting energy expenditure, 250 mg nitrogen [N]/kg/d) with or without adjuvant rhGH. Group H (n = 10) randomly received daily (8 AM) rhGH (0.15 mg/kg/d) and group C (n = 10) received the vehicle of infusion. Adjuvant rhGH treatment in intravenously fed trauma patients (1) increases plasma insulin-like growth factor-1 (IGF-1) and insulin concentrations, (2) improves N balance, and (3) exaggerates the hyperglycemic response without affecting endogenous glucose output, glucose oxidation, or recycling. The mechanism for the hyperglycemic hyperinsulinemia in trauma may be due to a defective nonoxidative glucose disposal, as well as inhibition of glucose transport activity into tissue cells.

Adjuvants, Pharmaceutic↗

PubMed1996

Ornithine-alpha-ketoglutarate (OKG) supplementation is more effective than its component salts in traumatized rats.

Addition of an anabolic stimulus during nutritional support seems to be a reasonable adjunct to augment protein synthesis. Ornithine-alpha-ketoglutarate (OKG) has been used for this purpose in many pathological situations, but the mechanism of action is poorly understood. We have evaluated the relative metabolic efficacy of four isonitrogenous diets with or without the addition of alpha-ketoglutarate (alpha KG) or ornithine (ORN), in a rat trauma (bilateral femur fracture) model. Both control and traumatized rats were starved for 2 d. Then for 4 d, the control rats were pair-fed to the traumatized rats, one of the four isonitrogenous diets: the basal diet was a casein-based liquid diet; the ORN and OKG diets were the basal diet in which 10% of the dietary nitrogen was replaced by ORN- or OKG-nitrogen, respectively; the alpha KG diet contained equivalent amounts of alpha KG as were present in the OKG diet. Body weight gain per gram of nitrogen intake was similar in all four diet groups of both control and traumatized rats. The fraction of nitrogen intake that was retained in the body was significantly higher in OKG-fed traumatized rats (23%) than in the corresponding basal diet-fed rats. Plasma and muscle free amino acid concentrations were comparable in OKG- and ORN-fed rats but not in OKG- and alpha KG-fed rats. Our data suggest that the mechanism of OKG action may be associated with increases in growth hormone and insulin, as well as the production of metabolites of ORN and alpha KG. OKG has better metabolic benefits than its two components given separately in the nutritional support of injured rats.

Amino Acids↗

PubMed1996

Arterial-jugular vein free amino acid levels in patients with head injuries: important role of glutamine in cerebral nitrogen metabolism.

Traumatic brain injury is the single largest contributor of trauma center deaths. Injury to the brain cannot be considered as an isolated event, affecting only this organ. Profound hypoglutaminemia commonly seen in patients with head injuries may be caused by the diminished release of glutamine from the brain to the systemic circulation. To assess this hypothesis, we have simultaneously measured the free amino acid (AA) levels in systemic arterial (A, radial artery), cerebral venous (JV, jugular bulb), and systemic venous (PA, pulmonary artery) plasma in 11 adult patients with severe head injuries once within 48 hours of the initial injury before starting nutritional support and again after 3 to 4 days of enteral feeding. Cerebral organ (A-JV) changes of AA levels were compared with whole body systemic (A-PA) changes. Arterial total AA levels when compared with reported normal values are diminished by 46% in patients with isolated severe injuries. Cerebral outflow of glutamine is 6% of the total AA output compared with 73% in normals. The systemic outflow of glutamine in patients with brain injuries is 28% of total AA flow. Despite this high systemic output, significant hypoglutaminemia persists. Feeding for 3 days did not appreciably change the arterial plasma AA levels except that of glutamate and citrulline. A significant (p = 0.01) linear relationship between glutamine (product) and glutamate (precursor) was seen in JV samples but not in A or PA samples. The ratio of plasma glutamine to glutamate was decreased significantly only in JV during nutritional support, and this was caused mainly by an increase in glutamate levels. This may be owing to defective amidation to glutamine, inasmuch as gamma aminobutyric acid (GABA) levels were only minimally affected. Nutritional support improves the net release of glutamine from the brain. This suggests that supplementing the diet with glutamine may be beneficial to support systemic requirements in patients with severe head injuries.

Adolescent↗

PubMed1996

Metabolic changes in rats during a continuous infusion of recombinant interleukin-1.

The effects of recombinant interleukin-1 (IL-1), given as a continuous infusion for 6 days, on host responses were determined in rats. The development of fever, change in food intake and body weight, and key components of the acute-phase response in energy and protein metabolism were assessed. The effects of IL-1 were compared with those observed in a matched pair-fed group (semistarved), to distinguish the contribution from anorexia, and in a group that received IL-1 for 4 h acutely. IL-1 significantly increased core temperature, plasma levels of IL-6, and acute-phase protein production and decreased food intake and the circulating zinc level. The catabolic effects of IL-1 on nitrogen loss and muscle protein breakdown were independent of, and additive to those from malnutrition. The changes in energy expenditure, cumulative urinary nitrogen, and hydroxyproline excretion in the chronic IL-1 group were increased over semistarved animals. Finally, changes in muscle protein kinetics were only seen with chronic IL-1 infusion, and the changes in acute-phase protein were greater.

Acute-Phase Proteins↗

PubMed1995

Plasma levels of insulin-like growth factor binding protein-3 in acute trauma patients.

Insulin-like growth factors (IGFs) are a family of polypeptides that regulate cell growth. Their action and bioavailability are modified by binding proteins such as IGF binding protein-3 (IGFBP-3). Plasma IGFBP-3 level was found to be growth hormone (GH)-dependent, which makes detection of IGFBP-3 useful in the evaluation of GH secretion. In the early catabolic flow phase of severe injury, when plasma levels of GH and IGF-1 are low versus uninjured levels, the role of IGFBP-3 has not been investigated. We have measured basal levels of these polypeptide hormones in 16 adult (13 men and three women aged 47 +/- 7 years) severely injured (Injury Severity Score, 32 +/- 2), hypermetabolic resting energy expenditure [REE] to basal energy expenditure [BEE] ratio, 1.30 +/- 0.05), ventilator-dependent, multiple-trauma patients within 48 to 60 hours of injury when the patients were receiving maintenance fluids without calories or nitrogen. These basal values were compared with those of 16 age-matched postabsorptive normals. In the catabolic flow phase of injury, plasma levels of GH, IGF-1, and IGFBP-3 were significantly reduced by 50%, 46%, and 45%, respectively. There was a significant linear inverse relationship between IGFBP-3 and age and also a positive correlation between IGFBP-3 and IGF-1 in both control and injured subjects. The ratio of IGFBP-3 to IGF-1 was not changed in trauma victims. Measurement of plasma IGFBP-3 levels has potential as a marker for monitoring GH therapeutic efficacy.

Adult↗

PubMed1995

Pulsatile nature of growth hormone levels in critically ill trauma victims.

BACKGROUND: Circulating growth hormone (GH) levels in normal persons fluctuate widely because of pulsatile GH secretion. It is not known whether this pulsatile nature and rhythmicity exist in severe injury. These data become necessary to decide the timing of supplementary GH administration for its optimal utilization. The purpose of this study was to investigate the GH circadian variation with respect to that of insulin-like growth factor-1 (IGF-1), insulin, C-peptide, and cortisol in the early flow phase of injury. METHODS: Plasma GH, IGF-1, insulin, C-peptide, and cortisol levels were measured at 1-hour intervals during 24 hours (8 AM to 8 AM) in 10 severely injured adults with multiple trauma during the early catabolic flow phase 24 to 48 hours after injury, when patients received maintenance fluids without calories or nitrogen. RESULTS: The 24-hour integrated GH concentration is not different from either 12-hour mean diurnal or 12-hour mean nocturnal or mean 8 AM GH concentration. Pulsatile GH bursts persist in injured patients during both day and night. Pulsatile bursts do not exist for IGF-1, insulin, and C-peptide. The plasma levels of cortisol show time-dependent daily maximum and minimum levels. CONCLUSIONS: Pulsatile GH bursts persist in injured patients but less frequently than seen in normal persons. The time of bolus administration of GH to augment the anabolic GH action in patients with trauma does not matter; however, for convenience morning administration may be preferable for patients in the intensive care unit.

Activity Cycles↗

PubMed1995

Altered brain and muscle amino-acid levels due to remote injury during glutamine supplementation.

Glutamine (GLN) has aroused considerable interest among clinicians and nutritionists after studies demonstrated conclusively profound GLN depletion during critical illness. Although the brain plays an important role in GLN metabolism, little is known concerning changes in cerebral handling of GLN following injury. We have evaluated in a rat trauma (bilateral femur fractures) model, the nutritional efficacy of GLN-rich diet and the remote injury-induced changes in amino-acid (AA) contents of brain and muscle tissues. Both control and traumatised rats were starved for 2 days and then pair-fed for 4 days, either a basic liquid diet (BioServ # F1259) or an isonitrogenous test diet which contained the same basic diet from which 10% nitrogen (N) was replaced by GLN-N. Protein efficiency ratio as well as plasma levels of anabolic growth hormone and insulin did not change due to GLN-enriched diet. Remote injury-induced changes in GLN and glutamic acid (GLU) during GLN-rich diet were minimal in brain tissues; whereas GLN levels were decreased in plasma and muscle, GLU levels were increased in plasma and decreased in muscle tissues. The AA levels of brain tissues, in general, were maintained within narrow limits during GLN supplementation in control and injured rats. An increased influx of tryptophan and increased synthesis of the neurotransmitter serotonin were suggested due to GLN-enriched diet.

Journal Article↗

PubMed1995

Adjuvant recombinant human growth hormone stimulates insulin-like growth factor binding protein-3 secretion in critically ill trauma patients.

The early catabolic phase of severe injury is associated with acute growth hormone (GH), insulin-like growth factor-1 (IGF-1), and insulin-like growth factor binding protein-3 (IGFBP-30 deficiency. The metabolic half-life of circulating IGF-1 is prolonged by its binding to IGFBP-3. The role of this binding protein in nutritionally repleted multiple-injury patients has not been previously evaluated. We have measured plasma levels of these polypeptides and nitrogen (N) balance in 18 adult (15 males/3 females; mean age, 45 years), severely injured, hypermetabolic, and highly catabolic trauma patients within 48 to 60 hours after injury, when they were receiving maintenance fluids without calories or N and during 6 days of total parenteral nutrition (TPN). Before instituting TPN, the patients were randomized to receive (group H, n = 9) or not to receive (group C, n = 9) daily recombinant human growth hormone (rhGH), 0.15 mg/kg IM. Adjuvant rhGH significantly increases plasma levels of GH, IGF-1, IGFBP-3, and insulin. In addition, it shows better improvement in N balance. The bioavailability of IGF-1 is increased, as indicated by the decrease in IGFBP-3:IGF-1 ratio. A significant correlation between IGF-1 and IGFBP-3 levels is present in the trauma patients who received TPN and rhGH. A GH/IGF-1/IGFBP-3 axis that closely regulates the metabolic status of the patient is established in trauma.

Adult↗

PubMed1994

Influence of diet with or without amino acids on polyamine excretion in multiple trauma victims.

Elevated levels of urinary polyamines (PA) in severely injured trauma patients are further enhanced by total parenteral nutrition (TPN) that contains both glucose and amino acids (AAs). Since TPN solutions contain arginine, the AA precursor of PA, it is not certain whether the increased urinary PA are due to this substrate. Nutritional factors can evidently modify PA metabolism. We measured the daily excretion of the PA, putrescine (PU) and spermidine (SD) in 18 multiply injured (injury severity score [ISS], 32 +/- 2), hypermetabolic (resting energy expenditure [REE]/basal energy expenditure [BEE], 1.41 +/- 0.06), and highly catabolic (daily N loss, 17.2 +/- 1.8 g N/d) acute trauma patients for 5 days in the early flow phase of injury. The patients were fed only maintenance fluids without calories or nitrogen for the first day 60 to 72 hours after injury, and then were randomized to receive glucose alone ([GLUC] 4.1 mg/kg/min, 80% measured REE, n = 8) or the same amount of glucose with AAs (TPN, 275 mg N/kg/d, n = 10) for the following 4 days. There was no significant difference in the enhanced daily PA excretion either in the free or acetylated form between the two dietary regimens. The addition of AAs in the TPN mixture did not seem to further stimulate PA metabolism in the trauma patients. The source of the nutrient content of the diet appears to be important for enhancing total PA excretion in critically ill patients.

Adolescent↗

PubMed1994

Enhancement of protein synthesis efficiency in parenterally fed trauma victims by adjuvant recombinant human growth hormone.

In the early catabolic phase of severe injury, conventional nutritional support is inadequate to reverse negative nitrogen balance and an anabolic stimulus may be beneficial. The utilization efficiency of body energy sources after injury could be improved by adjuvant recombinant human growth hormone (rhGH) therapy. We measured the protein kinetic response to exogenous rhGH in trauma patients fed parenterally (TPN). Severely injured (mean ISS, 31 +/- 2), highly catabolic (mean nitrogen loss, 19 +/- 2 g/day), and hypermetabolic (mean BEE/REE, 1.41 +/- 0.05), adult (mean age, 46 +/- 5 years), multiple trauma victims (n = 20, 17 men/3 women) were investigated. Rates of whole-body protein kinetics (turnover [WBPT], synthesis [WBPS], breakdown [WBPB], and protein synthesis efficiency [PSE]--the fraction of nitrogen turnover utilized for protein synthesis) were measured using a primed-constant infusion of 18N glycine 48 to 60 hours after injury when the patients were receiving only maintenance fluids without calories or nitrogen. The patients were then fed glucose-based TPN (1.1 x REE; 250 mg N/kg/day) and randomized to receive or not to receive rhGH. Group H (n = 10) received daily rhGH (0.15 mg/kg/day, Somatropin, Genentech, Inc.) intramuscularly at 8 am and group C (n = 10) received only the vehicle of infusion. Protein kinetic measurements were repeated at the end of 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗