Criteria for choosing amino acid therapy in acute renal failure.
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Metabolic studies were performed on 19 patients with acute renal failure. Therapy included intravenous hyperalimentation using 15 to 20 g of essential amino acids or 20 to 40 g of essential plus nonessential amino acids and hypertonic glucose (37 to 50%). The effect of this parenteral feeding appears to be primarily pharmacological. Hypertonic glucose promotes the hyperinsulinemia important to be membrane function, the operation of the sodium pump, and cell metabolism. Administration of high biological value crystalline amino acdis potentiates the effect of insulin by inhibiting protein breakdown and promoting protein synthesis, particularly in muscle. This reduces tissue catabolism and urea formation, and promotes potassium, magnesium, and phosphate homeostasis. The branched-chain ketogenic amino acids valine, leucine, and isoleucine may be of particular importance. When indicated, administration of renal failure hyperalimentation and peritoneal or hemodialysis can be expected to complement each other and accelerate recovery. This intravenous fluid therapy, in turn, must be coordinated with proper hemodynamics, usually requiring a colloidal solution to maintain intravascular volume, and cardiotrophic agents such as digitalis and dopamine. Early use of renal failure can be expected to demonstrate the most striking response in terms of survival, early recovery from acute renal failure, and the preservation of physiological homeostasis. (+info)
Comparison between in vitro lipid peroxidation in fresh sheep platelets and peroxidative processes during sheep platelet ageing under storage at 4 degrees C.
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Incubation of sheep platelet crude membranes with xanthine oxidase (XO)/hypoxanthine/Fe(2+)-ADP revealed: (i) a fast peroxidative response - with a maximal linear rate of 14 nmol malondialdehyde (MDA) equivalents/mg protein, as evidenced by the thiobarbituric acid test - and a decrease in the polyunsaturated fatty acid (PUFA) content of the platelet crude membranes; (ii) a decrease in the lipid fluidity in the deep lipid core of the membranes but not at the membrane surface; (iii) a dramatic inhibitory effect on glucose 6-phosphatase (Glc-6-Pase) but not on acetylcholinesterase activity. Platelets were also aged by storage at 4 degrees C in their own plasma or in Seto additive solution. In these media, platelet aggregates were visible and the effects on platelet phospholipids, PUFA, lipid extract fluorescence, crude membrane fluidity and membrane-bound enzyme activities were assessed for comparison with those observed in in vitro lipid peroxidation. The sensitivity of membranes from stored platelets to lipid peroxidation was also assessed. Storage of platelets in plasma for 5 days was associated with different changes in their crude membranes such as decreases in arachidonic acid contents, the decrease not being avoided by the presence of phospholipase A(2) inhibitors, increases in MDA equivalents, conjugated dienes and lipid extract fluorescence, decreases in the amounts of MDA equivalents formed by platelet crude membranes treated with the oxidizing agents, changes in membrane fluidity and inhibition of Glc-6-Pase. All these alterations were less pronounced or even abolished after platelet storage in Seto. These findings suggest that platelet lipid peroxidation due to XO/hypoxanthine/Fe(2+)-ADP and platelet membrane alterations observed after platelet ageing under storage at 4 degrees C share common features. Also, as regards the prevention of peroxidative processes, Seto solution permits better storage of sheep platelets than plasma. (+info)
Enhanced mucosal re-epithelialization induced by short chain fatty acids in experimental colitis.
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The short chain fatty acids (SCFA) are the best nutrients for the colonocytes. Glucose is poorly used as a fuel but may be transformed into SCFA by colonic bacteria. The aim of this study was to investigate the effect of SCFA or glucose on experimental colitis. Colitis was induced in 30 Wistar rats by colonic instillation of 4% acetic acid. Five days later they were randomized to receive twice a day colonic lavage containing saline (controls, N = 10), 10% hypertonic glucose (N = 10) or SCFA (N = 10) until day 8 when they were killed. At autopsy, the colon was removed and weighed and the mucosa was evaluated macro- and microscopically and stripped out for DNA assay. Data are reported as mean +/- SD or median [range] as appropriate. All animals lost weight but there was no difference between groups. Colon weight was significantly lower in the SCFA group (3.8 +/- 0.5 g) than in the control (5.3 +/- 2.1 g) and glucose (5.2 +/- 1.3 g) groups (P<0.05). Macroscopically, the severity of inflammation was less in SCFA (grade 2 [1-5]) than in control (grade 9 [4-10]) and glucose-treated (grade 9 [2-10]) animals (P<0.01). Microscopically, ulceration of the mucosa was more severe in the glucose and control groups than in the SCFA group. The DNA content of the mucosa of SCFA-treated animals (8.2 [5.0-20.2] mg/g of tissue) was higher than in glucose-treated (5.1 [4.2-8.5] mg/g of tissue; P<0.01) and control (6.2 [4.5-8.9] mg/g of tissue; P<0.05) animals. We conclude that SCFA may enhance mucosal re-epithelialization in experimental colitis, whereas hypertonic glucose is of no benefit. (+info)
Barbiturate anesthesia and brain proton spectroscopy.
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BACKGROUND AND PURPOSE: Thiopentone reduces CBF and metabolic rate. Still, it is widely used for sedation during MR spectroscopy. We investigated whether barbiturate anesthesia and preanesthetic fasting have an effect on metabolic ratios in proton MR spectroscopy of the brain. METHODS: Eight healthy, consenting, male volunteers were studied twice in a random, crossover fashion. The study sessions were conducted during fasting (F) and nonfasting (nonF), with glucose infusion mimicking the fed state. During both sessions, two sets of spectroscopic data were collected, one during the awake state (F or nonF) and one under barbiturate anesthesia (F+B or nonF+B), using TEs of 135 and 270. Spectral areas of N-acetylaspartate (NAA), choline-containing compounds (Cho), and creatine plus phosphocreatine (Cr) were calculated, and the presence of lactate or lipid was noted. Venous blood samples for glucose, beta-hydroxybutyrate, lactate, and electrolytes were collected. RESULTS: Barbiturate anesthesia caused a 42% reduction in blood lactate levels during fasting, but not during glucose infusion. There were no differences in NAA/Cho, NAA/Cr, or in Cho/Cr between the groups F, nonF, F+B, or nonF+B. No lactate or lipid resonances were detected. CONCLUSION: Barbiturate anesthesia with preanesthetic fasting can be used for proton spectroscopy at TEs of 135 or 270 without interference from NAA/Cho, NAA/Cr, or Cho/Cr or from the appearance of lactate or lipid. (+info)
Thermogenesis induced by intravenous infusion of hypertonic solutions in the rat.
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1. Intravenous administration of 20-60 % glucose, 3.2-9.7 % NaCl or 20 % mannitol solutions (1.66 ml kg(-1)) for 5 min increased oxygen consumption in urethane-anaesthetized rats, whereas administration of physiological saline had no effect. Administration of 7.7-18.3 % urea slightly increased the oxygen consumption, but the increase was significantly smaller than that measured after the administration of other hypertonic solutions. The magnitude of the thermogenic effect correlated with the osmolality of the applied solutions. These results suggest that the thermogenesis was caused mainly by changes in osmolality rather than by a specific action of the different solute molecules. 2. Neither pretreatment with the ganglion blocker hexamethonium (20 mg kg(-1), I.P.) or the beta-adrenergic antagonist propranolol (10 mg kg(-1), I.P.), nor bilateral cervical vagotomy or bilateral adrenalectomy had any effect on the osmotically induced thermogenesis. Therefore, the autonomic nervous system and the adrenal gland were not involved in this metabolic response. 3. In response to osmotic stimulation, the temperature of the skeletal muscle increased significantly, whereas that of brown adipose tissue did not change and that of the colon and liver decreased. Accordingly, the site of osmotic thermogenesis is probably in the skeletal muscle, although osmotic stimulation was not accompanied by electromyographic activity and was not blocked by pretreatment with muscle relaxants such as dantrolene sodium or pancuronium bromide, or with the Na(+)-Cl(-) co-transport inhibitor bumetanide. 4. The increases in plasma osmolality observed after the administration of 20 % (1.3 osmol kg(-1)) glucose and 4.1 % (1.3 osmol kg(-1)) NaCl were 4.50 +/- 0.88 and 5.57 +/- 0.71 mosmol kg(-1), respectively. Since the slight increase in osmolality is well within the physiological range of changes that occur after food ingestion, diet-induced thermogenesis may have a component that is mediated by an increase in plasma osmolality, which results from the prandial increase in circulating nutrients. (+info)
High concentration of glucose inhibits endothelium-dependent vasorelaxation of rabbit aortic artery.
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AIM: To determine whether high concentration of glucose inhibits endothelium-dependent vasorelaxation of rabbit aortic artery and possible mechanisms. METHODS: The organ-bath of rings of rabbit aorta was used to determine changes of tension of vessel in response to different concentrations of acetylcholine (ACh) and sodium nitroprusside (SNP) after removal of endothelium, coincubated with nitric oxide synthase (NOS) inhibitor L-NMMA, different concentrations of glucose, vitamin C, and cell-permeable superoxide dismutase-mimetic and oxygen-derived free radical scavenger manganese (III) tetrakis (1-methyl-4-pyridyl) porphyrin (MnTMPyP). RESULTS: ACh induced concentration- and endothelium-dependent aortic vasorelaxation. High concentration of glucose markedly inhibited this vasorelaxation, and vitamin C and MnTMPyP could not antaganize this inhibitory effect by high concentrations of glucose. SNP induced concentration-dependent and endothelium-independent vasorelaxation, and high concentration of glucose had no effect on the vasorelaxation by SNP. CONCLUSION: High concentration of glucose inhibited endothelium-dependent vasorelaxation and this effect was unlikely mediated through activating oxygen-derived free radical production. (+info)
Hypertonicity suppresses ionophore-induced product formation and translocation of 5-lipoxygenase in human leukocytes.
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5-Lipoxygenase (5-LO) initiates the biosynthesis of proinflammatory leukotrienes from arachidonic acid (AA). Here, we demonstrate that hypertonicity suppresses ionophore-induced 5-LO product formation reversibly in isolated human polymorphonuclear leukocytes (PMNL) and in Mono Mac 6 cells. Hypertonicity blocked the liberation of AA and abrogated translocation of 5-LO to the nuclear membrane. Accordingly, in the presence of exogenous AA, 5-LO product formation was less affected. The effects of hypertonicity were a result of cell shrinkage and not cytosolic hyperosmolarity. Hypertonicity did not inhibit the rapid increase in intracellular Ca(2)(+) induced by ionophores but prevented the ionophore-induced activation of p38 MAPK-regulated MAPKAP kinases, which can phosphorylate and activate 5-LO (and cPLA(2)). In summary, we show that hypertonicity blocks agonist-induced release of AA, 5-LO product formation, and translocation and in parallel, prevents activation of p38 MAPK and downstream 5-LO kinases in leukocytes. (+info)
Increased peritoneal membrane permeability is associated with abnormal peritoneal surface layer.
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OBJECTIVES: We recently showed that the peritoneal surface layer may be an important barrier in modulating peritoneal membrane permeability. In the present study, we investigated the relationship between an increased peritoneal transport rate and the peritoneal surface layer. METHODS: Male Sprague-Dawley rats (n = 8) received intraperitoneal injections of 4.25% glucose dialysate daily for 1 week. Forty-eight hours after the last injection, a 4-hour dwell study using 25 mL 4.25% glucose dialysate was performed in each rat. The results were compared with those from control rats that received no intraperitoneal injections (n = 8). The peritoneal fluid and small-solute transport characteristics were evaluated. The peritoneal surface layer was studied using an electron microscope. The phospholipids content of the dialysate was also evaluated. RESULTS: Peritoneal fluid removal was significantly reduced in the daily injection group (30.6 +/- 1.3 mL) as compared with the control group (38.2 +/- 0.6 mL). The peritoneal fluid absorption rate and small-solute transport rate were also significantly higher in the daily injection group as compared with the control group. The amounts of phospholipids in the dialysate were significantly lower in the daily injection group--especially the quantity of phosphatidylcholine. However, lysophosphatidylcholine increased significantly in the daily injection group. Electron microscopy showed that the peritoneal surface layer was almost completely gone in the daily injection group, but that a dense and thick (average 4 microm) peritoneal surface layer was present on the top of the mesothelial cells in the control group. CONCLUSIONS: Our results suggest that daily injection of hypertonic glucose dialysate significantly increased the peritoneal transport rate. The increased peritoneal transport rate was associated with a significant reduction in the peritoneal surface layer and the phospholipids content of the dialysis effluent. (+info)