Academic literature on the topic 'Plasma ketone'
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Journal articles on the topic "Plasma ketone"
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Bentourkia, M'hamed, Sébastien Tremblay, Fabien Pifferi, Jacques Rousseau, Roger Lecomte, and Stephen Cunnane. "PET study of 11C-acetoacetate kinetics in rat brain during dietary treatments affecting ketosis." American Journal of Physiology-Endocrinology and Metabolism 296, no. 4 (April 2009): E796—E801. http://dx.doi.org/10.1152/ajpendo.90644.2008.
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Normally, the brain's fuel is glucose, but during fasting it increasingly relies on ketones (β-hydroxybutyrate, acetoacetate, and acetone) produced in liver mitochondria from fatty acid β-oxidation. Although moderately raised blood ketones produced on a very high fat ketogenic diet have important clinical effects on the brain, including reducing seizures, ketone metabolism by the brain is still poorly understood. The aim of the present work was to assess brain uptake of carbon-11-labeled acetoacetate (11C-acetoacetate) by positron emission tomography (PET) imaging in the intact, living rat. To vary plasma ketones, we used three dietary conditions: high carbohydrate control diet (low plasma ketones), fat-rich ketogenic diet (raised plasma ketones), and 48-h fasting (raised plasma ketones). 11C-acetoacetate metabolism was measured in the brain, heart, and tissue in the mouth area. Using 11C-acetoacetate and small animal PET imaging, we have noninvasively quantified an approximately seven- to eightfold enhanced brain uptake of ketones on a ketogenic diet or during fasting. This opens up an opportunity to study brain ketone metabolism in humans.
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O’Malley, Trevor, Etienne Myette-Cote, Cody Durrer, and Jonathan P. Little. "Nutritional ketone salts increase fat oxidation but impair high-intensity exercise performance in healthy adult males." Applied Physiology, Nutrition, and Metabolism 42, no. 10 (October 2017): 1031–35. http://dx.doi.org/10.1139/apnm-2016-0641.
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This study investigated the impact of raising plasma beta-hydroxybutyrate (β-OHB) through ingestion of ketone salts on substrate oxidation and performance during cycling exercise. Ten healthy adult males (age, 23 ± 3 years; body mass index, 25 ± 3 kg/m2, peak oxygen uptake, 45 ± 10 mL/(kg·min)−1) were recruited to complete 2 experimental trials. Before enrollment in the experimental conditions, baseline anthropometrics and cardiorespiratory fitness (peak oxygen uptake) were assessed and familiarization to the study protocol was provided. On experimental days, participants reported to the laboratory in the fasted state and consumed either 0.3 g/kg β-OHB ketone salts or a flavour-matched placebo at 30 min prior to engaging in cycling exercise. Subjects completed steady-state exercise at 30%, 60%, and 90% ventilatory threshold (VT) followed by a 150-kJ cycling time-trial. Respiratory exchange ratio (RER) and total substrate oxidation were derived from indirect calorimetry. Plasma glucose, lactate, and ketones were measured at baseline, 30 min post-supplement, post–steady-state exercise, and immediately following the time-trial. Plasma β-OHB was elevated from baseline and throughout the entire protocol in the ketone condition (p < 0.05). RER was lower at 30% and 60% VT in the ketone compared with control condition. Total fat oxidation was greater in the ketone versus control (p = 0.05). Average time-trial power output was ∼7% lower (–16 W, p = 0.029) in the ketone condition. Ingestion of ketone salts prior to exercise increases fat oxidation during steady-state exercise but impairs high-intensity exercise performance.
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Nestler, James R. "Metabolic substrate change during daily torpor in deer mice." Canadian Journal of Zoology 69, no. 2 (February 1, 1991): 322–27. http://dx.doi.org/10.1139/z91-052.
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Various metabolic substrates were measured in plasma (glucose, free fatty acids (FFA), ketones, lactate), heart, liver, and skeletal muscle (glycogen, ketones, lactate) of deer mice (Peromyscus maniculatus) in association with their daily torpor cycle. Immediately after feeding, substrate levels were similar to those observed in other mammals. However, within 8–10 h carbohydrate indices (glucose, glycogen) decreased significantly in plasma, liver, and skeletal muscle, with prominent increases in FAA and ketones. Thus the metabolic condition of normothermic deer mice (body temperature 35–38 °C) resembled that seen during acute starvation. Conditions during the actual torpor bout (body temperature 19–24 °C) were similar to those immediately prior to torpor entrance. Glycogen levels in heart were actually highest during daily torpor, possibly as an 'anticipatory' response prior to arousal. Following arousal no repletion of glucose or glycogen was noted, while ketone levels exceeded 5 mM (plasma) and 5 μmol/g (tissues). Adjustments in FFA and ketone utilization may be important in sparing carbohydrate and protein during daily torpor, enabling foraging activity necessary for restoration of endogenous fuel following arousal.
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Avogaro, A., P. E. Cryer, and D. M. Bier. "Epinephrine's ketogenic effect in humans is mediated principally by lipolysis." American Journal of Physiology-Endocrinology and Metabolism 263, no. 2 (August 1, 1992): E250—E260. http://dx.doi.org/10.1152/ajpendo.1992.263.2.e250.
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To quantify epinephrine's effects on acetoacetate and beta-hydroxybutyrate kinetics, we infused subjects with 0.3 and 2.5 micrograms/min epinephrine, either alone or with a concomitant somatostatin infusion with insulin, glucagon, and growth hormone replaced at postabsorptive levels (islet clamp). Additional subjects received no epinephrine but sequential infusions of heparin plus 10% Intralipid at rates of 0.5 and 3.0 ml/min. Both epinephrine and Intralipid increased ketone body appearance (unaffected by islet clamp), augmented the interconversion rates between ketone bodies and, during the 2.5 micrograms/min infusion, caused a marked increase in beta-hydroxybutyrate appearance. The fraction of plasma free fatty acid (FFA) flux appearing as plasma ketones increased from 6 to 7% in the basal state to 11% at the high-epinephrine infusion. This fraction was also unaffected by the islet clamp and was not different from values obtained at similar Intralipid plus heparin-induced elevations in plasma FFA levels. We conclude that epinephrine's ketogenic effect in humans is primarily the result of its lipolytic effect, is accompanied by a significantly increased rate of ketone body interconversion, is manifest largely as an increase in plasma beta-hydroxybutyrate appearance at high plasma epinephrine values, and is not limited by portal insulin at post-absorptive levels.
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Leshem, M., F. W. Flynn, and A. N. Epstein. "Brain glucoprivation and ketoprivation do not promote ingestion in the suckling rat pup." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 258, no. 2 (February 1, 1990): R365—R375. http://dx.doi.org/10.1152/ajpregu.1990.258.2.r365.
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We examined the possibility that brain glucose or ketone availability may control suckling or precocious feeding in the preweanling rat. Brain glucoprivation induced by 5-thio-D-glucose injection into the 4th ventricle did not increase feeding on orally infused milk until 30 days of age, although hyperglycemia was evoked as early as 9 days by the same treatment. Plasma ketone levels varied with suckling status, but pharmacological blockade of hepatic free fatty acid oxidation, which restricts ketone availability (ketoprivation), failed to increase suckling. Because the suckling rat can switch energy substrates under nutritional duress, we combined glucoprivation and ketoprivation. Feeding was suppressed, and suckling was not affected. Finally, we injected ketones into the 3rd brain ventricle and found that they increased feeding. Thus, in contrast to the adult rat, reduced glucose or ketone utilization by the brain does not increase food intake in the preweanling, but increased circulating and brain ketone concentrations may arouse feeding.
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Valenzuela, Pedro L., Javier S. Morales, Adrián Castillo-García, and Alejandro Lucia. "Acute Ketone Supplementation and Exercise Performance: A Systematic Review and Meta-Analysis of Randomized Controlled Trials." International Journal of Sports Physiology and Performance 15, no. 3 (March 1, 2020): 298–308. http://dx.doi.org/10.1123/ijspp.2019-0918.
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Purpose: To determine the acute effects of ketone supplementation on exercise performance (primary outcome) and physiological and perceptual responses to exercise (secondary outcomes). Methods: A systematic search was conducted in PubMed, Web of Science, and SPORTDiscus (since inception to July 21, 2019) to find randomized controlled trials assessing the effects of acute ketone supplementation compared with a drink containing no ketones (ie, control intervention). The standardized mean difference (Hedges g) between interventions and 95% confidence interval (CI) were computed using a random-effects model. Results: Thirteen studies met all inclusion criteria. No significant differences were observed between interventions for overall exercise performance (Hedges g = −0.05; 95% CI, −0.30 to 0.20; P = .68). Subanalyses revealed no differences between interventions when analyzing endurance time-trial performance (g = −0.04; 95% CI, −0.35 to 0.28; P = .82) or when assessing the separate effects of supplements containing ketone esters (g = −0.07; 95% CI, −0.38 to 0.24; P = .66) or salts (g = −0.02; 95% CI, −0.45 to 0.41; P = .93). All studies reported increases in plasma ketone concentration after acute ketone supplementation, but no consistent effects were reported on the metabolic (plasma lactate and glucose levels), respiratory (respiratory exchange ratio, oxygen uptake, and ventilatory rate), cardiovascular (heart rate), or perceptual responses to exercise (rating of perceived exertion). Conclusions: The present findings suggest that ketone supplementation exerts no clear influence on exercise performance (from sprints to events lasting up to ∼50 min) or metabolic, respiratory, cardiovascular, or perceptual responses to exercise. More research is needed to elucidate if this strategy could provide ergogenic effects on other exercise types (eg, ultraendurance exercise).
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Ferrier, B., M. Martin, B. Janbon, and G. Baverel. "Transport of beta-hydroxybutyrate and acetoacetate along rat nephrons: a micropuncture study." American Journal of Physiology-Renal Physiology 262, no. 5 (May 1, 1992): F762—F769. http://dx.doi.org/10.1152/ajprenal.1992.262.5.f762.
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The transport of ketone bodies across the luminal membrane of the nephron was studied by means of micropuncture techniques in rats in normal acid-base state. The concentration of beta-hydroxybutyrate (beta-HB) and acetoacetate (AcAc) in plasma, tubular fluid and urine was measured by an ultramicromethod using enzymatic cycling. At endogenous plasma ketone body concentration, approximately 80% of the filtered load of beta-HB and AcAc was reabsorbed in the proximal convoluted tubule, the remaining fraction being almost completely reabsorbed between the late proximal convoluted and the distal tubule; under these conditions, the urinary excretion of ketone bodies was less than 1% of the filtered load. A progressive elevation to steady-state levels of plasma beta-HB resulted in a progressive reduction of the fractional reabsorption of beta-HB and AcAc in the proximal convoluted tubule, which means that reabsorption of ketone bodies in this nephron segment is saturable. No net secretion of ketone bodies could be demonstrated along the nephron even at the highest plasma ketone body concentrations reached. In clearance experiments, the capacity of the rat kidney for reabsorbing both beta-HB and AcAc was found to be limited by a maximal tubular capacity (Tm). The data suggest that, in the young Wistar rat nephron, most of the reabsorption of ketone bodies is carrier mediated.
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Rittig, Nikolaj, Mads Svart, Henrik Holm Thomsen, Esben Thyssen Vestergaard, Jens Frederik Rehfeld, Bolette Hartmann, Jens Juul Holst, Mogens Johannsen, Niels Møller, and Niels Jessen. "Oral D/L-3-Hydroxybutyrate Stimulates Cholecystokinin and Insulin Secretion and Slows Gastric Emptying in Healthy Males." Journal of Clinical Endocrinology & Metabolism 105, no. 10 (July 27, 2020): e3597-e3605. http://dx.doi.org/10.1210/clinem/dgaa483.
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Abstract Background D-3-hydroxybutyrate (D-3-OHB) is a ketone body that serves as an alternative nutritional fuel but also as an important signaling metabolite. Oral ketone supplements containing D/L-3-OHB are becoming a popular approach to achieve ketosis. Aim To explore the gut-derived effects of ketone supplements. Methods Eight healthy lean male volunteers were investigated on 2 separate occasions: An acetaminophen test was performed to evaluate gastric emptying and blood samples were obtained consecutively throughout the study period. Results We show that oral consumption of D/L-3-OHB stimulates cholecystokinin release (P = 0.02), elevates insulin (P = 0.03) and C-peptide (P < 0.001) concentrations, and slows gastric emptying (P = 0.01) compared with matched intravenous D/L-3-OHB administration. Measures of appetite and plasma concentrations of glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were unaffected by interventions. Conclusion Our findings show that D/L-3-OHB exert incretin effects and indicate luminal sensing in the gut endothelium. This adds to our understanding of ketones as signaling metabolites and displays the important difference between physiological ketosis and oral ketone supplements.
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Kanikarla-Marie, Preeti, and Sushil K. Jain. "Role of Hyperketonemia in Inducing Oxidative Stress and Cellular Damage in Cultured Hepatocytes and Type 1 Diabetic Rat Liver." Cellular Physiology and Biochemistry 37, no. 6 (2015): 2160–70. http://dx.doi.org/10.1159/000438573.
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Background/Aims: Type 1 diabetic (T1D) patients have a higher incidence of liver disease. T1D patients frequently experience elevated plasma ketone levels along with hyperglycemia. However, no study has examined whether hyperketonemia per se has any role in excess liver damage in T1D. This study investigates the hypothesis that hyperketonemia can induce oxidative stress and cellular dysfunction. Methods: STZ treated diabetic rats, FL83B hepatocytes, and GCLC knocked down (GSH deficient) hepatocytes were used. Results: The blood levels of ALT and AST, biomarkers of liver damage, and ketones were elevated in T1D rats. An increase in NOX4 and ROS along with a reduction in GSH and GCLC levels was observed in T1D rat livers in comparison to those seen in non-diabetic control or type 2 diabetic rats. MCP-1 and ICAM-1 were also elevated in T1D rat livers and ketone treated hepatocytes. Macrophage markers CCR2 and CD11A that interact with MCP-1, and ICAM-1 respectively, were also elevated in the T1D liver, indicating macrophage infiltration. Additionally, activated macrophages increased hepatocyte damage with ketone treatment, which was similar to that seen in GCLC knockdown hepatocytes without ketones. Conclusion: Hyperketonemia per se can induce macrophage mediated damage to hepatocytes and the liver, caused by GSH depletion and oxidative stress up regulation in T1D.
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Mey, Jacob T., Adithya Hari, Christopher L. Axelrod, Ciarán E. Fealy, Melissa L. Erickson, John P. Kirwan, Raed A. Dweik, and Gustavo A. Heresi. "Lipids and ketones dominate metabolism at the expense of glucose control in pulmonary arterial hypertension: a hyperglycaemic clamp and metabolomics study." European Respiratory Journal 55, no. 4 (February 27, 2020): 1901700. http://dx.doi.org/10.1183/13993003.01700-2019.
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Individuals with idiopathic pulmonary arterial hypertension (PAH) display reduced oral glucose tolerance. This may involve defects in pancreatic function or insulin sensitivity but this hypothesis has not been tested; moreover, fasting nutrient metabolism remains poorly described in PAH. Thus, we aimed to characterise fasting nutrient metabolism and investigated the metabolic response to hyperglycaemia in PAH.12 participants (six PAH, six controls) were administered a hyperglycaemic clamp, while 52 (21 PAH, 31 controls) underwent plasma metabolomic analysis. Glucose, insulin, C-peptide, free fatty acids and acylcarnitines were assessed from the clamp. Plasma metabolomics was conducted on fasting plasma samples.The clamp verified a reduced insulin response to hyperglycaemia in PAH (−53% versus control), but with similar pancreatic insulin secretion. Skeletal muscle insulin sensitivity was unexpectedly greater in PAH. Hepatic insulin extraction was elevated in PAH (+11% versus control). Plasma metabolomics identified 862 metabolites: 213 elevated, 145 reduced in PAH (p<0.05). In both clamp and metabolomic cohorts, lipid oxidation and ketones were elevated in PAH. Insulin sensitivity, fatty acids, acylcarnitines and ketones correlated with PAH severity, while hepatic extraction and fatty acid:ketone ratio correlated with longer six-min walk distance.Poor glucose control in PAH could not be explained by pancreatic β-cell function or skeletal muscle insulin sensitivity. Instead, elevated hepatic insulin extraction emerged as an underlying factor. In agreement, nutrient metabolism in PAH favours lipid and ketone metabolism at the expense of glucose control. Future research should investigate the therapeutic potential of reinforcing lipid and ketone metabolism on clinical outcomes in PAH.
Dissertations / Theses on the topic "Plasma ketone"
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Gravis, David. "Etude de l’influence de la physicochimie et de la texturation de surface sur l’adhérence métal - Poly(Ether Ether Ketone) (PEEK)." Thesis, Le Mans, 2019. http://www.theses.fr/2019LEMA1009.
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La faible densité et les propriétés mécaniques remarquables des composites polymères en font des matériaux de choix pour remplacer les métaux. Cependant, leurs propriétés physicochimiques rendent leurs surfaces peu adhésives pour divers types de revêtements. Pour améliorer l’adhérence de revêtements métalliques sur des substrats de PEEK, et pour mieux comprendre les mécanismes de l’adhésion, les propriétés de surface du matériau ont été modifiées par des procédés physiques en voie sèche.D’une part, cette étude montre que les traitements par plasma oxydants (à basse pression, ou à pression atmosphérique) permettent d’améliorer la mouillabilité de la surface et l’adhérence de revêtements métalliques, par l’augmentation de la polarité de la surface, quantifiée par XPS. D’autre part, cette étude montre que l’ablation laser infrarouge à impulsion femtoseconde permet la gravure d’un motif dense, induisant de meilleures tenues mécaniques de l’assemblage. Enfin, cette étude montre que la modification de la chimie et de la topographie combinées améliore davantage ce potentiel d’adhérence.Le but de cette étude est d’ouvrir une voie vers un modèle décrivant les mécanismes de l’adhésion, influencés par la chimie de surface et la géométrie d’un motif, en s’appuyant sur un modèle mécanique permettant de décrire la dynamique des contraintes se propageant au travers de l’interface, en tenant compte des propriétés mécaniques des matériauxThanks to their low densities and good mechanical properties, polymer composites are good candidates for metal alloys substitutes. However, their physicochemical properties limit their adhesion potential towards several types of coatings. In order to improve metallic thin films adhesion on PEEK substrates, and to better comprehend adhesion mechanisms, dry-phase methods have been used to alter the surface properties of the material.First, this study shows that oxidative plasma treatments (at low or at atmospheric pressure) improve the wettability and the practical adhesion of metallic coatings, by an increase of the polar component of the surface, as measured by XPS. Second, this study shows that dense patterns etched by an infrared femtosecond laser allow good practical adhesion of the metallic thin films on the substrate. Finally, this study shows that the modification of both surface chemistry and the surface topography at the same time further improves the practical adhesion of the metallic thin films.The goal of this study is to propose a route towards a model describing the combined influence of surface texture and chemistry, with the support of a mechanical model describing the dynamics of the stress dissipation through the interface while taking into account the mechanicals properties of the interfacial materials
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Daw, Rosamund. "Plasma co-polymer surfaces of acrylic acid/octa-1,7-diene and methyl vinyl ketone/octa-1,7-diene : surface characterisation and behaviour of osteoblast-like cells." Thesis, University of Sheffield, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.301905.
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Vandenberghe, Camille. "Élévation aigüe de la cétonémie : effets cétogènes de produits alimentaires dérivés de l’huile de noix de coco et influence d’une combinaison avec de l’exercice de type aérobie." Mémoire, Université de Sherbrooke, 2017. http://hdl.handle.net/11143/10500.
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Depuis maintenant plus de 30 ans, il est reconnu qu’au début de la maladie
d’Alzheimer, le cerveau utilise moins bien le glucose, son principal carburant.
Cependant, ce problème énergétique précoce dans la maladie semblerait limité au
glucose et ne concernerait pas un autre carburant, celui-ci dérivé des gras, les cétones.
Ces dernières sont produites par le corps après un exercice physique d’intensité
modérée. Leur production est également stimulée avec la prise de suppléments
alimentaires à base d’huile de noix de coco, un aliment riche en triglycérides de
moyennes chaînes (MCT). La capture des cétones au cerveau augmente
proportionnellement à leur concentration plasmatique. Ainsi, des conditions élevant la
cétonémie augmentent aussi la capture cérébrale des cétones. Par conséquent,
l’élévation de l’apport en cétones pourrait constituer une approche novatrice qui
permettrait de potentiellement ralentir le développement de la maladie d’Alzheimer.
Notre objectif général était d’optimiser le type de supplément MCT à utiliser afin
d’élever la cétonémie de manière aigüe et, en second lieu, d’employer ce dernier en
combinaison avec une seconde stratégie cétogène, l’exercice physique de type aérobie
(EA). Lors de la première phase de ce projet, l’effet cétogène de différents produits
alimentaires dérivant de l’huile de noix de coco (acide caprylique [C8], acide caproïque
[C10], mélange de MCT typique [C8+C10]) était comparé chez 9 participants jeunes
sains. Des échantillons sanguins étaient récoltés toutes les 30 min pendant 8 h. Lors de
la seconde phase, le potentiel cétogène de la combinaison d’EA à une supplémentation
MCT était évalué chez 10 femmes âgées saines pendant 5 jours. Les cétones
plasmatiques sous ces différentes conditions étaient mesurées. Lors de cette étude, le
C8 était le produit le plus cétogène testé suivi du supplément C8+C10. L’huile de noix de
coco n’a pas induit une cétonémie plus élevée qu’un 8 h sans MCT. De plus, l’ajout de 5
jours d’EA a potentialisé la cétonémie observée suite à la prise de MCT C8+C10 seul.
Ainsi, la combinaison de stratégies cétogènes, tant au niveau de la diversité des
molécules utilisées ou des stratégies cétogènes employées, permet d’augmenter la
présence de cétones dans le sang.Abstract : Brain glucose consumption deteriorates with age, a situation that worsens with the onset of Alzheimer's disease. However, this early energy problem in the disease is limited to glucose and does not affect brain ketone uptake. Ketones are the main alternative fuel for the brain when glucose concentrations are decreased. They are produced endogenously after moderate aerobic exercise (AE) or with a medium chain triglyceride (MCT) exogenous supplement. Ketone brain uptake increases in proportion to their plasma concentration. Thus, providing a daily ketogenic fuel could help support brain energy needs during aging. Our aim was to optimize the type of MCT to use in a ketogenic supplementation and to combine this supplement with another ketogenic strategy, AE. In the first phase of this project, the acute ketogenic effect of products derived from coconut oil was compared. Nine healthy adults took various MCT supplements (coconut oil, caprylic acid [C8], capric acid [C10], classic MCT mix [C8+C10]). Blood was sampled every 30 min over 8 h. In the second phase, we evaluated the acute ketogenic potential of the combination of AE and MCT supplementation. Ten healthy older women took C8+C10 MCT supplement for 5 days combined with a 5-days AE program. Automated spectrophotometric assays where used to measure plasma ketones under these different conditions. Our results show that in this 8 h experimental design, C8 was the most ketogenic MCT followed by C8+C10. Coconut oil alone did not induce more net ketosis than an 8 h visit with no added MCT. Furthermore, the combination of AE and MCT supplementation enhanced the ketogenic response over 4 h compared to the control day. Thus, the combination of ketogenic strategies, both in terms of the diversity of the molecules or the ketogenic strategy employed, makes it possible to increase the presence of ketones in the blood.
Book chapters on the topic "Plasma ketone"
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Pastor, A., A. Sünder, and F. Liebert. "Branched-chain α-keto acids in plasma of growing chicken: when is the time for blood sampling?" In Energy and protein metabolism and nutrition in sustainable animal production, 425–26. Wageningen: Wageningen Academic Publishers, 2013. http://dx.doi.org/10.3920/978-90-8686-781-3_156.
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Reed, Donald J., and Darren L. Warren. "In Vivo Model for Vitamin E Depletion in Plasma and Liver of Rats with Methyl Ethyl Ketone Peroxide or 1,2-Dibromoethane1." In Oxidative Damage & Repair, 65–70. Elsevier, 1991. http://dx.doi.org/10.1016/b978-0-08-041749-3.50017-6.
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Butler, Gary, and Jeremy Kirk. "Hypoglycaemia." In Paediatric Endocrinology and Diabetes, 253–72. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198786337.003.0007.
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• Hypoglycaemia is defined as ‘A plasma glucose concentration low enough to cause symptoms and/or signs of impaired brain function’. • Cut-offs are contentious, ranging from <2.2 to <4.0 mmol/L, and are dependent on age, diagnosis, and also availability/usage of alternative metabolic fuels such as ketones. • May be transient or persistent, dependent on diagnosis. • Causes broadly due to: ◦ decreased glucose including prematurity, inborn errors of metabolism, hypopituitarism, adrenal insufficiency (primary and secondary), and prolonged fasting ◦ increased glucose utilization including infant of diabetic mother, hyperinsulinaemia, perinatal asphyxia, and various syndromes, e.g. Beckwith–Wiedemann. • Endocrine causes of hypoglycaemia include growth hormone deficiency, adrenal insufficiency (primary and secondary), and (?) hypothyroidism. • Metabolic disorders cause hypoglycaemia via impaired: ◦ mobilization of glucose stores ◦ gluconeogenesis ◦ alternative energy sources ◦ liver function. • Hyperinsulinaemic hypoglycaemia presents with increased glucose requirements (>8 mg/kg/minute) and non-ketotic hypoglycaemia. Diagnosis confirmed by demonstrating raised/detectable insulin/C-peptide during hypoglycaemia. Genotyping may assist with not only diagnosis but direct therapy (medical and surgical).
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Clark, Gregory O., and William J. Kovacs. "Glucose, Lipid, and Protein Metabolism." In Textbook of Endocrine Physiology. Oxford University Press, 2011. http://dx.doi.org/10.1093/oso/9780199744121.003.0018.
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The maintenance of life requires a constant supply of substrate for the generation of energy and preservation of the structure of cells and tissues. The process in principle is simple, yet the individual metabolic pathways and the regulation of substrate fluxes through these pathways can be complex. Energy is derived when fuel substrates are oxidized to carbon dioxide and water in the presence of oxygen, generating adenosine triphosphate (ATP). A portion of the ingested foodstuff is also utilized, either directly or after transformation into other substrates, to repair and replace cell membranes, structural proteins, and organelles. The remainder is stored as potential energy in the form of glycogen or fat. Under normal circumstances, each individual remains in a near-steady state where weight and appearance are stable over prolonged periods. In the short term, fuel metabolism changes dramatically several times a day during alternating periods of feeding and fasting. An anabolic phase begins with food ingestion and lasts for several hours. Energy storage occurs during this period when caloric intake exceeds caloric demands. The catabolic phase usually begins 4 to 6 hours after a meal and lasts until the person eats once again. During this phase, utilization shifts from exogenous to endogenous fuels, a change heralded by the mobilization of substrate stored in liver, muscle, and adipose tissue. Both anabolic and catabolic phases are characterized by specific biochemical processes regulated by distinct hormonal profiles. In the anabolic phase that follows ingestion of a mixed meal, substrate flux is directed from the intestine through the liver to storage and utilization sites. Glucose, triglyceride, and amino acid concentrations increase in plasma, whereas those of fatty acids, ketones (acetoacetic and β -hydroxy-butyric acids), and glycerol decrease. Both glycogen and protein synthesis begin in liver and muscle, while fatty acid synthesis and triglyceride esterification are stimulated in hepatocytes and adipose tissue. In the catabolic phase, the biochemical activities are reversed and the flux of fuel is directed from storage depots to liver and other utilization sites.
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Crowell, Pamela L., Robert H. Miller, and Alfred E. Harper. "[7] Measurement of plasma and tissue levels of branched-chain α-keto acids by gas-liquid chromatography." In Methods in Enzymology, 39–46. Elsevier, 1988. http://dx.doi.org/10.1016/s0076-6879(88)66009-5.
Full textConference papers on the topic "Plasma ketone"
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Wakelin, Edgar, Giselle Yeo, Alexey Kondyurin, Michael Davies, David McKenzie, Anthony Weiss, and Marcela Bilek. "Bio-functionalisation of polyether ether ketone using plasma immersion ion implantation." In SPIE Micro+Nano Materials, Devices, and Applications, edited by Benjamin J. Eggleton and Stefano Palomba. SPIE, 2015. http://dx.doi.org/10.1117/12.2202506.
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Wang, Z. Y., L. Zhang, and Y. L. Su. "EFFECT OF POLLEN TYPHAE ON 6-KETO-PGF , TXB2, TOTAL CHOLESTEROL AND HDL-C IN RABBITS WITH CHRONIC HYPERLIPIDEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643409.
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62 NZW rabbits were divided into 4 groups: (1) Control (C), (2) rabbits fed with high lipids diet (H), (3) H+pollen Typhae (H+P), (4) H+VitE (H+E). The following parameters were determined: (1) total cholesterol of aortic wall (WTC), (2) Serum TC (STC), High density lipoprotein cholesterol (HDL-C), (3) Plasma 6-keto-PGF1 (6-keto) and thromboxane B2 (TXB2), (4) 6-keto of aortic wall, (5) ratio of STC/HDL-C and plasma TXB2/6-ketoThe results showed that: (1) the level of WTC, STC and STC/HDL-C was significantly higher in the group H than in the group C, while that of 6-keto was lower (P < 0.01), (2) STC, WTC and plasma TXB2, TXB2 /6-keto all were significantly lower in the group H+P than m the group H, while wall's 6-keto was higher (P < 0.01).There was inverse correlation between plasma 6-keto and STC/HDL-C (P < 0.01), while positive correlation has been found between STC/HDL-C and plasma TXB2/6-keto (P < 0.05).In the group H+E, the plasma TXB2/6-keto, was lower than in the group H, the wall's 6-keto was higher, but there was no difference between the groups H+E and H+P. The STC and WTC were higher in the group H+E than in the group H+P, although lower than in the group H.It has been demonstrated in our Department that the Chinese traditional medicine Pollen Typhae had preventive effect on the experimental atherosclerosis in rabbit fed with high lipids diet, the mechanism would not only due to its effect lowering the STC, WTC and STC/HDL-C, but also to its action on the metabolism of prostaglandins. Its action on lowering STC and WTC appeared to be better than VitE, however, the latter had similar effect on the metabolism of prostaglandins as compared with Pollen Typhae.
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Fitscha, P., T. Simmet, B. A. Peskar, V. Tilsner, Waltraud Rogatti, and H. Sinzinger. "EFFECTS OF I.V. AND I.A. PGE1-INFUSION IN DIFFERENT DOSES ON FIBRINOLYTIC ACTIVITY, PLATELET FUNCTION AND STABLE PGE1 METABOLITES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643388.
Full textAbstract:
As it is well known that PGE1 is degraded during lung passage to a major extent, we examined what the optimal route and dosage concerning platelet function and plasmatic coagulation would be.6 patients with peripheral vascular disease (PVD) stage lib according to Fontaine were treated either i.a. (1,25 or 2,50 ng PGE1 [Prostavasin]/kg/min) or i.v. (5 or 10 ng/PGEl/kg/min) for 120 minutes.Various parameters reflecting platelet function (βTG, PF4, serum TXB2, ADP-induced aggregation, platelet sensitivity to PGI2, intraplatelet cAMP) plasmatic coagulation and fibrinolytic activity were measured. Blood was drawn from the contralateral cubital vein avoiding occlusion before and 5,30,120,125 and 185 minutes after starting PGE1. Fibrinopeptide A (1,03±0,38 → 2,57±1,32; p<0,01), plasminogen (108,5+10,7 → 1,24±11,5; p<0,01), plasmin changed, whereas α2-anti-plasmin tissue plasminogen activator (72,7±34,7 → 94,0±32,5) and urokinase did not change (1,00±.0,41 → 1,30±0,95) significantly. The long-lasting influence on the fibrinolytic activity can not be explained by a direct action of PGE1 or 15-keto-13,14 DH-PGE1. RIA determination of 15-keto-13,14 DH-PGE1 exhibited a certain dose-dependent effect of PGE1 on the plasma levels of the immunoreactive substance. The findings are suggestive for a process persisting even after complete disappearance of the causative agent, or for a biological capacity of a so far unknown long-lived PGEl-metabolite. PGE1 did not significantly affect the platelet function parameters.
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Broeseker, T. A., M. D. P. Boyle, and R. Lottenberg. "PATHOGENIC BACTERIA HAVE HIGH AFFINITY RECEPTORS SPECIFIC FOR PLASMIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644391.
Full textAbstract:
Binding of the key fibrinolytic enzyme, plasmin, to certain pathogenic group A streptococci was studied. In these experiments the ability of a group A streptococcal strain, 64/14, to bind either 125I-human plasminogen or the same label following activation with urokinase was measured. It was found that this strain bound <10% of the labeled plasminogen but >70% of labeled plasmin. This property distinguishes the plasmin receptor from streptokinase. These bacteria did not express a common serine protease receptor/inhibitor since they failed to bind labeled trypsin or urokinase. Maximal binding of plasmin occurred between pH 6.0 and 8.0 and in the ionic strength range of 50-200 mM salt. The Kd of plasmin binding to bacteria was approximately 10-10 M at pH 7.4 in 150 mM salt. This was determined by a non-linear least squares analysis of equilibrium binding data. Binding was reversibly inhibited by either epsilon aminocaproic acid (I50 of 0.2 mM) or lysine (I50 of 3.0 mM) suggesting the involvement of the high affinity lysine binding site of plasmin in its binding to bacteria. Bacterial bound plasmin retains its enzymatic activity, being capable of cleaving chromogenic substrates and solubilizing a fibrin- clot. The bacterial bound enzyme activity was inhibited by the low molecular weight inhibitors aprotinin and phe-pro-arg chloromethyl ketone but not by alpha-2 plasmin inhibitor. The ability of bacteria to acquire membrane associated proteolytic activity which cannot be physiologically inhibited may contribute to their tissue invasive properties.
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Jakubowski, J. A., and D. Deykin. "NIACIN-INDUCED PROSTACYCLIN (PGI2) GENERATION AND THE SEARCH FOR THE IDEAL DOSE OF ASPIRIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643370.
Full textAbstract:
We have previously reported that chronic administration of 80 mg/day of enteric-coated aspirin (ECA) in three divided doses of 27 mg each day for 7 days produced over 90% inhibition of platelet thromboxane production. What we wanted to know was whether that dose of aspirin spared PGI2 production. We developed a sensitive plasma assay for PGI2 (measured as 6-keto-PGF1a). We confirmed the reports of others that normal plasma levels are very low, less than 2 pg/ml. We selected niacin as a provocative challenge to raise plasma levels of PGI2 to test the ability of a given aspirin regimen to spare or suppress PGI2 production in vivo. In 5 normal subjects an oral dose of 3 mg/kg of niacin produced a 3-fold rise in 6-keto-PGF1a from 0.86 to 2.64 pg/ml. A dose of 5 mg/kg produced a rise to 6.6 pg/ml. Administration of 323 mg of regular aspirin/day for 7 days completely abolished niacin-induced elevation of plasma PGI2. The lowest dose of ECA that we have found effective in suppressing platelet thromboxane production in vitro, 80 mg/day in divided doses of 27 mg three times a day for 7 days, also completely suppressed niacin-induced elevation of PGI2. Our data do not support the hyypothesis that a very low dose of ECA selectively suppress platelet thromboxane production but spares generation of PGI2
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Moriau, M., Ch Col-De Beys, B. Golinska, and E. Lavenne-Pardonge. "IMPORTANCE OF SOME MOLECULAR MARKERS OF HEMOSTATIC ACTIVATION FOR THE DIAGNOSIS, THE CHOICE AND THE CONTROL OF PREVENTIVE AND CURATIVE THERAPY OF D.V.T. AND P.P.S." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644811.
Full textAbstract:
The measurement, before and after treatment, of some molecular markers of hemostatic activation (βTG, PF4, TXB2, FPA, 6 keto PGFlα) and the determination of their increased coefficient ratio (Δ+/βTG/Δ+Δ FPA, 4+βTG/4+ PF4,4+ 6 keto PGF1α/Δ+ TXB2 combined with the estimation of other parameters (F.VIII:Ċ/F.VIIIR:AG), AT III, PROT. C, ELT with and without ischemia) permlted us to subdivide the deep venous thromboses in two groupsThe first one or "simple D.V.T." was observed in normal subjects with or without varicoses, and without other main pathology and was consecutive to a simple plasma factors activation, the second one or "complicated D.V.T." appeared in patients with other pathology (infections, neoplasms, trauma, metabolic disorders) and was consecutive to a combined activation of plasma factors and plateletsA:before treat.,B:after anticoagul.,C:after anticoagul. + platelet inhibitors / * extreme values (MV ±2ŊIf anticoagulants (Heparine ancjfor VKA) alone were effective and sufficient for the treatment of "simple DVT" they were little or non active in the "complicated" forms and must be combined with platelet inhibitors to give the same result. The prevention of DVT in venous insuffisancy, consecutive or not to DVT, must be performed in the same way. A comparative study with various types of platelet inhibitors permited us to establish a scale of activity and to observe a benefic synergism with some combinations
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Croset, M., E. Vericel, M. Rigaud, Ph Coupron, M. Dechavanne, and M. Lagarde. "DECREASE OF PLATELET AGGREGATION AFTER INTAKE OF SMALL AMOUNTS OF PURIFIED EICOSAPENTAENOIC ACID IN ELDERLY PEOPLE. POSSIBLE ROLE OF VITAMIN E." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643805.
Full textAbstract:
Platelet hyperactivity is believed to be involvedin the thrombotic complications of elderly people.Since it has been proposed that eicosapentaenoic acid(EPA) can reduce platelet functions in normal humans,we have investigated its effect in elderly people. The daily intake (100 mg EPA) was at least 20 fold lower than usually tested. In a randomized, double blind study, eight people ingested EPA given as a pure triglyceride (1,3-didecanoyl,2-eicosapentaenoyl-glycerol) for 2 months and eight people ingested a placebo containing the same amount of vitamin E than in EPA preparation. Platelet aggregation, the oxygenatedmetabolism of arachidonic acid (AA), and vitamin E content of both plasma and platelets were investigated. Ingestion of EPA resulted in a slight but significant reduction of platelet-rich plasma aggregation in response to epinephrine and AA. The same decrease was observed with washed platelets when triggered bythrombin or collagen. EPA intake failed to affect the oxygenated metabolism of AA, measured by the formation of TXB2, HHT and 12-HETE from either exogenous or endogenous (thrombin stimulation) AA. Formation of AA oxygenated products including 6-keto-PGFla in clotted blood was unaffected. Excretion of urinary TXB2, 6-keto-PGFlα and their 2,3-dinor metabolites wasleft unchanged by ingestion of EPA. Platelet, but not plasma α- and γ-tocopherols were significantly increased by EPA intake. We conclude that, in our experiment, the reduction of platelet aggregation could not be explained by modification of AA metabolism. Since vitamin E has been associated with a decrease ofplatelet aggregation, at least in vitamin E deficiency, and platelet vitamin E being reduced with age, we speculate that the decreased platelet aggregation after EPA intake might be related to the increased platelet tocopherols.
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Landolfi, R., R. De Cristofaro, S. De Carolis, G. Ciabattoni, and B. Bizzi. "PLACENTAL-DERIVED PGI2 INHIBITS CORD PLATELET FUNCTION: POSSIBLE ROLE OF PGI2 IN THE TRANSIENT HYPOREACTIVITY OF NEWBORN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644274.
Full textAbstract:
Previous studies on newborn platelets hyporeactivity have been performed on cord blood. In this study we demonstrated that fresh cord platelet poor plasma (C-PPP) contains a labile antiaggrega-ting substance which, added to adult platelet rich plasma (PRP), is able to reverse ADP-induced platelet aggregation. Measurements of 6-Keto-prostaglandin (PG) Fl± levels in C-PPP obtained from10 different normal newborns gave anaverage value of 1050 ± 361(SD) pg/mL. Significantly lower levelsof this prostaglandin were found in plasma samples obtained from two newborns 2 hours after the birth (mean = 150 pg/mL) and in PPP of ten control adults (mean = 25 ± 34 pg/mL). In three newborns, platelet aggregation was studied using both C-PRP and PRP obtained 2 and 48 hours after the birth. A marked reductionof platelet response to ADP and collagen was evident in C-PRP. Such hyporeactivity was mild at 2 hours and absent in the third day of life. These results show that PGI2 inhibits cord platelets and might be the cause of a transient platelet hyporeactivity in the newborn. Finally we demonstrated that washed newborn platelets, compared to adult platelets, have a significant increase ofthe apparent affinity constant (Ka)for fibrinogen and that fetal and adult fibrinogen have similar Ka for platelets.
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Egberg, Nils, Krister Gréen, Jan Jacobsson, Ole Vester-gvist, Bjöm Wiman, and Michael Gallimore. "EFFECTS OF PLASMA KALLIKREIN AND BRADYKININ ON FIBRINOLYSIS AND THROMBOXANE PROSTACYKLIN FORMATION STUDIED IN MINIPIGS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644334.
Full textAbstract:
The effect of plasma kallikrein and bradykinin infusions into pigs on hemodynamic and hemostatic variables have been investigated. Both substances caused a pronounced decrease of the systemic blood pressure. The leucocyte count in periferal blood fell markedly, reaching a minimun within one hour after infusion of either of the substances.Signs that could be interpreted as a progressive disseminated intravascular coagulation with decrease of fibrinogen and platelet count was observed after kallikrein as well as bradykinin infusions. A pronounced increase of the plasma tissue plasminogen activator concentration followed both plasma kallikrein and bradykinin infusions. However, the peak concentration was found 5 minutes after bradykinin infusion but 60-120 minutes after kallikrein infusion, suggesting different mechanisms leading to the t-PA release. Concomittant with the maximun t-PA concentration there was a marked reduction of the plasminogen activator inhibitor (PAI) concentration. Three hours after drug infusions the PAI concentration was at or above preinfusion level. Kallikrein infusions caused a 10-20 fold increase of the urinary excretion of 2,3-dinor thromboxane B2 (metabolite of TxA2) and a 3-42 fold increase of 2,3-dinor-6-keto-PGFlalpha (metabolite of PGI2) excretion respectively. Corresponding data for bradykinin infusions were, 1.6-5 fold and 2-10 fold increases respectively. Possible links between leucocyte aggregation, prostanoid formation and fibrinolytic variables will be discussed.
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Kindel, G., J. Fareed, and U. Cornelli. "EFFECTS OF DEFIBROTIDE TREATMENT ON THE PLASMA AND SERUM INDUCED CONTRACTION OF RABBIT AORTIC STRIP IN RELATION TO THE PATHOPHYSIOLOGY OF MYOCARDIAL INFARCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643147.
Full textAbstract:
Several clinical and experimental studies have demonstrated the efficacy of a polydeoxyribonucleotide (Defibrotide) in myocardial ischemic disorders and peripheral arterial diseases. In attempts to investigate the mechanisms of action of this agent, we used a modified rabbit model of hemodynamics and an isolated rabbit aortic strip preparation. Intravenous bolus administration of Defibrotide at 5-50 mg/kg did not produce any changes in the mean arterial blood pressure up to 3 hours. Defibrotide treated rabbits also resisted human serum-stasis and stasis alone induced venous and arterial thrombus formation. Serum and plasma from Defibrotide treated animals were tested for their direct contractile and procontractile (synergistic with an epinephrine stimulus) activities on rabbit aortic strips. In contrast to plasma and serum from saline treated rabbits, both serum and plasma produced relatively weak or no effects. The dose-contrac-tion responses were shifted to the right suggesting that serum from Defibrotide treated animals contained much lesser amounts of contractile substances. This data indicates blood from Defibrotide treated rabbits is compositionally different than normal, either due to lack of cellular product formation (thromboxane B 2, serotonin) or due to the generation of endothelial products which are inhibitory to the contractile effects of substances generated during the formation of a thrombus. Plasma thromboxane B2/6 keto-PGFia ratios were also found to be much higher in Defibrotide treated groups when compared to the saline groups. The observed therapeutic effect of Defibrotide in acute myocardial infarction may be linked with the inhibition of the formation of thrombus and with the mediation of vascular spasm due to the generation of inhibitory substances or the lack of generation of spasmogenic substances.