Actividad de la lactato deshidrogenasa en fluídocrevicular gingival y saliva en fumadores conperiodontitis crónica / Lactate dehidrogenase activity in gingival crevicular fluid and saliva of smoker with chronic periodontitis

Existe un alto porcentaje de enfermedad periodontal atribuido al hábito del tabaco. La respuesta del organismo a esta enfermedad incluye la liberación de enzimas intracelulares relacionadas con la muerte y destrucción celular, como la Lactato Deshidrogenasa (LDH). Objetivo: Comparar los valores de LDH en fluido crevicular gingival (FCG) y saliva de pacientes fumadores y no fumadores con Periodontitis crónica (PC). Metodología: Participaron 15 pacientes hombres mayores de 30años; 6 fumadores, 6 no fumadores con PC y 3 sujetos control. Se recolectaron muestras de saliva total y de FCG de bolsas periodontales de = 6 mm. El volumen del FCG se determinó pesando las puntas de papel antes y después del muestreo obteniendo los valores en gramos y convertidos a unidades de volumen (ml). La actividad de LDH se determinó por medio de espectrofotometría. Los resultados se convirtieron a unidades de actividad enzimática expresados en mM. El volumen de FCG fue de 0,78 μL en sujetos sanos, en no fumadores con PC 1.12 y en fumadores con PC 1,32. Los valores de LDH correspondieron a; saliva de sujetos sanos 0,845, en no fumadores con PC 1,325 yen fumadores con PC 1,7895 mM. En FCG la actividad fue 0,4568 en sujetos sanos, en no fumadores con PC 0,987 y en fumadores con PC 1,2546 mM. Conclusiones: Las técnicas utilizadas permitieron determinar diferencia entre los valores de la actividad de LDH en ambos fluidos en fumadores y no fumadores con PC (AU)

The response of the body to periodontal disease includes the production of intra-cellular enzymes like Lactate Dehydrogenase (LDH) which is released by damaged periodontal cells. The LDH can be found in the gingival crevicular fluid (GCF) and saliva as a result of cellular death and damage. Objective: To compare LDH activity in GCF and saliva of smoker and non-smoker patients with Chronic Periodontitis. Methods: 15 male patients (30 to 50 years of age) participated in this study; 6 smokers with Chronic Periodontitis, 6 non-smokers with Chronic Periodontitis and 3 health subjects. Samples of stimulated total saliva as well as four samples of gingival crevicular fluid while probing periodontal lpockets (= 6 mm deep) with standarized #30 endodontic paper points were obtained. The enzymatic activity of LDH was recorded and was quantified by espectrophotometry. Results: GCF volume was 0.78 μL in health subjects, 1.12 μL non-smokers with Chronic Periodontitis and 1.32 μLsmokers with Chronic Periodontitis. LDH activity in saliva of smoker was 1.7895 mM. non-smoker patients with Chronic Periodontitis 1.325 and health subjects 0.845 mM. In FCG the activity was0.4568 mM of health subjects , non-smokers with Chronic Periodontitis 0.987 and smoker with Chronic Periodontitis was 1.2546 mM. The enzymatic activity of LDH in gingival crevicular fluid and saliva was greater in smoking patients compared to non-smoking patients. Conclusions: These results suggest that LDH activity in saliva and gingival crevicular fluid can be used to evaluate the progression of periodontal disease as well as the effects of smoking (AU)

Testis specific lactate dehydrogenase as target for immunoliposomes.

PROBLEM: Is it possible to deliver therapeutic agents to testis through specific targeting? METHOD OF STUDY: Immunoliposomes are designed by incorporating antibodies to lactate dehydrogenase-C4 (LDH-C(4)), which is the product of a testis specific gene. Their targeting and delivering ability is investigated in vitro and in vivo. RESULTS: It is observed that LDHC(4)-immunoliposomes are able to discriminate and recognize antigens on spermatozoa and testes both in vitro and in vivo. CONCLUSION: Specific targeting through LDH-C(4) appears to be a feasible strategy for delivering therapeutic as well as anti-spermatogenic agents to testis.

Impact of excipients on the absorption of P-glycoprotein substrates in vitro and in vivo.

The efflux transporter, P-glycoprotein (P-gp), located in the apical membranes of intestinal absorptive cells, can reduce the bioavailability of a wide range of orally administered drugs. A number of surfactants/excipients have been shown to inhibit P-gp, and thus potentially enhance drug absorption. In this study, the improved everted gut sac technique was used to screen excipients for their ability to enhance the absorption of digoxin and celiprolol in vitro. The most effective excipients with digoxin were (at 0.5%, w/v): Labrasol > Imwitor 742 > Acconon E = Softigen 767 > Cremophor EL > Miglyol > Solutol HS 15 > Sucrose monolaurate > Polysorbate 20 > TPGS > Polysorbate 80. With celiprolol, Cremophor EL and Acconon E had no effect, but transport was enhanced by Softigen 767 > TPGS > Imwitor 742. In vivo, the excipients changed the pharmacokinetic profile of orally administered digoxin or celiprolol, but without increasing the overall AUC. The most consistent change was an early peak of absorption, probably due to the higher concentration of excipient in the proximal intestine where the expression of P-gp is lower. These studies show that many excipients/surfactants can modify the pharmacokinetics of orally administered drugs that are P-gp substrates.

Interaction between lactate dehydrogenase and Tween 80 in aqueous solution.

PURPOSE: The weak aqueous interaction between the protein lactate dehydrogenase (LDH) and the nonionic surfactant Tween 80 has been investigated, because weak protein-amphiphile interactions are of significant importance in pharmaceutical formulations, but are experimentally hard to determine. The system LDH/sodium dodecyl sulphate (SDS) was used as reference because SDS, by its strong protein binding, denatures LDH completely. METHODS: Fluorescence spectroscopy with pyrene and 1,3-bis(lphenyl)propane (P3P) as probes, intrinsic protein fluorescence and NMR spectroscopy have been used. RESULTS: The fluorescence probe pyrene monitors a weak Tween-LDH interaction, detectable below the critical micelle concentration of ordinary Tween micelles. The microviscosity probe P3P shows a surfactant-induced denaturation in the case of LDH/SDS but not in the case of LDH/Tween 80. Intrinsic LDH fluorescence verifies this behavior. Pulsed-gradient spin-echo NMR was also used to verify the weak LDH-Tween 80 interaction. CONCLUSIONS. A weak interaction between LDH and Tween 80 occurs at hydrophobic zones of the protein, but it is not strong enough to denature LDH. The experimental outline used here provides a useful approach for mapping the very weak protein-amphiphile interactions often present in pharmaceutical formulations.

Metabolic inhibition induces opening of unapposed connexin 43 gap junction hemichannels and reduces gap junctional communication in cortical astrocytes in culture.

Rat cortical astrocytes in pure culture are functionally coupled to neighboring cells via connexin (Cx) 43 gap junctions under ordinary conditions. Small fluorescent molecules such as Lucifer yellow (LY) pass between cell interiors via gap junctions, but do not enter the cells when externally applied. Subjecting rat and mouse cortical astrocytes to "chemical ischemia" by inhibition of glycolytic and oxidative metabolism induced permeabilization of cells to Lucifer yellow and ethidium bromide before loss of membrane integrity determined by dextran uptake and lactate dehydrogenase release. The gap junction blockers octanol and 18alpha-glycyrrhetinic acid markedly reduced dye uptake, suggesting that uptake was mediated by opening of unapposed hemichannels. Extracellular La(3+) also reduced dye uptake and delayed cell death. The purinergic blocker, oxidized ATP, was ineffective. Astrocytes isolated from mice with targeted deletion of the Cx43 coding DNA exhibited greatly reduced dye coupling and ischemia-induced dye uptake, evidence that dye uptake is mediated by Cx43 hemichannels. Dye coupling was reduced but not blocked by metabolic inhibition. Blockade of lipoxygenases or treatment with free radical scavengers reduced dye uptake by rat astrocytes, suggesting a role for arachidonic acid byproducts in hemichannel opening. Furthermore, permeabilization was accompanied by reduction in ATP levels and dephosphorylation of Cx43. Although hemichannel opening would tend to collapse electrochemical and metabolic gradients across the plasma membrane of dying cells, healthy cells might rescue dying cells by transfer of ions and essential metabolites via Cx43 gap junctions. Alternatively, dying astrocytes might compromise the health of neighboring cells via Cx43 gap junctions, thereby promoting the propagation of cell death.

Glomerular charge selectivity for proteins larger than serum albumin as revealed by lactate dehydrogenase isoforms.

It is well known that macromolecules like albumin are markedly restricted in their passage across the glomerular capillary wall. However, the relative importance of solute size, charge and shape is currently debated since much of the previous work is based on dextran in neutral or charge-modified forms. These polymers have certain drawbacks that make them less suitable for analysis of capillary permeability and the notion of a glomerular charge barrier has therefore been questioned. Moreover, macromolecules larger than albumin (mol. wt. 69,000) have been suggested to pass through nonselective 'shunt' pathways. In order to study glomerular permeability, isolated rat kidneys were perfused with albumin solutions containing trace amounts of two differently radiolabelled isoenzymes of lactate dehydrogenase (LDH) at low temperature to inhibit tubular function. The isoenzymes have similar size (mol. wt. 140,000) and shape but differ in charge, one carrying a negative net surface charge (LDH1, -19) and the other being slightly cationic (LDH5, +2). The urine and perfusate samples were subjected to high pressure liquid chromatography (HPLC) gel-filtration to allow for measurements of intact LDH. The fractional clearance was 0.11% +/- 0.04% for the anionic LDH1 and 0.56% +/- 0.07% for LDH5, whereas that for albumin was 0.21% +/- 0.03% at a glomerular filtration rate of 0.11 +/- 0.01 mL min-1 g-1 kidney wet weight. The results were analysed using a homogenously charged membrane model and are compatible with a charge density of 35 mEq L-1, with 95% confidence interval of 26-41 mEq L-1. These findings suggest a significant glomerular charge selectivity for proteins substantially larger than albumin. The charge density is, however, far less than estimated from dextran studies.

The role of neutrophil elastase in human pulmonary artery endothelial cell injury.

Neutrophils are thought to play a key role in tissue injury. We investigated the role of human neutrophil-derived elastase in the induction of injury to human pulmonary artery endothelial cells. Incubation of endothelial cells with neutrophils increased the release of lactate dehydrogenase activity, thrombomodulin, and preloaded fura-2 from endothelial cells, indicating that neutrophils induce endothelial cell injury. Attachment alone of neutrophils to endothelial cells appeared to induce activation because elastase release and N-formyl-mentionyl-leucyl-phenylalanine (fMLP)-induced superoxide (O2) production from neutrophils incubated with endothelial cells were greater than from neutrophils only. When endothelial cell were incubated with neutrophils stimulated by fMLP or phorbol myristate acetate, the amount of elastase in the medium and endothelial cell damage was further enhanced. However, when neutrophils were blocked from direct attachment to endothelial cells using a membrane filter, endothelial cell damage was ameliorated, while exogenous neutrophil elastase and medium containing neutrophil-released elastase did not induce endothelial cell injury. An inhibitor of neutrophil elastase, ONO-5046 Na, as well as erythromycin, which reduces neutrophil-derived elastase, dramatically inhibited neutrophil-induced endothelial cell injury. Superoxide dismutase (SOD) partially inhibited injury. Injury was completely inhibited by treatment with a combination of ONO-5046 Na and SOD. These results suggest that attachment of neutrophils to endothelial cells is important for endothelial cell damage and that neutrophil-derived elastase plays an important role in endothelial cell injury in combination with O2. In addition, ONO-5046 Na and erythromycin may be useful in treating diseases worsened by excessive neutrophil activity.

Protein engineering tests of a homology model of Plasmodium falciparum lactate dehydrogenase.

This paper describes the testing of a homology model of Plasmodium falciparum lactate dehydrogenase (pfLDH) by protein engineering. The model had been validated in structural terms. It suggests explanations of the unusual properties of pfLDH (compared with all other LDHs). These unusual features are a lack of substrate inhibition, high activity with the synthetic coenzyme 3-acetylpyridine adenine dinucleotide (APAD+) and changes in residues at previously conserved positions. pfLDH shows several amino acid insertions and deletions in an alignment with protein sequences from all other known LDHs. The most notable is a five amino acid insertion into the active-site loop. In addition, a conserved serine at position 163 is replaced by leucine. The results showed that when the unique pfLDH structural features were engineered into Bacillus stearothermophilus lactate dehydrogenase, the thermophilic enzyme acquired the properties previously uniquely associated with the malarial enzyme. We conclude that the homology model of the malarial enzyme is adequate for the prediction of successful redesigns and, in the regions tested, is accurate.

Cytotoxicity of ethylene oxide/propylene oxide copolymers in cultured mammalian cells.

Cytotoxicity was measured in vitro for 8 ethylene oxide/propylene oxide copolymers (EO/PO copolymers) using lactate dehydrogenase release from cultured mammalian cells as the endpoint. Three cell types were used in these assays: Chinese hamster ovary cell line (AS52), rat lung epithelial cell line (LEC), and freshly isolated rat alveolar macrophages (RAM). A range of cytotoxicity was seen with toxic effects observed from 20 to > 20,000 micrograms/ml. The same relative order of toxicities were observed for all 3 cell lines although RAM cells appeared to be somewhat more sensitive. The in vitro cytotoxicity, as measured by LDH release and microscopic observations of the cells, correlated poorly with the in vivo inhalation toxicity. The most lethal compounds following acute inhalation (UCON 50-HB-5100 and UCON 50-HB-2000) were among the least toxic in the in vitro cytotoxicity screen. Conversely the 2 compounds which were the most toxic in vitro (Pluronic 17 R1 and Pluronic L64) did not produce any unusual degree of toxicity in inhalation studies. The results of these experiments indicate that these in vitro mammalian cell assays will not be useful, at least for these classes of chemistry, in prediction of in vivo inhalation toxicity.

[Kinetics of lipid peroxidation induced by UV beta rays in human keratinocyte and fibroblast cultures]. / Cinétique de la lipoperoxydation induite par les UVB dans les cultures de kératinocytes et de fibroblastes humains.

Lipid peroxidation has been implicated in skin damage by ultraviolet radiation. The aim of the study was to determine the kinetic of lipid peroxidation induced by ultraviolet beta (UVB) in adult keratinocytes and fibroblasts in culture. The keratinocytes were obtained from a single primary culture and the fibroblasts were in the same subculture (4 to 10 transfers). For UVB irradiation, the cells were maintained in a small volume of Hanks balanced salt solution and were irradiated (0.75, 1.5, 3 and 4.5 Jcm-2). Then cells were cultured for 3 to 48 hours. Lipid peroxidation was estimated by free MDA determination in both extracellular medium and cells using a size exclusion chromatography coupled to an HPLC procedure. In addition, LDH release in culture media was evaluated as in indice of cytotoxicity. An increase of total free MDA was observed 3 hours after cell irradiation which was dose-dependent from 0.75 to 3 Jcm-2 for keratinocytes and fibroblasts. MDA was detected both in cells and in culture media. As soon as 3 hours after irradiation 90% in total MDA was present in the culture media. Kinetic of lipid peroxidation: for 0.75 Jcm-2, an elevation of MDA was observed 12 hours after irradiation in both cultures. A further increase in MDA was noted 24 hours after fibroblasts irradiation but not in irradiated keratinocytes. LDH release in culture media increased with post irradiation time until 48 hours. The cytotoxic effect of UVB irradiation on keratinocytes and fibroblasts cultures was shown by an enhancement of lipid peroxidation which was detectable during 48 hours after irradiation. An increase of LDH release was observed simultaneously.

Dipyridamole increases oxygen-glucose deprivation-induced injury in cortical cell culture.

BACKGROUND AND PURPOSE: Adenosine transport inhibitors attenuate ischemic central neuronal damage in vivo, but the locus of this protective action is presently unknown. To help address the question of whether adenosine transport inhibitors have a protective effect directly on brain parenchyma, we tested the effect of the adenosine transport inhibitor dipyridamole on neuronal loss induced by oxygen-glucose deprivation in vitro. METHODS: Murine cortical cultures were exposed to combined oxygen and glucose deprivation, N-methyl-D-aspartate, or kainate. The extracellular concentrations of glutamate and adenosine were measured by high-performance liquid chromatography; neuronal cell death was assessed by morphological examination and measurement of lactate dehydrogenase release. RESULTS: Cultures exposed to oxygen-glucose deprivation for 30 to 75 minutes exhibited an insult-dependent increase in extracellular adenosine, followed shortly by an increase in extracellular glutamate and 24 hours later by neuronal death. Addition of the A1 receptor antagonist 8-cyclopentyltheophylline during oxygen-glucose deprivation enhanced both glutamate release and neuronal damage. Addition of 10 mumol/L dipyridamole decreased extracellular adenosine and also enhanced extracellular glutamate and neuronal death. In contrast, dipyridamole increased the levels of extracellular adenosine stimulated by N-methyl-D-aspartate or kainate. CONCLUSIONS: These results are consistent with the idea that endogenous adenosine has a neuroprotective effect directly on cortical cells exposed to oxygen-glucose deprivation. However, inhibition of adenosine transport with dipyridamole was surprisingly not an effective strategy for enhancing this protective effect. The beneficial effects of adenosine transport inhibitors observed in vivo may be mediated indirectly--for example, by effects on the vasculature.

Ultraviolet A-induced cellular membrane damage in the photosensitivity dermatitis/actinic reticuloid syndrome.

Abnormal photosensitivity of skin in the photosensitivity dermatitis/actinic reticuloid syndrome (PD/AR) correlating to an abnormal photosensitivity of dermal fibroblasts from these patients has been established previously. Cultured human skin fibroblasts from normal infant and adult donors, foreskin tissue and patients with PD/AR were assayed for oxidative stress induced membrane damage following ultraviolet A (UVA) radiation (340-450 nm) and hydrogen peroxide treatment by measurement of lactate dehydrogenase release. Skin fibroblasts from PD/AR patients were, in general, 2- and 4-fold more sensitive than normal controls regarding membrane-induced damage to UVA radiation and hydrogen peroxide treatment, respectively. Cells from one patient where biopsies were taken during full disease flair and 2 years later, following disease remission by immunosuppressive therapy, showed the same cellular sensitivity. In addition, fibroblasts from foreskin tissue were resistant to UVA radiation as measured by lactate dehydrogenase release, suggesting that this frequently used source of cell culture does not provide the best control group for comparison with photosensitive disease states. All these results suggest that the target for the cellular sensitivity seen in cells from PD/AR patients is the membrane.

Permeability of parietal pleura to liquid and proteins.

The permselectivity of the parietal pleura was determined in spontaneously breathing anesthetized rabbits and dogs. In rabbits, we injected intrapleurally 5 ml of 1-g/dl albumin solution containing 100 microCi of 131I-labeled albumin plus 100 microCi of either lactate dehydrogenase (LDH) or alpha 2-125I-macroglobulin. Dogs received 100 ml of 1-g/dl albumin solution containing 100 microCi of 131I-albumin plus 100 microCi of alpha 2-125I-macroglobulin. A transpleural pressure gradient was set, lowering the intracapsular pressure to -30 cmH2O. The solvent drag reflection coefficients (sigma f) were calculated as the ratio between tracer concentrations in capsular and pleural liquid collected at 60-180 min. In rabbits sigma f was 0.44 +/- 0.2 (SD) for albumin, 0.84 +/- 0.1 for LDH, and 0.93 +/- 0.05 for alpha 2-macroglobulin. In dogs sigma f was 0.30 +/- 0.19 for albumin and 0.53 +/- 0.15 for alpha 2-macroglobulin. The hydraulic conductivity of the parietal pleura was 2.18 +/- 1.54 microliters.h-1.cmH2O-1.cm-2 in rabbits and 1.22 +/- 1.13 microliters.h-1.cmH2O-1.cm-2 in dogs. The parietal pleura could be modeled by two pore populations with radii of 83-89 and 156-222 A. The permeability coefficient averaged 0.08-0.21 x 10(-6) cm/s for albumin, 0.06-0.09 x 10(-6) cm/s for LDH, and 0.01-0.03 x 10(-6) cm/s for alpha 2-macroglobulin.

Protection by gabexate mesilate (FOY) of the exocrine pancreas in rats with acute pancreatitis induced by a supramaximal dose of caerulein.

Earlier studies have reported that interstitial oedematous pancreatitis characterized by hyperamylasaemia can be seen during the early stage of stimulation of supramaximal dose of caerulein. The present study investigated the changes in both cellular and lysosomal fragility and the protective effects of a synthetic protease inhibitor gabexate mesilate (FOY) on this non-invasive model of experimental pancreatitis. The infusion of FOY (50 mg/kg/h) prevented the caerulein-induced increase in serum amylase and pancreatic oedema formation and reduced the elevated amylase content significantly. The administration of FOY with caerulein also reduced the increased lactic dehydrogenase (LDH) discharge significantly and inhibited the cathepsin B leakage from lysosomes in an in vitro incubation system. These results indicate that FOY plays its protective role at the subcellular level--that is, in lysosomes by inhibiting some proteases such as phospholipase A2. The importance of esterases in the pathogenesis of acute pancreatitis is demonstrated. This type of esterase inhibitor may be valuable clinically in the treatment of acute pancreatitis and these results also suggest the role of lysosomal fragility in the pathogenesis of progression of acute pancreatitis.

Actinobacillus actinomycetemcomitans serotypes and leukotoxicity in Korean localized juvenile periodontitis.

Actinobacillus actinomycetemcomitans is though to play an important role in the pathogenesis of localized juvenile periodontitis (LJP). Preliminary data suggested that the serotype distribution of A. actinomycetemcomitans in Korea and the United States differ. This study evaluated A. actinomycetemcomitans prevalence, serotype distribution, and leukotoxicity in Korean LJP patients by culture, enzyme-linked immunosorbent assay, indirect immunofluorescence, and lactate dehydrogenase release from polymorphonuclear leukocytes exposed to A. actinomycetemcomitans. A. actinomycetemcomitans occurred in 75% of LJP lesions and 6% of normal sites with approximately equal distribution of serotype a, b, and c. Single serotypes were isolated from nine patients while three patients harbored two serotypes either in the same or different disease sites. A. actinomycetemcomitans leukotoxicity occurred in 22% isolates with a 69% prevalence. Individual sites harbored both leukotoxic and non-leukotoxic strains with no serotype association. The distribution of serotypes and leukotoxic strains of A. actinomycetemcomitans in Korean LJP patients differed from those reported in the United States. This suggests that serotype b may not be more important in the pathogenesis of LJP.

Reactivity and toxicity of atracurium and its metabolites in vitro.

Cytotoxicity of atracurium and of its metabolites was tested in vitro. Exposure of isolated rat hepatocytes to atracurium produced cellular damage evidenced by extrusion of an intracellular enzyme, lactate dehydrogenase (LDH), into the incubation medium. Leakage of LDH was directly related to the concentration of atracurium in the medium (250 to 800 microM). If the spontaneous degradation of atracurium (presumably via Hofmann elimination) was first carried out in vitro and the degradation products subsequently added to the isolated hepatocytes, the leakage of LDH was also dose-dependent but larger than that observed after the addition of the parent drug. When l-cysteine was admixed to the products of the spontaneous degradation of atracurium prior to their addition to the liver cells, no leakage of LDH was observed. The results are compatible with the working hypothesis that atracurium itself and, even more so, acrylates formed in Hofmann elimination of atracurium, are reactive toward nucleophiles and damage the cells by alkylating nucleophiles present in cellular membranes. Antecedent covalent binding of acrylates to the nucleophile cysteine, i.e., the formation of acrylate-cysteine adducts, saturated the reactive capacity of acrylates for nucleophiles and thus prevented the reactive metabolites from alkylating the endogenous nucleophiles. Possible clinical consequences resulting from in vivo generation of reactive metabolites are not clear at the present time but are projected to be related to (a) the dose of atracurium administered, (b) the amount of acrylates generated, (c) the functional importance of the endogenous nucleophiles alkylated, and (d) the pathway and the speed of detoxification of atracurium and its metabolites.

Release characteristics of enzymes used in the diagnosis of myocardial infarction.

Release characteristics of S-LD, S-LD1, S-ASAT, S-CK and S-CK-MB were studied in 47 consecutive AMI patients. In addition, previously obtained data for serum myoglobin (S-MYO) were compared. Serum was sampled at regular intervals after admission to the Coronary Care Unit (CCU). The release rate and half lives of the enzymes were calculated according to a one-compartment kinetic model. The time to peak values, the time of total release and the half lives were interrelated in the following order: MYO less than CK-MB less than CK less than ASAT less than LD1 less than LD which coincides with the wellknown appearance and disappearance rates in serum. The ratio between mean peak values and upper reference limits followed the reverse order. The finding that the release rate of enzymes and half-lives co-vary is hypothetically suggested to be attributed to differences in rate of membrane diffusion. There is indirect evidence that a slow indicator such as LD1 reflects infarct size better than fast indicators with rapid release and removal such as MYO or CK-MB. However, these fast markers have a better signal to noise ratio, whereby they probably reflect changes in the infarction process better.