Buenos Aires 01 de Diciembre del 2020
Búsqueda Bibliográfica: Acido Láctico (2000-2010)
- Chin Med J (Engl). 2009 Nov 5;122(21):2547-53.
Relationship of plasma creatinine and lactic acid in type 2 diabetic patients without renal dysfunction.
Liu F(1), Lu JX, Tang JL, Li L, Lu HJ, Hou XH, Jia WP, Xiang KS.
(1)Department of Endocrinology and Metabolism, Shanghai Jiao Tong University
Affiliated Sixth People's Hospital, Shanghai 200233, China.
BACKGROUND: As one of most widely-used biguanides, metformin can induce the lactic acidosis in patients with renal failure though its incidence is very low.
However, lactic acidemia induced by metformin was reported in patients without renal dysfunction. It is unclear that whether lactatemia exists in diabetic patients with normal renal function in Chinese or not and its influencing factors. This study aimed to clarify the influencing factors of lactic acid, and identify a practiced clinical marker to predict the hyperlactacidemia in diabetics with normal renal function.
METHODS: The clinical data and venous blood samples of 1024 type 2 diabetic patients treated with (n = 426) or without metformin (n = 599) were collected.
The lactic acid was assayed by enzyme-electrode method. The biochemical indexes included creatinine (Cr) and hepatase were measured with enzymatic procedures.
The lactic acid concentrations of different Cr subgroups were compared, and the correlation and receiver operating characteristic curve analysis were used.
RESULTS: The mean lactic acid level and the proportion of hyperlactatemia of metformin group were significantly higher than that of non-metformin group (P < 0.01), but no lactic acidosis was found in all patients. The correlation and multiple stepwise regression analysis indicated that the correlative factors of lactic acid in turn were Cr, metformin, alanine transferase (ALT), body mass index (BMI), Urine albumin (Ualb), and blood urea nitrogen (BUN) in total patients; and Cr, ALT, BMI and BUN in non-metformin treated patients; Cr and ALT in metformin-group. The lactate concentration increased with the increment of Cr levels, and reached its peak at Cr 111-130 micromol/L, and the optimal cutoff of Cr in predicting hyperlactacidemia was 96.5 micromol/L.
CONCLUSIONS: Metformin can increase the incidence of lactatemia in type 2 diabetic patients without renal dysfunction. Cr, ALT, and BMI are independent associated factors of blood lactic acid levels. There is low proportion of lactatemia in type 2 diabetics without metformin therapy, the optimal cutoff of Cr to predict lactatemia in these patients is 96.5 micromol/L.
PMID: 19951568 [Indexed for MEDLINE]
- Ultrasound Med Biol. 2009 Nov;35(11):1854-62. doi: 10.1016/j.ultrasmedbio.2009.06.1098. Epub 2009 Sep 19.
Plasma sterilization of poly lactic acid ultrasound contrast agents: surface modification and implications for drug delivery.
Eisenbrey JR(1), Hsu J, Wheatley MA.
(1)School of Biomedical Engineering, Science and Health Systems, Drexel
University, Philadelphia, PA 19128, USA.
Poly lactic acid (PLA) ultrasound contrast agents (CA) have been developed previously in our laboratory for ultrasound (US) imaging, as well as surface coated with doxorubicin to create a potential targeted platform of chemotherapeutic delivery using focused US. However, we have previously found it impossible to sterilize these agents while at the same time maintaining their acoustic properties, a task that would probably require fabrication within a clean facility. The purpose of this paper is to investigate the feasibility of using plasma to sterilize these CA while maintaining maximum echogenicity, a step that would greatly facilitate in vivo investigations. Effects of plasma exposure time (1, 3 and 6 min) and intensity (low-10 mA, 6.8 W; medium-15 mA, 10.5 W; and high-25 mA, 18 W) on the CAs' acoustic properties, surface morphology, zeta potential, capacity to carry chemotherapeutics and overall sterility are described. Both increases in plasma intensity and exposure time increased CA zeta potential and also significantly increased drug payload.
High-intensity plasma exposure for 3 min was found to be an optimal sterilization protocol for maximal (100%) preservation of CA echogenicity.
Plasma exposure resulted in sterile samples and maintained original CA enhancement of 20 dB and acoustic half-life over 75 min, while increasing CA zeta potential by 11 mV and doxorubicin loading efficiency by 10%. This study not only shows how a highly temperature- and pressure-sensitive agent can be sterilized using plasma, but also that surface modification can be used to increase surface binding of the drug.
PMID: 19766380 [Indexed for MEDLINE]
- Clin Res Cardiol. 2009 Jan;98(1):52-8. doi: 10.1007/s00392-008-0723-0. Epub 2008 Oct 13.
Post-exercise heart rate recovery in healthy, obeses, and COPD subjects: relationships with blood lactic acid and PaO2 levels.
Ba A(1), Delliaux S, Bregeon F, Levy S, Jammes Y.
(1)UMR MD2 (P2COE), IFR Jean Roche, Faculty of Medicine, University of Mediterranee, Bd. Pierre Dramard, 13916, Marseille Cedex 20, France.
Because blood acidosis and arterial oxygenation (PaO(2)) play key roles in the chemoreflex control of cardiac activity, we hypothesized that heart rate (HR) decay rate after maximal exercise may be linked to post-exercise increase in blood lactate (LA) level and/or the resting PaO(2). Twenty healthy subjects and thirty five patients at risks of cardiovascular diseases (20 obeses; 15 patients with chronic obstructive pulmonary disease, COPD) performed a maximal cycling exercise. During the recovery period, HR was continuously measured for consecutive 10-s epochs allowing to compute linear or second order polynomial equations and to calculate every minute HR variations compared to peak HR value (DeltaHR). PaO(2) was measured at rest and post-exercise maximal LA level was determined. A second order polynomial equation (y = a(2) x (2) + b(2) x + c) best fitted the post-exercise HR decay rate. The a(2) and b(2) coefficients and DeltaHR did not depend on age, sex, and body mass index. Despite a large scattering of HR decay rate, even present in healthy subjects, a(2) and DeltaHR were significantly lower in obeses and COPDs. In the whole population, both a(2) coefficient and DeltaHR were negatively correlated with maximal post-exercise LA level. DeltaHR was lowered in hypoxemic patients. Thus, the slowest post-exercise HR decay rate was measured in subjects having the highest peak LA increase or hypoxemia. Thus, even in healthy subjects, the post-exercise HR decay rate is lowered in individuals having an accentuated exercise-induced LA increase and/or hypoxemia. The mechanisms of delayed post-exercise HR recovery are only suspected because significant correlations cannot assess cause-to-effect relationships.
PMID: 18853089 [Indexed for MEDLINE]
- Biomed Chromatogr. 2008 May;22(5):450-3. doi: 10.1002/bmc.966.
Simultaneous clinical monitoring of lactic acid, pyruvic acid and ketone bodies in plasma as methoxime/tert-butyldimethylsilyl derivatives by gas chromatography-mass spectrometry in selected ion monitoring mode.
Paik MJ(1), Cho EY, Kim H, Kim KR, Choi S, Ahn YH, Lee G.
(1)Metabolomic Analysis Laboratory, Institute for Neuroregeneration and Stem Cell Research, Ajou University, Wonchon-dong, Yeongtong-gu, Suwon 443-721, South Korea.
Simultaneous determination of lactic acid, pyruvic acid, 3-hydroxybutyric acid and acetoacetic acid for clinical monitoring of lactic acidosis and ketone body formation in human plasma (20 microL) was performed by gas chromatography-mass spectrometry in selected ion monitoring (SIM) mode after generating methoxime/tert-butyldimethylsilyl derivatives. All of the targeted carboxylic acids were detected by characteristic fragment ions, which permitted sensitive and selective identification in the presence of co-extracted free fatty acids and other acidic metabolites at much higher levels. The method was linear (r>or=0.9991), reproducible (% relative standard deviation=1.2-5.8), and accurate (% relative error=-7.2-7.6), with detection limits of 0.05-1.7 ng/mL.
This rapid, accurate and selective method using minimal plasma samples (20microL) is useful in the clinical monitoring of lactic acidosis and ketone body formation in plasma.
PMID: 18254151 [Indexed for MEDLINE]
- Intensive Care Med. 2007 Nov;33(11):1967-71. doi: 10.1007/s00134-007-0788-7. Epub 2007 Jul 28.
The first demonstration of lactic acid in human blood in shock by Johann Joseph Scherer (1814-1869) in January 1843.
Kompanje EJ, Jansen TC, van der Hoven B, Bakker J.
Lactic acid was first found and described in sour milk by Karl Wilhelm Scheele (1742–1786) in 1780. The German physician–chemist Johann Joseph Scherer (1841–1869) demonstrated the occurrence of lactic acid in human blood under pathological conditions in 1843 and 1851. In this article we honour the forgotten observations by Scherer and describe the influence of Scherer's finding on further research on lactic acid at the end of the 19th century.
We conclude that Scherer's 1843 case reports should be cited as the first description of lactic acid in human blood after death and also as the first demonstration of lactic acid as a pathological finding in septic and haemorrhagic shock. Carl Folwarczny was, in 1858, the first to demonstrate lactic acid in blood in a living patient.
PMID: 17661014 [Indexed for MEDLINE]
- FEMS Immunol Med Microbiol. 2007 Mar;49(2):192-6. doi:10.1111/j.1574-695X.2006.00199.x.
Identification of lactic acid bacteria isolated from human blood cultures.
Svec P(1), Sevcíková A, Sedlácek I, Bednárová J,Snauwaert C,Lefebvre K,Vandamme P, Vancanneyt M.
(1)Czech Collection of Microorganisms, Faculty of Science, Masaryk University,
Brno, Czech Republic. email@example.com
Fifteen lactic acid bacterial strains were isolated from blood cultures from 15 different patients in the Faculty Hospital in Brno, Czech Republic. All strains were identified using biochemical tests and repetitive PCR using the (GTG)5 primer. Doubtful identification results were confirmed by whole-cell protein analysis. The strains were assigned to the genera Lactobacillus (eight strains representing seven species), Leuconostoc (six strains representing four species) and Weissella (one strain). Antibiotic susceptibility testing was performed using the E-test and revealed high-level resistance to cotrimoxazol, metronidazole, vancomycin and teicoplanin, but nearly all strains were susceptible to erythromycin, clindamycin, ampicillin and penicillin.
PMID: 17328753 [Indexed for MEDLINE]
- J Biomater Sci Polym Ed. 2007;18(11):1387-400. doi: 10.1163/156856207782246812.
Effects of oxygen plasma treatment on adipose-derived human mesenchymal stem cell adherence to poly(L-lactic acid) scaffolds.
Hanson AD(1), Wall ME, Pourdeyhimi B, Loboa EG.
(1)Joint Department of Biomedical Engineering, 2142 Burlington Nuclear
Engineering Laboratories, Campus Box 7115, North Carolina State University,
Raleigh, NC 27695, USA.
Plasma treatment of substrate surfaces can be utilized to improve adhesion of cells to tissue engineered scaffolds. The purpose of this study was to enhance cell adhesion to non-woven poly(L-lactic acid) (PLLA) scaffolds using oxygen plasma treatment to increase surface hydroxyl groups and thereby enhance substrate hydrophilicity. It was hypothesized that oxygen plasma treatment would increase the number of adipose-derived human mesenchymal stem cells (hMSCs) that adhered to melt-blown, non-woven PLLA scaffolds without affecting cell viability. The number of cells that adhered to the oxygen plasma-treated (10 min at 100 W) or untreated PLLA scaffolds was assessed at 2, 4, 8, 12, 24 and 48 h post-seeding via DNA analysis. Cell viability and morphology were also assessed at 2, 4, 8, 12 and 24 h post-seeding via a live/dead assay and hematoxylin staining, respectively. Oxygen plasma treatment decreased the contact angle of water from 75.6 degrees to 58.2 degrees , indicating an increase in the surface hydrophilicity of PLLA. The results of the DNA analysis indicated that there was an increased number of hMSCs on oxygen plasma treated scaffolds for two of the three donors. In addition, oxygen plasma treatment promoted a more even distribution of hMSCs throughout the scaffold and enhanced cell spreading at earlier time points without altering cell viability. This early induction of cell spreading and the uniform distribution of cells, in turn, may increase future proliferation and differentiation of hMSCs under conditions that simulate the microenvironment in vivo.
PMID: 17961322 [Indexed for MEDLINE]
- J Physiol Pharmacol. 2006 Nov;57 Suppl 9:13-21.
Combined effect of different lactic acid bacteria strains on the mode of cytokines pattern expression in human peripheral blood mononuclear cells.
Gackowska L(1), Michalkiewicz J, Krotkiewski M, Helmin-Basa A, Kubiszewska I, Dzierzanowska D.
(1)Department of Immunology, Collegium Medicum in Bydgoszcz, Nicolaus Copernicus
University, Poland. firstname.lastname@example.org
The balance between immunogenic and tolerogenic activities in human immune system strongly depends on microflora-induced pro-and anti-inflammatory activities. Lactic acid bacteria (LAB) are important components of microflora.
The interactions of the different strains of LAB and the cells of immune system are largely unknown. To assess if LAB strains composition would have an effect on the cellular responses profile (proliferation, cytokines synthesis) peripheral blood mononuclear cells (PBMC) model system was used. PBMC were induced by three different strains of LAB: Lactobacillus acidophilus, Lactobacillus delbrueckii spp. bulgaricus, Bifidobacterium bifidum. Tested strains were mixed together, in combinations with each other (pairs) or alone.
Both, the LAB mixture as well as the pairs and the single LAB strains induced low lymphocyte proliferation (about 10% of ConA-induced response). However, the single LAB strains and their combinations were quite different cytokines inducers. First, L. acidophilus was much stronger IFN-gamma inducer than the LAB mixture, being a few times higher IL-12 stimulator than L. bulgaricus and B. bifidum. Second, L. bulgaricus and B. bifidum suppressed L.acidophilus-induced IFN-gamma synthesis to the level equal to that induced by the LAB mixture, limiting IL-12 production by about 30% and 70%, respectively. Third, the LAB strains were good IL-10 and TNF-alpha inducers, irrespectively of their combinations used. We conclude that LAB strains' pro or anti-inflammatory potentials are at least in part dependent on their composition. Low LAB mixture-induced IL-12 and IFN-gamma production and relatively high IL-10 and TNF-alpha expression may represent cellular activities normally induced in vivo by a combined action of bacterial antigens. Their presence is important to limit pro-inflammatory reactions (via IL-10) and to provide protection against infections (via TNF-alpha).
PMID: 17242484 [Indexed for MEDLINE]
- Asian J Surg. 2004 Oct;27(4):303-5. doi: 10.1016/S1015-9584(09)60056-7.
Plasma D-lactic acid level: a useful marker to distinguish perforated from acute simple appendicitis.
Demircan M(1), Cetin S, Uguralp S, Sezgin N, Karaman A, Gozukara EM.
(1)Department of Pediatric Surgery, Faculty of Medicine, Inonu University, Malatya, Turkey. email@example.com
Early diagnosis of perforated appendicitis is important for reducing morbidity rates. The aim of this study was to determine the value and utility of plasma D-lactic acid levels in identifying the type of appendicitis. In this clinical study, plasma D-lactic acid levels were assessed in 44 consecutive paediatric patients (23 with acute appendicitis, 21 with perforated appendicitis) before laparotomy. D-lactic acid levels were determined by an enzymatic spectrophotometric technique using a D-lactic acid dehydrogenase kit. Patients with perforated appendicitis had higher D-lactic acid levels (3.970 +/- 0.687 mg/dL) than patients in the control group (0.478 +/- 0.149 mg/dL) and patients with acute appendicitis (1.409 +/- 0.324 mg/dL; p < 0.05). For a plasma D-lactic acid level greater than 2.5 mg/dL, the sensitivity and specificity of the D-lactic acid assay were 96% and 87%, respectively. The positive predictive value was 87%, the negative predictive value was 96%, and the diagnostic value was 91%. These results suggest that the measurement of plasma D-lactic acid levels may be a useful adjunct to clinical and radiological findings in distinguishing perforated from acute non-perforated appendicitis in children.
PMID: 15564184 [Indexed for MEDLINE]
- Clin Infect Dis. 2004 Mar 1;38 Suppl 2:S73-9. doi: 10.1086/381449.
Nucleoside-related mitochondrial toxicity among HIV-infected patients receiving antiretroviral therapy: insights from the evaluation of venous lactic acid and peripheral blood mitochondrial DNA.
Montaner JS(1), Côté HC, Harris M, Hogg RS, Yip B, Harrigan PR, O'Shaughnessy MV.
(1)BC Centre for Excellence in HIV/AIDS and the Canadian HIV Trials Network, St. Paul's Hospital, Providence Health Care, University of British Columbia, Vancouver, Canada. firstname.lastname@example.org
Nucleoside analogues inhibit human DNA polymerase gamma. As a result, they can produce mitochondrial toxicity. We evaluated the possible role of random venous lactic-acid determinations as a tool for mitochondrial toxicity among patients receiving nucleoside therapy. More recently, we have developed an assay that can detect changes in mitochondrial DNA (mtDNA) levels in peripheral blood cells. Using this assay, we have characterized changes in mtDNA relative to nuclear DNA (nDNA) in peripheral blood cells from patients with symptomatic nucleoside-induced hyperlactatemia. Our results demonstrated that symptomatic hyperlactatemia was associated with markedly low mtDNA : nDNA ratios. A statistically significant increase in the mtDNA : nDNA ratio was observed after the discontinuation of antiretroviral therapy. Full validation of monitoring the mtDNA : nDNA ratio is currently under way.
PMID: 14986278 [Indexed for MEDLINE]
- Indian J Med Sci. 2000 Jan;54(1):21-5.
Levels of lactic acid, normal level & its relation to food, glucose, cholesterol, raised blood urea and phenformin therapy.
Patel JC(1), Sawant MS, Amin BM.
(1)Bombay Hospital, Bombay.
The level of lactic acid was found to be 25 mg percent in 95 percent of 186 normal Indians. There was no difference due to sex and age. 2. Level of lactic acid was estimated in blood of normal persons and diabetics Type II patients to observe the effects of food and glucose. There was no change except the level of lactic acid was in higher but in normal range. 3. Hyperglycemia of over 300 mg raised the blood lactic acid in 25 percent of patients. 4. Lactic acid was not affected by hypercholesteremia but was raised in 60 percent of cases with raised blood urea. 5. Lactic acid was found to remain within normal limits in 48 type
II diabetics treated with phenformin dose varying from 50 mg to 225 mg per day.
The duration of treatment varied from one year to seven years.
PMID: 11214517 [Indexed for MEDLINE]