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Biomedical subjects

J Suárez

Publications and source records attributed to J Suárez.

At least 19 recordsLinked to original sources
PubMed2001

Effect of chronic manganese treatment on adenosine tissue levels and adenosine A2a receptor binding in diverse regions of mouse brain.

In the present study the effects of chronic manganese (Mn) treatment on adenosine A2a receptor binding in mouse brain have been assessed. Male albino mice were divided in two groups: In the Mn-treated group, the animals were injected intraperitoneally (i.p.) with MnCl2 (5 mg/kg/day) five days per week during 9 weeks; in the control group, they were injected likewise with a saline solution. A significant decrease of the Kd without alteration of Bmax in the cerebellum and, an increase of the Kd and Bmax in hippocampus of mice treated with Mn were found. Also, an increase of Kd in frontal cortex was observed. The binding parameters in caudate nucleus, olfactory bulb and hypothalamus were not altered by Mn. A significant decrease in the adenosine concentration in caudate nucleus, olfactory bulb and hypothalamus, without significant changes in hippocampus, frontal cortex and cerebellum was also detected. These findings suggest that chronic administration of Mn could affect adenosine receptor function and turnover, depending on the brain region analyzed.

Adenosine↗
PubMed2001

Evolution of the mitochondrial control region in Palaearctic brown trout (Salmo trutta) populations: the biogeographical role of the Iberian Peninsula.

In order to extend present knowledge of brown trout phylogeography in the Palaearctic, we analysed the complete mitochondrial D-loop sequence (1025-1027 bp) of all mitochondrial haplotypes of Salmo trutta found in the Iberian Peninsula and one North African haplotype. Sequence variation in the mitochondrial control region serves to identify four major haplotype groups within the Iberian Peninsula, i.e. Atlantic, Duero, Mediterranean and Andalusian. Including the Iberian haplotypes, the five main European groups previously established were increased to six: (i) an Atlantic group including two different clusters, South European and North Atlantic; (ii) a group representing an endemism restricted to the Duero basin in the Iberian Peninsula; (iii) an Adriatic-Andalusian group found in two vicariant areas including Adriatic-Ionian populations in the Mediterranean and the Andalusian basins of the southern Iberian Peninsula; (iv) a Mediterranean group with a distribution range that extends from the southwestern basins of the Iberian Peninsula to the Ionian basins of the Greek Peninsula; (v) a Danube group of wide distribution in the Black, Aral and Caspian basins; and (vi) a group comprising the S. t. marmoratus subspecies confined to the Adriatic Sea. The Iberian Peninsula appears to have acted as a physical boundary between haplotypes corresponding to Atlantic- and Mediterranean-draining rivers. Owing to its geographical position, this area has played a major role in present Palaearctic species distribution, as illustrated by its haplotype diversity.

Animals↗
PubMed2000

Use of a sandwich-enzyme-linked immunosorbent assay (SEA) for the diagnosis of natural Fasciola hepatica infection in cattle from Galicia (NW Spain).

An indirect-enzyme immune-linked immunosorbent assay (IEA) was compared to a sandwich-enzyme-linked immunosorbent assay (SEA) to diagnose fasciolosis in naturally infected cattle. By means of a rabbit polyclonal IgG antibody to F. hepatica antigens, captured circulating antigens were detected by an SEA technique. A total of 85.1% of the samples examined was considered positive by using the IEA-test, whereas this percentage was of 37.3% by the SEA test. Using the two enzymatic probes, only the 38.3% resulted positive to both immunoassay probes. Our data indicate that circulating antigen detection assay in combination with results of antibody detection may offer a more reliable diagnostic technique than classic coprologic ones, with results very appropriate for epidemiologic studies carried out on a wide area.

Animals↗
PubMed2000

Mitochondrial haplotype variation and phylogeography of Iberian brown trout populations.

The biogeographical distribution of brown trout mitochondrial DNA haplotypes throughout the Iberian Peninsula was established by polymerase chain reaction-restriction fragment polymorphism analysis. The study of 507 specimens from 58 localities representing eight widely separated Atlantic-slope (north and west Iberian coasts) and six Mediterranean drainage systems served to identify five main groups of mitochondrial haplotypes: (i) haplotypes corresponding to non-native, hatchery-reared brown trout that were widely distributed but also found in wild populations of northern Spain (Cantabrian slope); (ii) a widespread Atlantic haplotype group; (iii) a haplotype restricted to the Duero Basin; (iv) a haplotype shown by southern Iberian populations; and (v) a Mediterranean haplotype. The Iberian distribution of these haplotypes reflects both the current fishery management policy of introducing non-native brown trout, and Messinian palaeobiogeography. Our findings complement and extend previous allozyme studies on Iberian brown trout and improve present knowledge of glacial refugia and postglacial movement of brown trout lineages.

Animals↗
PubMed1999

Flow stimulates nitric oxide release in guinea pig heart: role of stretch-activated ion channels.

Blood flow regulates vessel tone triggering the release of nitric oxide; however, the mechanism involved in this phenomenon is unknown. We investigated whether coronary flow induces nitric oxide release in the isolated perfused guinea pig heart and the role of the stretch-activated ion channels in the effect of flow. We used gadolinium (3 microM) in order to block these channels, and estimated nitric oxide release by an oxyhemoglobin method. The results have shown a flow-dependent stimulation of nitric oxide release (fivefold increase at perfusion flow of 25 ml/min). Gadolinium inhibited this effect in a dose-dependent fashion. Acetylcholine was able to stimulate nitric oxide release in presence of gadolinium. We concluded that coronary flow stimulates nitric oxide release in the guinea pig heart. Stretch-activated ion channels mediate this effect. Acetylcholine and flow stimulate nitric oxide release by different mechanisms of action.

Acetylcholine↗
PubMed1999

Refractive errors in children with cerebral palsy, psychomotor retardation, and other non-cerebral palsy neuromotor disabilities.

The aim of this study was to analyse the refractive state of four different groups of children: those with spastic cerebral palsy (CP), aged between 7 and 81 months (N=50); psychomotor retardation, aged between 19 and 70 months (N=16); other neuromotor dysfunctions, aged between 12 and 75 months (N=37); and without psychomotor retardation, aged between 9 and 73 months (N=181). Refractive errors were determined using cycloplegic retinoscopy and non-cycloplegic retinoscopy (Mohindra's technique). We found higher percentages of hyperopia, tendency toward hyperopia, and other refractive anomalies in all the pathological groups of children than in the non-pathological control groups. Children from both the non-CP pathological control group and the group with psychomotor retardation had similar or even higher levels of hyperopia than children from the group with spastic CP. Our results in different age groups indicate a less effective normal emmetropization course in all the pathological groups of children studied. The correction of refractive errors is needed in these children before the end of the neural plasticity period.

Cerebral Palsy↗
PubMed1999

Decrease in spontaneous motor activity and in brain lipid peroxidation in manganese and melatonin treated mice.

In the present study, we have evaluated whether melatonin (MEL) modulates Mn-induced decrease in spontaneous motor activity (SMA) and lipid peroxidation, estimated as malondialdehyde (MDA) formation, in several brain regions. In mice treated with manganese a decrease in SMA after 2 weeks of treatment was observed. In the group treated with Mn+MEL a significant greater reduction in SMA was detected at 4 weeks. MDA levels were reduced in both MEL and Mn treated mice. In the animals treated with MEL + Mn a higher reduction in MDA levels was observed. These results suggest that MEL modulates the effect of Mn on SMA and brain lipid peroxidation.

Animals↗
PubMed1999

Correlation between blood adenosine metabolism and sleep in humans.

Blood adenosine metabolism, including metabolites and metabolizing enzymes, was studied during the sleep period in human volunteers. Searching for significant correlations among biochemical parameters found: adenosine with state 1 of slow-wave sleep (SWS); activity of 5'-nucleotidase with state 2 of SWS; inosine and AMP with state 3-4 of SWS; and activity of 5'-nucleotidase and lactate with REM sleep. The correlations were detected in all of the subjects that presented normal hypnograms, but not in those who had fragmented sleep the night of the experiment. The data demonstrate that it is possible to obtain information of complex brain operations such as sleep by measuring biochemical parameters in blood. The results strengthen the notion of a role played by adenosine, its metabolites and metabolizing enzymes, during each of the stages that constitute the sleep process in humans.

Adenosine↗
PubMed1998

Tuberculous pleurisy: a study of 254 patients.

OBJECTIVES: To determine the age at which tuberculous pleural effusions occur, the radiological and biochemical characteristics of the effusions, the sensitivities of the various diagnostic tests, and the utility of combining clinical, radiological, and analytic data in diagnosis. METHODS: We studied the case histories of 254 patients in whom tuberculous pleural effusions were diagnosed with certainty between January 1, 1989, and June 30, 1997, in a Spanish university hospital in a region with a high incidence of tuberculosis. RESULTS: The mean (+/-SD) age of the patients was 34.1+/-18.1 years, and 62.2% were younger than 35 years. The effusion was on the right side in 55.9% of patients, on the left side in 42.5% of patients, and on both sides in 1.6% of patients. In 81.5% of patients, less than two thirds of the hemithorax was affected. Associated pulmonary lesions were detected in 18.9% of patients, of whom 14.6% exhibited cavitation. In 93.3% of the effusions, more than 50% of leukocytes were lymphocytes, and almost all had the biologic characteristics of exudates (98.8% had high total protein contents, 94.9% had high cholesterol levels, and 82.3% had high lactate dehydrogenase levels). All but 1 effusion (99.6%) had an adenosine deaminase (ADA) concentration higher than 47 U/L, 96.8% (123/127) of the effusions had high ADA2 levels, and 89% (73/82) of the effusions had high interferon gamma levels. Adenosine deaminase 2 contributed 72.2%+/-12.5% (mean +/- SD) of total ADA activity. Total ADA activity was significantly correlated with ADA2 (r = 0.83) and with interferon gamma (r = 0.30) levels. Definitive diagnosis was based on the observation of caseous granulomas in pleural biopsy tissue samples in 79.8% of patients, on the results of biopsy cultures in 11.7% of patients, and on pleural effusion cultures in the remaining 8.5% of patients. Results of the tuberculin skin test were positive in only 66.5% of patients. CONCLUSIONS: In these patients, lymphocyte-rich exudative pleural effusions occurred, on average, at a young age, with no preference for either the right or the left side; normally affected no more than two thirds of the hemithorax; and were generally unaccompanied by pulmonary infiltrates. High ADA concentration was a highly sensitive diagnostic sign and was caused by a rise in ADA2 concentration. The most sensitive criterion based on pleural biopsy was the observation of caseous granulomas, and culture of biopsy material further increased overall sensitivity. Negative skin test results were no guarantee of the effusion being nontuberculous. This, together with the low mean age of the patients and the low frequency of associated pulmonary lesions, suggests that tuberculous pleural effusion is a primary form of tuberculosis in this region.

Adenosine Deaminase↗
PubMed1997

Spasmolytic effects of tetrazepam on rat duodenum and guinea-pig ileum.

This study was designed to examine the inhibitory effects exerted by tetrazepam isolated rat duodenum and guinea pig ileum contractive responses and to further clarity the mechanisms involved. Tetrazepam produced concentration-dependent and complete relaxation of muscle contractions induced by KCl (80 mM) in guinea-pig ileum and this relaxant action was not antagonized by pretreatment with hexamethonium (0.1 mM), antagonist for nicotinic receptors, or atropine (1 microM), antagonist for muscarinic receptors, or PK 11195 (1 microM) antagonist for peripheral-type benzodiazepines receptors. Tetrazepam also modified the concentration-response curves of CaCl2 in calcium-free and high K/ depolarizing medium as soon as concentration-response curves of acetylcholine in Tyrode solution. The results suggested that tetrazepam inhibits the contractile responses to guinea-pig ileum and rat duodenum, probably through a reduction of calcium influx by way of calcium channels and these events are not related to high-affinity peripheral benzodiazepine binding sites.

Acetylcholine↗
PubMed1997

Vasodilating effects of tetrazepam in isolated vascular smooth muscles: comparison with cromakalim and diltiazem.

The vasodilating effects of tetrazepam (1,4-benzodiazepine derivative) were studied and compared with those of the K-channel activator, cromakalim and the Ca-channel blocker, diltiazem, in rat aorta smooth muscle and on the spontaneous contractile activity of the rat portal vein. In the aorta, tetrazepam (3 x 10(-7)-10(-4) M) and diltiazem (10(-8)-3 x 10(-6) M) concentration-dependently relaxed aortic rings contracted by 30 mM as well as 80 m KCl. Although cromakalim (10(-8)-3 x 10(-6) M) concentration-dependently relaxed aortic rings contracted by 30 mM KCl, it did not relax those contrated by 80 mm KCl. In the presence of the ATP-sensitive K-channel blocker, glibenclamide (10(-6) and 3 x 10(-6) M), 30 mM KCl concentration-response curves for the relaxant effect of tetrazepam and diltiazem were unaffected but cromakalim caused a progressive shift of these curves upwards. In the portal vein, tetrazepam inhibited spontaneous contractions, decreased amplitude and increased frequency. Similar behaviour was shown with diltiazem (10(-8)-10(-5) M) and in both cases, pre-treatment with glibenclamide (10(-6) M) was ineffective. Although cromakalim (10(-5)-10(-6) M) decreased both amplitude and frequency, this effect was blocked by glibenclamide. These results indicate that the vasodilator action of tetrazepam is not mediated to the opening of ATP-sensitive K-channels, unlike cromakalim. This may be mediated, like those of diltiazem, by the blockade of calcium movements across the cell membrane.

Animals↗
PubMed1997

Inhibition of S-adenosyl-L-homocysteine hydrolase by adrenaline in isolated guinea-pig papillary muscles.

Purified S-adenosyl-L-homocysteine hydrolase from Dictyostelium discoideum or rabbit erythrocytes is inactivated when incubated with cAMP. The aim of this study was to investigate whether adrenaline, which increases cytosolic cAMP and calcium concentrations, is able to modify in situ the activity of S-adenosyl-L-homocysteine hydrolase in the heart. The enzyme was assayed in a crude extract obtained from superfused guinea-pig papillary muscles with the different tested substances. Adrenaline was found to inhibit S-adenosyl-L-homocysteine hydrolase in papillary muscles in a concentration-dependent fashion. This inhibition was associated with an increase in the concentration of S-adenosyl-L-homocysteine (326%), and a decrease of adenosine (40%). beta-Adrenoceptors are involved in the effect of adrenaline, since isoproterenol, a beta-adrenergic agonist, inhibited the enzyme, whereas the beta-adrenergic blocker, propranolol, prevented this inhibition. Participation of calcium in the inhibitory effect of adrenaline was suggested because the calcium channel blocker, verapamil, suppressed this inhibition, and high calcium in the perfusion medium inhibited the enzyme. In vitro experiments with calcium were performed in a semi-purified fraction of the enzyme, resulting in a concentration-dependent inhibition of the enzyme. Calcium concentration, which inhibited the enzyme 50%, was in the millimolar range for control and in the micromolar range for the obtained enzyme from adrenaline-treated muscles, indicating a different sensitivity to calcium inhibition. We conclude that adrenaline inhibits S-adenosyl-L-homocysteine hydrolase in situ, probably by a calcium-modulated mechanism.

Adenosylhomocysteinase↗
PubMed1997

Sequential changes of energy metabolism and mitochondrial function in myocardial infarction induced by isoproterenol in rats: a long-term and integrative study.

Acute myocardial infarction is the second cause of mortality in most countries, therefore, it is important to know the evolution and sequence of the physiological and biochemical changes involved in this pathology. This study attempts to integrate these changes and to correlate them in a long-term model (96 h) of isoproterenol-induced myocardial cell damage in the rat. We achieved an infarct-like damage in the apex region of the left ventricle, occurring 12-24 h after isoproterenol administration. The lesion was defined by histological criteria, continuous telemetric ECG recordings, and the increase in serum marker enzymes, specific for myocardial damage. A distinction is made among preinfarction, infarction, and postinfarction. Three minutes after drug administration, there was a 60% increase in heart rate and a lowering of blood pressure, resulting possibly in a functional ischemia. Ultrastructural changes and mitochondrial swelling were evident from the first hour of treatment, but functional alterations in isolated mitochondria, such as decreases in oxygen consumption, respiratory quotient, ATP synthesis, and membrane potential, were noticed only 6 h after drug administration and lasted until 72 h later. Mitochondrial proteins decreased after 3 h of treatment, reaching almost a 50% diminution, which was maintained during the whole study. An energy imbalance, reflected by a decrease in energy charge and in the creatine phosphate/creatine ratio, was observed after 30 min of treatment; however, ATP and total adenine nucleotides diminished clearly only after 3 h of treatment. All these alterations reached a maximum at the onset of infarction and were accompanied by damage to the myocardial function, drastically decreasing left ventricular pressure and shortening the atrioventricular interval. During postinfarction, a partial recovery of energy charge, creatine phosphate/creatine ratio, membrane potential, and myocardial function occurred, but not of mitochondrial oxygen consumption, rate of ATP synthesis, total adenine nucleotides, or mitochondrial proteins. Interesting correlations of the sequential changes in heart and mitochondrial functions with energy metabolism were obtained at different stages of the isoproterenol-induced cardiotoxicity. These correlations could be useful to study and understand the cellular events involved in this pathology.

Animals↗
PubMed1996

Participation of adenosine in the renal hemodynamic abnormalities of hypothyroidism.

To investigate the participation of adenosine (ADO) in the abnormalities of renal function associated with hypothyroidism, glomerular hemodynamics were evaluated in normal (Nl) and 2-wk thyroidectomized (Htx) rats. Studies were performed before and during intravenous infusion of the ADO blocker 1,3-dipropyl-8-p-sulfophenyl xanthine (PSPX, 20 mM, 1.2 ml/h), intra-aortic ADO (100 nmol.kg-1.min-1), or vehicle. In addition, single-nephron glomerular filtration rate (SNGFR) was measured during the infusion of different intrarenal ADO doses (1, 10, and 35 nmol.kg-1.min-1); plasma and renal content of ADO were measured by high-performance liquid chromatography in additional groups. Decreased SNGFR, glomerular blood flow (QA), and ultrafiltration coefficient (Kf) were found in Htx rats. PSPX did not modify glomerular hemodynamics in Nl rats; in contrast, in Htx rats, the antagonist increased SNGFR, QA, and Kf, with a fall in afferent (RA) and efferent (RE) resistances. ADO infusion in Nl rats produced renal vasoconstriction characterized by a fall in SNGFR, QA, and Kf, with an increased RA and RE. Paradoxically, in Htx rats, ADO increased SNGFR, QA, and Kf, decreasing RA and RE. However, when ADO was infused through the renal artery, it induced a 20% reduction of SNGFR at 1 nmol.kg-1.min-1 that rose to control values at 10 nmol.kg-1.min-1 and increased to 38.3% to 35.kg-1.min-1. Renal ADO content was markedly low in Htx rats (4.37 +/- 0.79 and 115.46 +/- 14.9 nmol/g wet wt for Htx and Nl rats, respectively). Renal vasodilation induced by PSPX in Htx rats suggests predominant activation of A1 receptors in this condition. The vasodilatory response to exogenous ADO suggests additional activation of A2 receptors.

Adenosine↗