Muscle Satellite Cell Heterogeneity: Does Embryonic Origin Matter?

Muscle regeneration is an important homeostatic process of adult skeletal muscle that recapitulates many aspects of embryonic myogenesis. Satellite cells (SCs) are the main muscle stem cells responsible for skeletal muscle regeneration. SCs reside between the myofiber basal lamina and the sarcolemma of the muscle fiber in a quiescent state. However, in response to physiological stimuli or muscle trauma, activated SCs transiently re-enter the cell cycle to proliferate and subsequently exit the cell cycle to differentiate or self-renew. Recent evidence has stated that SCs display functional heterogeneity linked to regenerative capability with an undifferentiated subgroup that is more prone to self-renewal, as well as committed progenitor cells ready for myogenic differentiation. Several lineage tracing studies suggest that such SC heterogeneity could be associated with different embryonic origins. Although it has been established that SCs are derived from the central dermomyotome, how a small subpopulation of the SCs progeny maintain their stem cell identity while most progress through the myogenic program to construct myofibers is not well understood. In this review, we synthesize the works supporting the different developmental origins of SCs as the genesis of their functional heterogeneity.

Checklist of Benthic Cnidaria in the SW Atlantic Ocean (54ºS-56ºS).

In this study we provide an updated checklist of benthic Cnidaria from SW Atlantic Ocean that comprised the Marine Protected Areas Namuncurá I and II, located at Burdwood bank, and other neighbouring locations. A total of 88 taxa was recorded: 36 hydrozoans and 52 anthozoans from which 32 were octocorals, 10 scleractinian corals, 8 sea anemones and 2 zoanthids. Burdwood bank presented the highest richness considering that 87% of the recorded species inhabit this plateau or its slope. Besides some common species widely distributed in the studied sub-areas, at least 24 species represent new distributional records while few were exclusively recorded at Burdwood bank. The inventory here provided will help to identify key habitat-forming species in a complex habitat where marine animal forests and vulnerable marine ecosystems were previously detected. It will be also a very valuable tool for the management and monitoring of the sub-areas under protection.

Assessing cross-species transmission of hemoplasmas at the wild-domestic felid interface in Chile using genetic and landscape variables analysis.

The co-occurrence of domestic cats (Felis silvestris catus) and wild felids in rural landscapes can facilitate pathogen transmission. However, in the relatively-isolated regions of southern South America there have been no comprehensive studies to assess disease transmission risks between domestic cats and forest-dwelling wild felids such as guigna (Leopardus guigna). We evaluated hemoplasma infection and the possibility of transmission between domestic cats and guignas by comparing spatial and phylogenetic patterns of pathogen prevalence. Blood/spleen samples were collected from 102 wild guignas and 262 co-occurring rural domestic cats across the entire distribution range of guigna in Chile. Hemoplasma infection was assessed by direct sequencing of the 16S RNA gene. Infection with hemoplasmas was common and geographically widespread across different bioclimatic areas for both species. The most common feline Mycoplasma species in guigna and domestic cats were Candidatus M. haemominutum (CMhm) (15.7% guigna; 10.3% domestic cat) and Mycoplasma haemofelis (Mhf) (9.8% guigna, 6.1% domestic cat). A previously undescribed Mycoplasma sp. sequence was found in two guignas and one cat. Continuous forest-landscapes were associated with higher hemoplasma-prevalence in guignas. Shared hemoplasma nucleotide sequence types between guigna and domestic cats were rare, suggesting that cross-species transmission between guignas and domestic cats may occur, but is probably uncommon. Ectoparasites, which have been linked with hemoplasma transmission, were not found on guignas and were infrequent on domestic cats. Our results suggest that transmission pathways vary among hemoplasma species and, contrary to our predictions, domestic cats did not appear to be the main driver of hemoplasma infection in guignas in these human-dominated landscapes.

Enfermedad de Moya-Moya / Moya-Moya disease

Enfermedad esteno-oclusiva de la porción terminal de las arterias carótidas internas y de sus ramas principales (arteria carótida media y arteria carótida anterior), progresiva, prevalente en el este Asiático (Japón, Corea), muy rara en nuestro país como en el resto del mundo, de causa desconocida. Se manifiesta mas frecuentemente como un accidente cerebrovascular isquémico transitorio o permanente en los niños menores de 10 años y como accidente cerebrovascular hemorrágico en el adulto. El diagnóstico se realiza con la Angiografía Digital Cerebral y el tratamiento consiste en la revascularización cerebral, que mejora el cuadro neurológico y la calidad de vida.`Se presenta el caso de una niña de 3 años de edad con convulsiones, afasia de expresión, lúcida y hemiparesia izquierda, que luego de una franca mejoría vuelve a presentar una semana después, otra crisis más severa con compromiso de conciencia y hemiplejía derecha, cuyo estudio neurorradiológico reveló la imagen típica de volutas de humo de cigarrillo en la base del cerebro, característico de la enfermedad de Moya-Moya e intervenida quirúrgicamente con la revascularización cerebral por medio de la técnica: EncefaloDuroArterioSinangiosis (EDAS), con buen resultado.

Moya-Moya is a progressive steno-occlusive disease of the internal carotid arteries and its major branches (middle cerebral artery, and anterior cerebral artery) whose cause is unknown, and which is reported primarily in east Asia (Japan and Korea) but rare in Paraguay and the rest of the world. In children under age 10, it presents most commonly as a transient or permanent ischemic attack and in adults as a hemorrhagic stroke. Diagnosis is done by digital subtraction cerebral angiography, and treatment consists of cerebral revascularization to improve the neurological profile and quality of life. We present the case of a 3-year old female child with seizures and motor aphasia who was lucid, with left hemiparesis, and who after complete recovery presented again a week later with a more severe attack, with impaired consciousness and right hemiplegia. Radiological study revealed a typical image of swirls of 'cigarette smoke' at the base of the brain that are characteristic of Moya-Moya disease, and who was operated on using encephaloduroarteriosynangiosis (EDAS), with good results.

Calidad de vida relacionada con la salud en edad preescolar / Quality of life and health in preschoolers

Objective: Parents' perception of quality of life (QOL) was correlated to the health status of children between three and five years eleven months of age. Method: TAPQOL questionnaires were utilized to evaluate parents or guardians of 483 children who attenden private, semiprivate and public kindergardens. Average age of the children was 51.7 months, 47% were girls. Results: QOL was found to be disturbed through anxiety and behavior problems. Some differences were found along the dimensions of gender, type of institution, and presence of illness. Conclusions: Our results allow us to focus on those preschoolers whose parents report a worse QOL, to develop intervention plans. Those are children who have suffered a disease, the youngest, or those who attend public preschools. Positive behavioral signs, anxiety and communication are special areas of interest for medical intervention.

Objetivo: Bajo un diseño transversal, se evalúa la percepción de los padres sobre la calidad de vida relacionada con la salud (CVRS) en niños entre tres y cinco años once meses. Método: Se aplicó el cuestionario específico de CVRS para menores en edad preescolar TAPQOL a los padres o tutores de 483 infantes que asistían ajardines infantiles particulares, públicos y subvencionados. El promedio de edad de los menores fue de 51,7 meses, siendo el 47% de estos mujeres. Resultados: La CVRS de los menores se ve más afectada en las dimensiones de ansiedad y problemas de conducta. Se encontraron diferencias en los reportes de las distintas dimensiones dadas por el sexo, el tipo de establecimiento al que acudían los menores y por la presencia de enfermedad. Conclusiones: Los resultados obtenidos nos permiten focalizar la atención en aquellos preescolares cuyos padres reportan una menor CVRS, siendo estos los que han padecido o padecen una enfermedad, los más pequeños y los que asisten a establecimientos públicos, especialmente en las áreas de emociones positivas, ansiedad y comunicación, entregando información para posibles planes de intervención con el objeto de mejorar el bienestar de los menores.

Formación de enfermeras en prevención y tratamiento de conductas adictivas. Los planes de estudio de la Universidad Nacional Autónoma de México / Formation of nurses in the prevention and treatment of addictive behaviors, the related study plans in the National School of Nursing and Obstetrics

El uso y dependencia de sustancias adictivas se relaciona con un amplio conjunto de problemas de salud y de exclusión social, así mismo representan un factor significativo en el incremento de la morbilidad a nivel nacional. En este artículo se presentan los resultados de la revisión y análisis de los planes de estudios correspondientes a la Licenciatura en Enfermería en tres centros de la Universidad Nacional Autónoma de México (UNAM): La ENEO, FESZ y FESI), desde la perspectiva de la formación en prevención y tratamiento de conductas adictivas. Se trata de un estudio descriptivo, evaluativo, transversal, de tipo investigación documental, que analiza la transversalidad de los contenidos sobre la temática de adicciones en los planes y programas de las tres dependencias de la UNAM. Proyecto MP6-20 El análisis comparativo de los planes de estudio permite mostrar que la temática de adicciones, aparece de manera diferencial en los proyectos de formación universitaria de enfermería. Los proyectos curriculares analizados, adolecen de un modelo pedagógico que permita identificar como problema de salud, las conductas adictivas; y en consecuencia se desarrollen estrategias que permitan paulatinamente desarrollar competencias profesionales para la prevención específica, el tratamiento y la reinserción social de las personas con conductas adictivas.

The use and dependence of addictive substances is related with a wide group of problems of health and of social exclusion, likewise they represent a significant factor in the increment from the mobility to national level. In this paper present the results of the revision and analysis of curriculum corresponding to bachelor nursing in three dependences of UNAM: The ENEO, FESZ and FESI, from the perspective of the formation in prevention and treatment of addictive behaviors. It is a descriptive study, evaluative, cross transverse, of type documental investigation that analyzes the transversal of the contents on the thematic of addictions in the curriculum of the three dependences of the UNAM. The comparative analysis of the study plans allows explains that the thematic of addictions appears in a differential way in the projects of university formation of nursing. The analyzed curriculum lack of a pedagogic model that allows identifying as problem of health the addictive behaviors and in consequence strategies are developed that allow gradually developing professional competitions for the prevention it specifies, the treatment and the social reinsertion of people with addictive behaviors.

Disponibilidad de médicos en Chile al año 2004 / Availability of physicians in Chile at the year 2004

Background: The number of physicians available in a given country, their efficiency, quality and specialization is of utmost epidemiological importance. Aim: To evaluate the availability of physicians in Chile. Material and methods: The information about the number of physicians in Chile up to the year 2004, was obtained from the Ministry of Health, national universities and the register of immigrant physicians since 1950. Results: The total number of physicians licensed to practice was 25,542, of whom 2,700 are immigrants. The physician/inhabitant ratio increased from 1/921 in 1998 to 1/612 in 2004. The greater impact in the increment of available physicians was given by the immigration of professionals and by the increase in the number of physicians graduated from national universities, mainly from the new private universities. Forty two percent of physicians work at public services and 61 percent of these are certified specialists. The regional distribution of general practitioners and basic specialists is adequate. Along the country, the mean physician/beneficiary ratio is 8.45/10,000, the specialist/beneficiary ratio is 4.9/10,000 and the general practitioner/beneficiary ratio is 2.3/10,000. Conclusions: The national information of available physicians, especially in the private sector, should be improved. Immigration of physicians should be regulated, maintaining validation examinations and a National Medical Test to assess medical proficiency should be instituted.

Nuclear factor kappaB activation by muscarinic receptors in astroglial cells: effect of ethanol.

Activation of muscarinic receptors leads to proliferation of astroglial cells and this effect is inhibited by ethanol. Among the intracellular pathways involved in the mitogenic action of muscarinic agonists, activation of the atypical protein kinase C zeta (PKC zeta) appears to be of most importance, and is also affected by low ethanol concentrations. PKC zeta has been reported to activate nuclear factor kappaB (NF-kappaB), a transcription factor that has been shown to play an important role in cell proliferation. The aim of this study was, therefore, to determine whether muscarinic receptors would activate NF-kappaB in astroglial cells, whether such activation would play a role in the mitogenic action of muscarinic agonists, and whether it would represent a possible target for ethanol. Carbachol activated NF-kappaB in human 1321N1 astrocytoma cells, as evidenced by translocation of the p65 subunit of NF-kappaB to the nucleus, phosphorylation and degradation of IkappaBalpha in the cytosol, and increase NF-kappaB binding to DNA. Carbachol also induced translocation of p65 to the nucleus in primary rat astrocytes. Carbachol-induced NF-kappaB activation was mediated by the M3 subtype of muscarinic receptors and appeared to involve Ca(2+) mobilization and activation of PKC epsilon and PKC zeta, but not PI3-kinase and mitogen-activated protein kinase. The NF-kappaB peptide inhibitor SN50, but not the inactive peptide SN50M, strongly inhibited carbachol-induced astrocytoma cells proliferation and p65 translocation to the nucleus. Increased DNA synthesis was also antagonized by the IkappaBalpha kinase inhibitor BAY 11-7082. Ethanol (25-100 mM) inhibited the translocation of p65 and the binding of NF-kappaB to DNA in both 1321N1 astrocytoma cells and primary rat cortical astrocytes. Together, these results suggest that activation of NF-kappaB by muscarinic receptors in astroglial cells is important for carbachol-induced DNA synthesis and that ethanol-mediated inhibition of cell proliferation may be due in part to inhibition of NF-kappaB activation.

Testicular damage from anabolic treatments with the beta(2)-adrenergic agonist clenbuterol in pigs: a light and electron microscope study.

The morphological consequences of anabolic clenbuterol treatment on the testicular parenchyma were investigated in 30 pigs at morphological and ultrastructural levels. Clenbuterol was given with food (1 ppm). In the first group (n=10), treatment was maintained until slaughter (experimental period 3 months). In the second group (n=10), clenbuterol was withdrawn 2 weeks before slaughter (experimental period 2.5 months). A third group (n=10) of pigs not fed with clenbuterol served as controls. Animals were slaughtered at 9 months of age and samples of testicular parenchyma were collected for light and electron microscope studies. In the clenbuterol-treated groups, the interstitial cells showed a considerable increase in the organelles involved in testosterone production, with an increased development of the mitochondria, smooth endoplasmic reticulum, Golgi apparatus and lipid droplets compared to the control group. The seminal epithelium displayed many lipid vacuoles and evident signs of tubular involution, such as degenerating and multinucleate germ cells. Sertoli cells gave evidence of metabolic alterations such as large lipid deposits and cytolysosomes.

Mercuric ion attenuates nuclear factor-kappaB activation and DNA binding in normal rat kidney epithelial cells: implications for mercury-induced nephrotoxicity.

Mercuric ion (Hg(2+)), one of the strongest thiol-binding agents known, mediates the toxicity associated with elemental, inorganic, and organic mercurial compounds. Studies of cellular events associated with Hg(2+) toxicity have focused largely on disruption of cell membranes and impairment of mitochondrial functions. In contrast, few studies have sought to define the specific molecular mechanisms through which Hg(2+) might affect toxicity via alteration of thiol-dependent signal transduction pathways that regulate cell proliferation and survival. Of particular interest in this regard is the effect of Hg(2+) on nuclear factor-kappaB (NF-kappaB), a pleiotropic transcriptional factor that is known to require reduced cysteine moieties at critical steps of activation and DNA binding. Here, we evaluated the effects of Hg(2+) on the expression of NF-kappaB in normal rat kidney epithelial (NRK52E) cells, a principal target of Hg(2+) toxicity. The lipopolysaccharide (LPS)-inducible form of NF-kappaB was readily detected in kidney cells and has been characterized as the p50p65 heterodimer. NF-kappaB-DNA binding was prevented in a dose-related manner by Hg(2+) (0-55 microM) in vitro when added to DNA binding reactions containing the nonthiol reducing agent Tris(2-carboxyethyl)phosphine hydrochloride (TCEP). Similarly, Hg(2+) at the same concentrations prevented DNA binding of a human recombinant wild-type p50p50 homodimer in binding reactions, and this effect was attenuated using a mutant form of the p50 protein containing a cys(62)-->ser(62) mutation. The inhibition of p50-DNA binding by Hg(2+) was reversible in a dose-related manner in vitro by competitive thiols DTT, GSH, and l-cysteine in binding reactions. In contrast, competitive thiols added to nuclear binding reactions were unable to reverse attenuation of LPS-mediated NF-kappaB-DNA binding affinity when cells were pretreated in vivo with Hg(2+) at concentrations as low as 2 microM prior to LPS administration. Immunoblot analyses indicted that Hg(2+) pretreatment of kidney cells substantially diminished, in a dose-related manner, the concentration of p65 translocated into the nucleus following LPS administration. Additionally, Hg(2+) pretreatment impaired both the phosphorylation and degradation of IkappaBalpha, suggesting a specific effect on NF-kappaB activation at the level of IkappaBalpha proteolysis. Finally, Hg(2+) at concentrations as low as 5 microM significantly diminished NF-kappaB-mediated transcriptional activity when administered to kidney cells transiently transfected with an NF-kappaB-driven luciferase reporter gene (pLuc-4xNF-kappaB) prior to LPS treatment. These findings demonstrate that Hg(2+), at low cellular concentrations, attenuates NF-kappaB activation at sites associated with IkappaBalpha phosphorylation and degradation, nuclear translocation of the p50p65 heterodimer, and association of p50-cys(62) with the DNA kappaB binding site. Attenuation of NF-kappaB activation by Hg(2+) through these mechanisms may underlie apoptotic or other cytotoxic responses that are known to be associated with low level Hg(2+) exposure in kidney epithelial cells.

Inhibition of NF-kappaB-DNA binding by mercuric ion: utility of the non-thiol reductant, tris(2-carboxyethyl)phosphine hydrochloride (TCEP), on detection of impaired NF-kappaB-DNA binding by thiol-directed agents.

Mercuric ion (Hg(2+)), a potent thiol inhibitor, prevents expression of nuclear factor kappaB (NF-kappaB) by mercaptide bond formation with a critical cysteine moiety (cys(62)) on the p50 subunit required for DNA binding. NF-kappaB-DNA binding is typically measured in reaction mixtures in which dithiothreitol (DTT) or other thiol reductants are used to maintain cys(62) in the reduced state. However, the presence of thiol reductants prevents accurate assessment of the Hg(2+) concentration required to prevent NF-kappaB-DNA binding because of competitive mercaptide bond formation. In the present studies we evaluated the efficacy of tris(2-carboxyethyl)phosphine-HCl (TCEP), a non-thiol reducing agent which does not bind Hg(2+), on NF-kappaB-DNA binding in vitro, using recombinant p50 protein and a (32)P-labelled kappaB oligonucleotide. We also measured the minimal Hg(2+) concentration required to prevent this interaction in the presence of either reagent. DTT promoted NF-kappaB-DNA binding in concentrations from 0.25 to 2.6mM in binding reactions. However, in the presence of 0.25mM DTT, inhibition of NF-kappaB binding was seen only at Hg(2+) concentrations greater than 100 microM and results were highly variable. In contrast, TCEP promoted NF-kappaB-DNA binding in a dose-related manner in concentrations from 0.25 to 6mM. In the presence of even 6mM TCEP, Hg(2+) prevented NF-kappaB-DNA binding at concentrations as low as 20 microM in binding reactions. Similar findings were observed with regard to the thiol alkylating agent N-ethylmaleimide (NEM). These findings demonstrate the utility of TCEP as reductant in nuclear binding reaction assays involving the interaction of thiol constituents. They also demonstrate inhibition of NF-kappaB-DNA binding at Hg(2+) concentrations comparable to those known to initiate toxicity and apoptotic cell death in vivo.

Activation of NF-kappaB in normal rat kidney epithelial (NRK52E) cells is mediated via a redox-insensitive, calcium-dependent pathway.

Renal tubular epithelial cells are largely resistant to oxidant-induced injury despite their capacity to accumulate relatively high concentrations of potentially damaging prooxidant and thiol-depleting agents. In the present study, we tested the hypothesis that such resistance may be attributable to a lack or deficiency of signaling transduction pathways through which reactive oxidants have been shown to promote the activation of NF-kappaB, a transcriptional factor that is known to mediate the inducible expression of a wide variety of genes that are involved in inflammatory and other cytotoxic reactions in numerous cell types. NF-kappaB was found to be readily activated following exposure of cultured normal rat kidney epithelial (NRK52E) cells to bacterial lipopolysaccharide (LPS). However, in contrast to findings with many other cell types, the activation of NF-kappaB by LPS was not substantially altered either by pretreatment of cells with the thiol antioxidant, N-acetylcysteine, or by glutathione (GSH) depletion. Moreover, reactive oxidants and oxidative stress-generating chemicals were completely without effect with respect to NF-kappaB activation in NRK52E cells, even following GSH depletion. In contrast, LPS activation of NF-kappaB was substantially attenuated by the intracellular Ca2+ chelator, Quin 2AM, and by the Ca-channel inhibitor, ruthenium red. Moreover, thapsigargin, a Ca-ATPase inhibitor, promoted NF-kappaB activation comparable to that observed by LPS. Additionally, staurosporine, a Ca-dependent protein kinase C inhibitor, substantially decreased LPS-mediated NF-kappaB activation. These results demonstrate that the LPS-inducible expression of NF-kappaB in renal epithelial cells, in contrast to many other cell types, is not responsive to oxidative stress and is regulated, at least in part, by redox-insensitive modulation of intracellular calcium levels. These findings provide a basis for the highly tissue-specific expression and function of NF-kappaB in kidney epithelial cells, which may underlie their resistance to oxidant-mediated cytotoxicity.

Estudio preliminar en pacientes discrásicos tratados en base a ácido tranexámico / Preliminary study in discrasies patients treated with tranexamic acid

The aim of the present clinical investigation was to evaluate the effect of tranexamic acid in the treatment of discrasies patients. In the study we observed that antifibrinolytic therapy with tranexamic acid used with ystemic therapy significantly reduces the incidence of postoperative bleeding

A behavioral treatment program as a therapy in the control of primary hypertension.

In order to assess the effects of a Behavioral Treatment Program in the control of primary hypertension, twenty one unmedicated hypertensives were randomly allocated to three groups: first, a treatment group (BHG) receiving a Behavioral Treatment which included: deep muscle relaxation, peripheral temperature Biofeedback and anxiety management training; second, the placebo attention control group (PHG) and third, a control group of hypertensives too (CHG). Additionally, were compared with seven normotensives subjects (CNG). The post-treatment measures showed a significant reduction (p < 0.001) in systolic and diastolic values only in the (BHG). In a six months follow-up the (BHG) group still showed a significant reduction in the systolic and diastolic BP (p < 0.02; p < 0.01). Moreover individual variations in response to treatment were observed in this group, (BHG).

Echocardiographic assessment of doxazosin on left ventricular mass in patients with essential hypertension.

A single daily dose of doxazosin taken during a 12-week period produced a significant reduction in blood pressure and left ventricular mass index in patients with mild or moderate hypertension. The systolic shortening coefficient was also increased and a trend in the improvement of ejection fraction, rate of circumferential fiber shortening, systolic contraction time, and preejective/ejective ratio was observed. No change in heart rate was recorded and no patients had side effects. The serum lipid profile was modified favorably, particularly with regard to the low-density lipoprotein cholesterol/high-density lipoprotein cholesterol ratio. By producing a reduction in blood pressure and left ventricular mass while favorably modifying the serum lipid profile, doxazosin produced a beneficial change in the overall coronary heart disease risk profile.

Impaired glucose metabolism in hypertensive patients.

We have studied glucose tolerance under carefully controlled conditions in 79 patients with arterial hypertension. The results show that, in patients with arterial hypertension but without clinical diabetes mellitus, the glucose tolerance was abnormal in 77.3% and normal in 22.3%. The corresponding figure in the control group of normotensive subjects was 0%. In each test the responses to glucose administration were analyzed by plotting the logarithm of the blood glucose concentration against time. For the points between 60 and 120 min, corresponding to the periods following glucose administration, a linear relationship was obtained and showed a decline at an exponential rate, as noted by other observers. An estimate of the volume of distribution of glucose was obtained as follows. Values observed in hypertensives with a pathological percent fall in blood glucose per minute (Kg) were 29.8 +/- 12.0 (mean +/- SD) liters and those in normal subjects with normal Kg values had a mean of 14.35 +/- 2.98, the difference being highly significant (p less than 0.0001). The results of the theoretical glucose concentration are also presented. Those obtained from subjects with normal Kg values (359.0 +/- 58.4 mg/dl) are significantly higher than in subjects with pathological Kg values (257.6 +/- 51.3 mg/dl; p less than 0.0001). All patients with either pathological or normal Kg values had normal glucose concentration levels, fasting blood sugar and no glucose in the urine specimen. The difference between pathological Kg values (107.0 +/- 25.8 mg/dl) and normal Kg values (90.6 +/- 13.0 mg/dl) was not found to be statistically different (p greater than 0.05). The distribution and means of glucose half time in controls with normal Kg values and hypertensives with pathological Kg values were: 63.5 +/- 11.5 and 137.8 +/- 48.1 min, respectively. The difference between normal and pathological Kg values being statistically significant at a confidence level above 99.5%. We also studied the free glucose pool at zero time. A significantly higher level was found in hypertensives with pathological Kg values, again indicating an impairment in glucose metabolism in this group: 90.6 +/- 26.5 vs. 65.0 +/- 5.4 g (p less than 0.0001). Another study showed an estimate of the mean cellular glucose uptake (MCUg) per minute and per kilogram body weight. The MCUg following glucose loading decreased considerably in hypertensives with pathological Kg values. The percentage reduction ranged between 50 and 55% hypertensives with pathological Kg values 4.1 +/- 0.8, and normotensives with normal Kg values, 8.0 +/- 0.6 (p less than 0.0001).(ABSTRACT TRUNCATED AT 400 WORDS)

Acute hypotensive action of clonidine after intravenous infusion in hypertensive emergencies.

Clonidine was administered by intravenous infusion to 12 patients classified as having exaggerated arterial hypertension, their systolic (SAP), diastolic (DAP) and mean (MAP) arterial pressures were significantly reduced from the third min. The maximal percentage reduction (Mean +/- SEM) reached 30.1 +/- 3.1% (SAP) and 24.7 +/- 2.9% (DAP) after 30 to 110 min of infusion. Initially there were transitory initial increases in SAP (3 patients) and DAP (1 patient). The increases in blood pressure were related to low body surface area (BSA). The dose of clonidine per m2BSA able to reduce by 10% either SAP or DAP (active dose-10), and the dose able to reduce SAP or DAP by 10 mmHg in one minute (systolic or diastolic clonidine unit) were calculated, providing indices for detecting clonidine responsiveness in patients with exaggerated hypertension. This method is advantageous when using clonidine intravenously because it diminishes the risk of overdosage.