Cognitive and anxiety-like impairments accompanied by serotonergic ultrastructural and immunohistochemical alterations in early stages of parkinsonism.

Parkinson's disease (PD) is mostly known as a dopamine deficiency syndrome due the structural and functional changes in striatal projection neurons. However, studies have considered this pathology as a multi-systemic disease in which the neurodegenerative process extends beyond the dopaminergic system. Therefore, the purpose of the present study was to investigate the morphological and immunohistochemical changes associated with behavioral and cognitive alterations in a model of parkinsonism induced by low dose of reserpine. Animals showed anxiety-like behavior and deficits in short-term recognition memory. Besides, Tyrosine Hydroxylase (TH) immunoreactive cells decreased in reserpine (RES) group in CA1 and serotonin (5-HT) immunoreactive cells decreased in RES group in CA1, CA3 and medial prefrontal cortex (mPFC). Moreover, an increase in the area (µm2) of 5 H T labeled ultrastructure (axon terminal) was observed in RES group only in CA1 and mPFC. The evidence of alterations in 5-HT immunoreactive in the premotor phase of model of parkinsonism highlights the importance of looking beyond the nigrostriatal system to elucidate the underling mechanisms and deficits in other neurotransmitters systems. This provides vital information regarding novel interventions for the management of non-motor symptoms. Additionally, the low-dose reserpine treatment has an early effect on axonal ultrastructure. As the axonopathy in PD has been increasingly recognized, the focus on axonal neurobiology is noteworthy for both neuroprotective and restorative therapeutics, and the progressive reserpine rat model can be a useful tool in this search.

Are There Benefits from Teaching Yoga at Schools? A Systematic Review of Randomized Control Trials of Yoga-Based Interventions.

Introduction. Yoga is a holistic system of varied mind-body practices that can be used to improve mental and physical health and it has been utilized in a variety of contexts and situations. Educators and schools are looking to include yoga as a cost-effective, evidence-based component of urgently needed wellness programs for their students. Objectives. The primary goal of this study was to systematically examine the available literature for yoga interventions exclusively in school settings, exploring the evidence of yoga-based interventions on academic, cognitive, and psychosocial benefits. Methods. An extensive search was conducted for studies published between 1980 and October 31, 2014 (PubMed, PsycInfo, Embase, ISI, and the Cochrane Library). Effect size analysis, through standardized mean difference and Hedges'g, allowed for the comparison between experimental conditions. Results and Conclusions. Nine randomized control trials met criteria for inclusion in this review. Effect size was found for mood indicators, tension and anxiety in the POMS scale, self-esteem, and memory when the yoga groups were compared to control. Future research requires greater standardization and suitability of yoga interventions for children.

Electrolytic lesion of the nucleus incertus retards extinction of auditory conditioned fear.

Fear memory circuits in the brain function to allow animals and humans to recognize putative sources of danger and adopt an appropriate behavioral response; and research on animal models of fear have helped reveal the anatomical and neurochemical nature of these circuits. The nucleus (n.) incertus in the dorsal pontine tegmentum provides a strong GABAergic projection to forebrain 'fear centers' and is strongly activated by neurogenic stressors. In this study in adult male rats, we examined the effect of electrolytic lesions of n. incertus on different stages of the fear conditioning-extinction process and correlated the outcomes with anatomical data on the distribution of n. incertus-derived nerve fibers in areas implicated in fear circuits. In a contextual auditory fear conditioning paradigm, we compared freezing behavior in control (naïve) rats (n=23) and rats with sham- or electrolytic lesions of n. incertus (n=13/group). The effectiveness and extent of the lesions was assessed post-mortem using immunohistochemical markers for n. incertus neurons-calretinin and relaxin-3. There were no differences between the three experimental groups in the habituation, acquisition, or context conditioning phases; but n. incertus lesioned rats displayed a markedly slower, 'delayed' extinction of conditioned freezing responses compared to sham-lesion and control rats, but no differences in retrieval of extinguished fear. These and earlier findings suggest that n. incertus-related circuits normally promote extinction through inhibitory projections to the amygdala, which is involved in acquisition of extinction memories.

Cardiovascular effects of Hyptis fruticosa essential oil in rats.

In non-anesthetized normotensive rats, Hyptis fruticosa essential oil (HFEO, 5, 10, 20 and 40 mg/kg; i.v.) induced hypotension associated with tachycardia. In intact and isolated rings of rat superior mesenteric artery (control), HFEO (1-1000 microg/ml, n=6, cumulatively) induced concentration-dependent relaxations of tonus induced by 10 microM phenylephrine (Phe) (pD(2)=2.6+/-0.27; E(max)=64+/-8.3%). In denuded endothelium pre-contracted rings with Phe or K(+)-depolarizing solution (80 mM), the concentration-response curves to HFEO were not shifted (pD(2)=2.3+/-0.25 and 2.3+/-0.28, respectively), but their maximal responses were significantly (P<0.05 vs control) increased (E(max)=122.3+/-18.2% and 92+/-3.6%, respectively). HFEO was also capable of antagonizing the concentration-response curves to CaCl(2) (3 microM-30 mM) in a dose-dependent manner.

Lead effects on non-adrenergic non-cholinergic relaxations in the rat gastric fundus.

The effect of lead exposure on non-adrenergic non-cholinergic (NANC) relaxations in rat gastric fundus was evaluated in this work. Wistar rats were divided into four groups: The control group received tap water and the three other received 0.008% of lead acetate in their drinking water for 15, 30 and 120 days. NANC relaxations induced by electrical field stimulation (0.5-8 Hz, 1 ms, 60 V) of gastric fundus strips was inhibited in all groups treated with lead. The strips from groups, control and 120 days of lead treatment (LEAD 120), were incubated with L-NOARG (100 microM). The presence of this blocker did not produce any additional inhibition. Sodium nitroprusside (10(-10)-10(-6) M) and 8-Br-GMPc (3 x 10(-8)-3 x 10(-4) M) produced dose-dependent relaxations in strips of both groups control and LEAD 120, however, in the LEAD 120, the potencies were significantly reduced from 7.32 +/- 0.05 to 6.40 +/- 0.09 (n = 5) and 4.26 +/- 0.06 to 3.69 +/- 0.05 (n = 5), respectively. Our data suggest that the chronic exposure to lead inhibits NANC relaxations probably by modulating NO release from NANC nerves and/or by interacting with intracellular transducer mechanisms in rat gastric fundus.

Postnatal neurogenesis in the medial cortex of the tropical lizard Tropidurus hispidus.

Young, adult and presumed old specimens of the tropical lizard Tropidurus hispidus, living in an almost steady warm habitat, have been the subjects of a 5-bromodeoxiuridine immunocytochemical study to label proliferating brain cells. All animals showed abundant 5-bromodeoxiuridine-labeled nuclei in the ependyma of their telencephalic lateral ventricles, with these being especially abundant in the medial cortex ependyma. Surprisingly, adult animals displayed higher numbers of labeled nuclei when compared with those of young specimens. In a second experiment, in order to check the evolution of ependymal-labeled nuclei, adult specimens were allowed 4 h or 2, 4, 7, 15 or 30 days of survival after the 5-bromodeoxiuridine pulse. Most labeled nuclei appeared isolated at short survival times (4 h and 2 days after the 5-bromodeoxiuridine pulse) but from day 4 and beyond, labeled nuclei appeared in couples or groups usually located in the ependyma. Labeled nuclei with vertical fusiform appearance in the inner plexiform layer or even recruited in the medial cortex cell layer were assumed to be migratory. These presumed migratory nuclei were unexpectedly few (less than 30%) when compared with other lizards, and they appeared much later; at 15 and 30 days after the pulse. This situation resembles that of mammals where only a small proportion of postnatally generated neurons can develop and survive.

Central nervous system effects of the crude extract of Erythrina velutina on rodents.

The aqueous extract (AE) of Erythrina velutina prolonged the sleep duration induced by sodium pentobarbital (control: 6.4 +/- 1.2 min; extract 10 mg/kg, 47.1 +/- 3.9 min; extract 100 mg/kg, 109.4 +/- 7.2 min; F = 243, P < 0.001). In the open field, the extract at the doses of 10 and 50 mg/kg did not changed the number of crossings, rearings nor groomings. On the other hand, at the dose of 200 mg/kg it reduced the number of crossings (q = 6.25, P < 0.05) and groomings (q = 3.91, P < 0.05). When exposed during three consecutive days to the open field, the control animals showed habituation for crossings (F = 17.56, P < 0.001) and rearings (F = 14.01, P < 0.001). The same was not true for animals treated with 10 mg/kg of the extract (crossings: F = 3.59, P > 0.05; rearings: F = 3.62, P > 0.05). At the same dose, the extract blocked the acquisition of foot shock memory (P = 0.9219) when compared to the control values (P = 0.0078). Our data showed that the crude extract of Erythrina velutina at lower doses interferes with mnemonic process for different tasks, while at higher doses, the sedative and neuromuscular blocking actions are the main effects.

Antinociceptive and antiedematogenic effects of the aqueous extract of Hyptis pectinata leaves in experimental animals.

The aqueous leaf extract of Hyptis pectinata (L.) Poit (Lamiaceae), popularly known in Brazil as "sambaicatá" or "canudinho", was tested for its antinociceptive effects using the abdominal writhing, hot plate and formalin test models, and for its aniedematogenic effects using the carrageenin and arachidonic acid-induced rat paw edema. The aqueous extract of Hyptis pectinata administered orally at doses of 100, 200 and 400 mg/kg had a significant antinociceptive effect in the test of acetic acid-induced abdominal writhing, with 43, 51 and 54% reduction of writhes, respectively, compared to the control. An increase in hot-plate latency of 47 and 37.5% was also observed in animals receiving doses of 200 and 400 mg/kg, p.o. when placed on a hot plate. In the formalin test, doses of 200 and 400 mg/kg, p.o. had no significant effect during the first phase of the test (0-5 min), while the dose of 200 mg/kg, p.o. reduced the nociceptive effect by 70% during the second phase (20-25 min). At the dose of 600 mg/kg, p.o., the aqueous extract inhibited carrageenin-induced rat paw edema by 34.1%, and the dose of 300 mg/kg administered intraperitoneally inhibited the rat paw edema induced by subplantar injection of arachidonic acid by 32.8%. These results suggest that the aqueous extract from the Hyptis pectinata leaves produces antiedematogenic and antinociceptive effects. The antinocipetion observed with the hot-plate test probably involves the participation of the opioid system.

Differential effects of lead and zinc on inhibitory avoidance learning in mice.

We studied the effects of chronic intoxication with the heavy metals lead (Pb2+) and zinc (Zn2+) on memory formation in mice. Animals were intoxicated through drinking water during the pre- and postnatal periods and then tested in the step-through inhibitory avoidance memory task. Chronic postnatal intoxication with Pb2+ did not change the step-through latency values recorded during the 4 weeks of the test (ANOVA, P>0.05). In contrast, mice intoxicated during the prenatal period showed significantly reduced latency values when compared to the control group (day 1: q = 4.62, P<0.05; day 7: q = 4.42, P<0.05; day 14: q = 5.65, P<0.05; day 21: q = 3.96, P<0.05, and day 28: q = 6.09, P<0.05). Although chronic postnatal intoxication with Zn2+ did not alter a memory retention test performed 24 h after training, we noticed a gradual decrease in latency at subsequent 4-week intervals (F = 3.07, P<0.05), an effect that was not observed in the control or in the Pb2+-treated groups. These results suggest an impairment of memory formation by Pb2+ when the animals are exposed during the critical period of neurogenesis, while Zn2+ appears to facilitate learning extinction.

Differential effects of lead and zinc on inhibitory avoidance learning in mice

We studied the effects of chronic intoxication with the heavy metals lead (Pb2+) and zinc (Zn2+) on memory formation in mice. Animals were intoxicated through drinking water during the pre- and postnatal periods and then tested in the step-through inhibitory avoidance memory task. Chronic postnatal intoxication with Pb2+ did not change the step-through latency values recorded during the 4 weeks of the test (ANOVA, P>0.05). In contrast, mice intoxicated during the prenatal period showed significantly reduced latency values when compared to the control group (day 1: q = 4.62, P<0.05; day 7: q = 4.42, P<0.05; day 14: q = 5.65, P<0.05; day 21: q = 3.96, P<0.05, and day 28: q = 6.09, P<0.05). Although chronic postnatal intoxication with Zn2+ did not alter a memory retention test performed 24 h after training, we noticed a gradual decrease in latency at subsequent 4-week intervals (F = 3.07, P<0.05), an effect that was not observed in the control or in the Pb2+-treated groups. These results suggest an impairment of memory formation by Pb2+ when the animals are exposed during the critical period of neurogenesis, while Zn2+ appears to facilitate learning extinction

Lead increases tetrodotoxin-insensitive spontaneous release of glutamate and GABA from hippocampal neurons.

This study was aimed at investigating the effects of the environmental pollutant lead (Pb2+) on the tetrodotoxin (TTX)-insensitive release of neurotransmitters from hippocampal neurons. Evidence is provided that Pb2+ (>/=100 nM) increases the frequency of gamma-aminobutyric acid (GABA)- and glutamate-mediated miniature postsynaptic currents (MPSCs) recorded by means of the patch-clamp technique from cultured hippocampal neurons. Because Pb2+ changed neither the amplitude nor the decay-time constant of the MPSCs, Pb2+-induced changes in MPSC frequency are exclusively due to a presynaptic action of this heavy metal. Increase by Pb2+ of the action potential-independent release of GABA and glutamate was concentration dependent and was only partially reversible upon washing of the neurons with nominally Pb2+-free external solution. This effect was also Ca2+ independent and began approximately after 1-2-min exposure of the neurons to Pb2+. The latency for the onset of the Pb2+'s effect on the MPSC frequency and the inability of the chelator ethylenediaminetetraacetic acid (100 microM) to reverse the effect that remained after washing of the neurons with external solution suggested that Pb2+ acted via an intracellular mechanism. Of interest also was the finding that Pb2+ simultaneously increased the release of GABA and glutamate, overriding the ability of these neurotransmitters to decrease the release of one another. Given that synaptic activity is a key mechanism for the establishment of stable synaptic connections early in the development, it is possible that, by interfering with spontaneous transmitter release, Pb2+ has lasting effects on neuronal maturation and plasticity.

Glycine and calcium-dependent effects of lead on N-methyl-D-aspartate receptor function in rat hippocampal neurons.

The effects of lead (Pb++) on N-methyl-D-aspartate (NMDA) receptor function of rat hippocampal neurons in culture were studied by use of the whole-cell patch-clamp technique. Currents activated by NMDA (100 microM) in the presence of nonsaturating concentrations of glycine (0.01-0.05 microM) were potentiated in a voltage-independent manner by Pb++ (1-10 microM), and the potentiation was antagonized by 50 microM kynurenic acid. Increasing extracellular Ca++ from 1 to 10 mM similarly potentiated the NMDA-activated currents in the presence of a nonsaturating concentration of glycine (0.2 microM). The potentiation of NMDA-activated currents by low micromolar concentrations of Pb++ may be mediated by this cation's ability to increase the affinity of the NMDA receptor for glycine. In the presence of 10 microM glycine and 2 mM Ca++, Pb++ reduced the peak amplitudes of currents activated by NMDA (100 microM) in a voltage-independent manner (IC50 = 5.9 microM Pb++, Hill coefficient (nH) = 1.2). Also, steady-state currents activated by NMDA (50 microM) were inhibited by rapid application of Pb++ (IC50 = 3.2 microM, nH = 0.7). Increasing extracellular Ca++, in the presence of 10 microM glycine, reduced the NMDA-activated currents and shifted the Pb++ concentration-response curves to the right: at 0.2, 2 and 20 mM Ca++, the IC50 values of Pb++ were 3.0, 5.9 and 12.5 microM and the nH values were 0.9, 1.2 and 1.1, respectively. The finding that external Ca++ antagonized the inhibitory effect of Pb++ suggests that the noncompetitive inhibitory action of Pb++ with respect to glycine and NMDA may be mediated by Pb++ competition with Ca++ for a site on the NMDA receptor.

GSTM1 and NAT2 genotypes and urinary mutagens in coke oven workers.

The influence of the metabolic genotypes GSTM1 and NAT2 on the urinary excretion of mutagens in 46 coke oven workers (27 of them smokers) was studied. Exposure to polycyclic aromatic hydrocarbons (PAH) was estimated from urinary 1-pyrenol levels, which varied from 0.23 to 5.59 micromol/mol creatinine. Fourteen urine samples (30.4%), all but one belonging to smokers, were positive for mutagenic activity (i.e. at least one of the assayed doses was able to double the number of spontaneous revertants). Nine of the urine-positive subjects were both GSTM1-null and NAT2-ss (64.3%), while the same combination of genotypes was found in nine out of 31 urine-negative subjects (29.0%) (P < 0.05). Significantly more smoking workers with the genotype combination GSTM1-null/NAT2-ss showed positive urine mutagenicity than the other subjects (75.0 versus 28.6%, P < 0.05). Smokers with the slow acetylator genotype showed a significantly higher frequency of positive urine samples than smoking fast acetylators (64.7 versus 22.2%, P < 0.05). Our results suggest that smoking coke oven workers with genotypes unfavourable for detoxification of aromatic amines (NAT2-ss) and PAH (GSTM1-null) may have an increased risk of developing bladder cancer.

Mutagenicity and contents of polycyclic aromatic hydrocarbons in used and recycled motor oils.

Thirteen samples of used motor oil and 33 recycled fractions, obtained in the laboratory by means of a recovery process similar to that currently used in Italy (vacuum distillation followed by thermal clay treatment) were examined. The Ames test (standard and modified version according to Blackburn) was used to determine the mutagenicity of the extracts and their contents of polyaromatic fraction (PAF) (IP346/80 method) and polycyclic aromatic hydrocarbons (PAH) (Grimmer's method). Used motor oils are mutagenic, both directly and indirectly. The highest values have been found in used oils from motor vehicles using leaded petrol (up to 118.8 revertants/mg). Samples from vehicles using unleaded petrol or diesel fuel are less mutagenic (up to 31.1 and 16.4 rev/mg, respectively). The enrichment in mutagens due to the use of oil in the three types of engine ranges from mean values of 6.2, 1.1 and 0.4 rev/mg per 1000 km, respectively. Recycled oils are almost completely devoid of direct mutagenic activity (33 samples: mean +/- SD = 1.6 +/- 1.5 rev/mg). Most recycled distillates show considerable mutagenic activity in the presence of microsomial enzymes (up to 82.5 rev/mg), although this is reduced with respect to the original oils (recycled, mean +/- SD = 13.8 +/- 15.5 rev/mg; original oils, mean +/- SD = 30.7 +/- 35.2, Mann-Whitney U-test, z = 1.793, p < 0.05). Both PAF and PAH contents are high in used oils from the two types of petrol engine but not in those from diesel engines. Recycling reduces PAF contents only in used oils from petrol engines, from a mean value of 13.91 +/- 7.32 to 4.23 +/- 2.90% (comparison with original used oils, Mann-Whitney U-test, U = 8, p < 0.01). The light distilled fractions have greater concentrations of indirect mutagens, PAF and PAH than the others. The increase in PAH in light recycled products with respect to the original used oils is significant (Wilcoxon's t-test, z = 2.306, p < 0.05). Benzo[a]pyrene (BaP) is found in appreciable quantities (> 10 ppm) in all used oils from petrol engines and in most of their recycled products. Recycling generally recovers 50% of mutagens and PAF and about 80% of PAH. Considered together, recycled products have in any case contents of mutagens and PAF which are significantly lower than those in the parent oils, but not of PAH (Wilcoxon's t-test; mutagens, z = 2.935, p < 0.01; PAF, z = 3.145, p < 0.01; PAH, z = 1.397, not significant). Lastly, many recycled oils have PAH concentrations which are equal to or higher than those of the original used oils. The health risks linked to professional exposure to these types of oils and the inadequate recycling process currently used (redistillation and thermal clay treatment) in reducing mutagenic and cancerogenic substances from used motor oils are stressed.

Mutagenicity and contents of polycyclic aromatic hydrocarbons in new high-viscosity naphthenic oils and used and recycled mineral oils.

Mutagenic activity on the Ames test was evaluated in 15 samples of naphthenic high-viscosity mineral oils and 12 samples of used lubricants (recovered and pooled) and their recycled products. Bacterial mutagenesis was assayed using both the standard technique and Blackburn's modification. The contents of polycyclic aromatic hydrocarbons (PAH) was also evaluated, as polynuclear aromatic fraction (PAF) and total PAH, determined respectively with the semi-quantitative dimethylsulphoxide-refractive index method and the Grimmer method. Only four samples (three acid-treated naphthenic oils and one recycled fraction of a used oil) showed mutagenic activity higher than 6 revertants/mg of oil, considered by Blackburn and coworkers as indicating a potential carcinogenic risk for these compounds. Limited mutagenicity was found in all used and recycled oils, but also in samples of acid- or solvent-treated oils. No hydrogen-treated naphthenic oils turned out to have any mutagenic activity. PAF contents of oils were closely correlated with those of total PAH (n = 15, r = 0.83; n = 12, r = 0.91; p < 0.01 for both naphthenic and used/recycled oils respectively). No recycled oil had high PAF contents. Eleven samples had PAF contents higher than 3%, the arbitrary danger threshold suggested by the CONCAWE (1988). Of these 11 samples, the majority were acid-treated products, although there was one hydrogen-treated oil and one used and recycled oil. No mutagenic activity could be demonstrated in almost half the oils with PAF > 3%. In this study, the presence of mutagens was not correlated wither with PAF or with total or mutagenic PAH. The difficulty of predicting the mutagenicity of mineral oils is stressed. Most naphthenic and some recycled oils clearly have components which inhibit the metabolizing system in the bacterial mutagenesis test, with consequent possible false negative results.

Urinary excretion of mutagens in coke oven workers.

The influence of occupational exposure to polycyclic aromatic hydrocarbons (PAHs) on urinary mutagenic activity was assessed in 75 coke oven workers, using a highly sensitive bacterial mutagen technique (extraction with C18 resin and liquid micro-preincubation test on strain TA98 of Salmonella typhimurium in the presence of metabolizing and deconjugating enzymes). Exposure to PAHs was assessed according to the urinary excretion of 1-pyrenol; the main confounding factors were checked by the number of cigarettes smoked per day and the levels of nicotine and its metabolites in urine, or by ascertaining whether recommended dietary restrictions had been followed. Of the 20 urine samples which turned out to be positive (producing at least double the number of spontaneous revertants), 19 (95%) belonged to smokers. Only one non-smoker had obvious urinary mutagenic activity, and was highly exposed occupationally to PAHs (urinary 1-pyrenol of 3.930 mumol/mol of creatinine). Of the five urine samples from subjects who had not followed the recommended diet, two (40%) were clearly mutagenic. Multiple regression analysis (n = 67) showed that the presence of samples positive for urinary mutagenic activity depended only on smoking habits, if this confounding factor was assessed according to the number of cigarettes smoked per day, while the significant influence of exposure to PAH could be shown when the confounding factor was objectively estimated according to the urinary levels of nicotine and its metabolites. Assessment of the mutagenic potency of urinary extracts (net revertants/mmol creatinine) confirmed the strong influence of smoking habits on urinary mutagenic activity (all smokers 2156 +/- 2691 versus non-smokers 939 +/- 947 net revertants/mmol creatinine; Mann-Whitney test: P < 0.01). In smokers highly exposed to PAHs, greater excretion of mutagens with respect to low-exposure smokers was revealed (3548 +/- 4009 versus 1552 +/- 1227 net revertants/mmol creatinine; Mann-Whitney test: P < 0.01). Multiple regression analysis showed that the mutagenic potency of urinary extracts of coke oven workers depended on exposure to PAHs, tobacco smoking habits, and consumption of fried, grilled or barbecued meat. Increased urinary mutagenic activity strengthens epidemiological evidence of the increased risk of renal and urinary tract tumours in these workers. The presence of mutagenic metabolites in urine as a result of occupational exposure to PAH may be demonstrated only by using highly sensitive techniques for assessing urinary mutagenic activity in studies which include careful checking of the main confounding factors.

Predictors of mortality in very old subjects aged 80 years or over.

We studied 318 subjects aged 80 years of over included in the Cardiovascular Study in the Elderly (CASTEL). Some well known risk factors (left ventricular hypertrophy, glucose intolerance, cholesterol, ApoB/ApoA ratio, triglycerides, proteinuria, cigarette smoking, and ECG abnormalities), whose importance in cardiovascular risk is definitely accepted for young adults, were very poor predictors of mortality in our survey. On the contrary, FEV1 reduction and blood uric acid were strong predictors.

Mortality in relation to Minnesota code items in elderly subjects. Sex-related differences in a cardiovascular study in the elderly.

The prognostic value of electrocardiographic abnormalities has not been widely studied in the elderly. We examined the Minnesota code ECG items in 2254 elderly subjects of the Cardiovascular Study in the Elderly (CASTEL), performed on an Italian general population. In our experience, codes for ischaemia, 1st-degree atrio-ventricular block, bundle branch blocks, myocardial infarction, atrial fibrillation or sinus tachycardia were predictors of overall mortality in females, while only the former three items were predictors in men. Although ischaemia, left bundle branch block and atrial fibrillation were predictors of cardiovascular mortality in both sexes, right bundle branch block, supraventricular arrhythmias and left ventricular hypertrophy were predictors only in men, and 1st-degree atrio-ventricular block were predictors only in women. Surprisingly, left anterior haemiblock and bifascicular blocks were not predictive of mortality.

Blood pressure, left ventricular hypertrophy and diabetes among 179 very old hypertensives from an Italian general population. The CASTEL (Cardiovascular Study in the Elderly).

Hypertension is common in elderly subjects, but old and particularly very old people have usually been excluded from major epidemiological trials. We studied 179 hypertensive subjects aged 80 years or more drawn from elderly people of an Italian town within the context of the CASTEL (Cardiovascular Study in the Elderly). Prevalence of hypertension declined from 66.7% (first visit, first measurement) to 56.3% (last visit, last measurement). Systolic but not diastolic blood pressure was a little higher among very old hyperglycemic hypertensive subjects than in normoglycemic ones, while left ventricular mass was independent of both blood pressure and glucose intolerance.