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Biomedical subjects

A Semplicini

Publications and source records attributed to A Semplicini.

126 records · Page 7Linked to original sources
PubMed1980

[Analysis of the variability of arterial pressure in patients with labile and stable hypertension and changes induced with atenolol].

Blood pressure variability was studied in 8 "labile" and in 8 "established" hypertensive patients by means of continuous unrestricted blood pressure recording for 24 hours. In 7 of the former and 5 of the latter the effect of atenolol (200 mg/day) was also investigated. Blood pressure variability as judged by circadian rhythm, standard deviation, coefficient of variation, indexes of skewness and kurtosis was similar in the two groups. The only significant difference consisted in the mean arterial pressure which was higher in the established than in the labile hypertensives. Atenolol produced in all subjects a fall in blood pressure but no significant changes in the standard deviation, coefficient of variation and index of skewness. On the contrary the index of kurtosis significantly increased suggesting a more stable blood pressure after treatment.

Adult↗
PubMed1980

Blood pressure variability in 'labile' and 'established' hypertension.

Blood pressure variability over a 24-hour period was compared between subjects with labile and those with established hypertension. For this purpose, a computer analysis of the blood pressure tracings, obtained with continuous unrestricted monitoring, was adopted, which characterizes the blood pressure variability in a quantitative manner. The following parameters were employed: the mean, the standard deviation, the coefficient of variation, the indexes of skewness and of kurtosis. No significant differences could be found between the two groups except for the mean value of the blood pressure. It is concluded, therefore, that the term 'labile hypertension' in inappropriate.

Adolescent↗
PubMed1978

[Acid-base metabolism in patients with hepatic cirrhosis treated with portacaval anastomosis at various intervals after the operation].

In a series of 68 cirrhotics subjected to portacaval anastomosis for digestive haemorrhage, alterations in the acid base balance, 3, 6, 12, 24 and 48 weeks after anastomosis, were examined. Following operation, an increase in the incidence of the usual acid base disturbances of liver cirrhosis is observed. Respiratory alkalosis increases with no direct relationship to teh postoperative increase in ammoniemia, the main stimulating agent of the resporatory centres. This is probably because the active fraction on the nerve cells is the non-ionized one only, freely diffusible through the haematoencephalic barrier, the plasma concentration of which is a function of blood pH. Postoperative metabolic alkalosis is secondary to the potassium and chloride depletion consequent on operative trauma, on the malnutrition syndrome and, in the case of potassium, on secondary hyperaldosteronism which, unlike what is observed in the other groups of cirrhotics, is uncorrected by anastomosis. After the shunt, metabolic acidosis may be the expression of an increase in lactates and pyruvates following on further liver function deterioration, and of a functional renal insufficiency which anastomosis makes more manifest.

Acid-Base Equilibrium↗
PubMed1976

[Benign muscular dystrophy with hypergonadotrophic hypogonadism and congenital cataract].

A syndrome characterized by benig muscular dystrophy, hypergonadotropic hypogonadism, congenital cataract and normal karyotype is reported. A similar condition was described by Bassöe. The patient's family tree revealed a number of isolated cases presenting some component of the syndrome, suggesting that this is connected with a recessive autosomic gene, probably with pleiotropic effect. The muscular disorder was absent in most of the other family members and its clinical signs were probably favoured by the low plasma level of testosterone with consequent reduced myotrophic action. The simultaneous presence of congenital cataract links the syndrome on the one hand to Steinert's myotonic dystrophy, although there were no clinical or electromyographic signs of myotonia, and on the other to other hereditary or familial neuroectodermal syndromes, compared to which it presents specific differential traits.

Adult↗
PubMedDate not supplied

Type I insulin-dependent diabetic patients show an impaired renal hemodynamic response to protein intake.

Human kidney responds to a meat meal with an increase in glomerular filtration rate (GFR), but the mechanisms regulating kidney hemodynamics following protein intake are poorly understood in Type I insulin-dependent diabetes. In the present study we investigated GFR response to protein intake (600 gr/1.73 m2 meat meal) in nine normal subjects and 21 Type I insulin-dependent diabetic patients with normal albumin excretion rates as well as proximal tubular sodium reabsorption rates and distal sodium delivery (PRNa and DDNa). The same study was reperformed in normal subjects and diabetic patients, with less than a 5 year diabetes duration, following one week of indomethacin treatment. Normal subjects showed a 38% increase in GFR following protein intake, whereas diabetic patients showed a significantly lower response (18%, p less than 0.01). The response of GFR to protein challenge was negatively related to diabetes duration but not to baseline glomerular filtration rate. Indomethacin treatment completely prevented the protein induced GFR increase in normal subjects but not in diabetic patients. Sodium reabsorption rate was increased following protein challenge both at the proximal and distal tubular level, as was net natriuresis.(ABSTRACT TRUNCATED AT 250 WORDS)

Diabetes Mellitus, Type 1↗
PubMedDate not supplied

Hypertension, coronary artery and cerebrovascular diseases in the population. Has epidemiology changed in the last decades?

Life expectancy has significantly increased in the last decades in many western populations, due to the fall of total and cardiovascular death rate. However, morbidity from cardiovascular diseases has decreased to a smaller extent. The overall population risk profile has improved, but it is still unsatisfactory. This is true for blood pressure control (with only 20% of hypertensive patients achieving normotension with antihypertensive drugs), hypercholesterolemia (with borderline-high serum cholesterol levels in 50% of the population), and smoking habits. Other potential causes of the poor cardiovascular prevention are: 1) a limited knowledge of the optimal blood pressure goal with antihypertensive treatment, 2) scanty information on the long term effects of antihypertensive drugs on cerebral and coronary circulation. Finally, little is being done to improve primary prevention in youth, when the slowly progressing atherosclerotic plaque formation is already on the way. To improve the cost / effectiveness of cardiovascular prevention, efforts must concentrate on the early identification of the subjects at the highest risk and on health promotion among youngsters. Large epidemiological trials conducted from the early 50s have provided convincing evidence of the multifactorial origin of cardiovascular diseases and encouraged the implementation of population based primary and secondary preventive measures, including antihypertensive treatment, as well as dietary and life-style modifications. It is now time to start asking ourselves whether or not we are satisfied with the results obtained in terms of reduced morbidity and mortality, whether these results are the direct consequence of these measures and whether or not we can do even better. The present work reviews some of the most recent comparative reports on the epidemiology of cardiovascular diseases in different populations, and some intervention trials to answer these questions and to help in identifying the most cost-effective approach to cardiovascular disease prevention in the next few years.

Cardiovascular Diseases↗
PubMedDate not supplied

Prediction and consistency of blood pressure salt-sensitivity as assessed by a rapid volume expansion and contraction protocol. Salt-Sensitivity Study Group of the Italian Society of Hypertension.

BACKGROUND: This multicenter trial in essential hypertensive patients (n=94) is aimed i) to evaluate the distribution of blood pressure salt-sensitivity by a rapid volume expansion/contraction protocol over three days; ii) to investigate the within-patient reproducibility and to identify predictors of the response to the test; iii) to compare this response with the response to dietary NaCl restriction. METHODS: The study design included: 1) screening for salt-sensitivity by the rapid test; 2) a controlled trial of dietary salt restriction; 3) repetition of the rapid test in a subgroup of patients. RESULTS: The mean BP response to the rapid test fitted a Gaussian curve. In multivariate regression analysis, controlling for the effect of potential confounders, the blood pressure increment during the intravenous saline infusion was the best independent predictor of the response to the test (r=0.713) with minor contributions by the 24-h urinary sodium excretion before the test and by baseline fasting serum insulin. These three variables together explained 61% of the overall variability of the response. The Spearman rank correlation coefficient between the BP response to the rapid test and the response to the dietary protocol was 0.21, p=0.05. Upon repetition of the rapid test, the correlation coefficient between the responses observed on the two occasions was 0.60 (n=19, p<0.01); there were no patients misclassified across the extreme tertiles of the distribution of salt-sensitivity. CONCLUSION: We conclude that the rapid test reproducibly identified patients in the upper and lower parts of the distribution of salt sensitivity. The analysis of possible predictors of the response to the test suggested that the evaluation of the blood pressure response to saline infusion, upon careful standardization of dietary NaCl intake, may represent an alternative to the completion of the whole test for the screening of the salt-sensitivity.

Adult↗
PubMedDate not supplied

[Arterial hypertension and oxidative stress induced by cyclosporin. Effect of carvedilol].

Cyclosporin-induced hypertension and endothelial dysfunction have been attributed to the effects of cyclosporin on factors controlling vasomotor tone. Endothelial nitric oxide (NO) regulates basal vasodilation, and an NO-mediated protective mechanism from cyclosporin-induced vasoconstriction has been proposed. In transplanted patients with cyclosporin-induced hypertension, we have recently demonstrated upregulation of the NO system and superoxide and free radical overproduction, which, by increasing NO metabolism, could induce hypertension, vascular remodeling and chronic rejection. In the present work, we have evaluated endothelial constitutive NO synthase (ecNOS), transforming growth factor beta and heme oxygenase-1 (protective against oxidative stress), mRNA production and plasma NO metabolites, peroxynitrite and antioxidant power in 15 kidney transplanted patients before and after 4 months of treatment with carvedilol alpha 1-beta-blocker and potent antioxidant. Our aim was to study the efficacy of the reduction of oxidative stress on complications such as endothelial dysfunction and fibrogenesis. Monocyte ecNOS and plasma NO metabolites remained higher versus those of control subjects and were unchanged by carvedilol, while antioxidant power and heme oxygenase-1 mRNA production increased. Peroxynitrite, as well as transforming growth factor beta mRNA, were reduced by carvedilol. It also normalized blood pressure. In conclusion, carvedilol reduces oxidative stress and normalizes blood pressure; ecNOS remains upregulated while mRNA for transforming growth factor beta, a key fibrogenic cytokine, is reduced by carvedilol, which seems to preserve protective mechanisms such as NO and heme oxygenase-1 against long-term complications of oxidative stress, e.g., endothelial dysfunction, fibrogenesis and chronic rejection.

Adult↗