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Biomedical subjects

R Ricci

Publications and source records attributed to R Ricci.

At least 181 records · Page 10Linked to original sources

Hyperplasia of myocyte nuclei in long-term cardiac hypertrophy in rats.

In contrast to observations made in the human heart, hyperplasia of myocyte nuclei has never been demonstrated in experimental cardiac hypertrophy. To test the hypothesis that the duration of the mechanical load more than the magnitude of ventricular hypertrophy may be the inciting stimulus for myocyte nuclei hyperplasia, constriction of the pulmonary artery was produced in rats and the hearts were examined 6 mo later. A 76% increase in right ventricular weight was measured. This hypertrophic response was accompanied by a 41% increase in the total number of myocyte nuclei in the ventricle. Furthermore, average myocyte cell volume per nucleus increased by 28%. No changes in weight, myocyte size, and nuclear number were observed in the left ventricle. In conclusion, myocyte nuclear hyperplasia and cellular hypertrophy both participate to the adaptive response of the right ventricular myocardium in long-standing pressure overload cardiac hypertrophy.

Animals↗

Effects of exercise on the capillary vasculature of the rat heart.

Effects on the myocardium, particularly those structural properties of the capillary network relevant to tissue oxygenation, were studied morphometrically in rats subjected to moderate exercise, strenuous exercise, and strenuous exercise preceded by a preconditioning period of moderate exercise. These different modalities of exercise were used to test the hypothesis that endurance training leads to capillary proliferation in the heart. The findings indicate that treadmill running produces right ventricular hypertrophy exclusively, which is accompanied by lengthening of the myocytes. Furthermore, a moderate running program results in an increase in the numerical density, luminal surface, and total length of capillaries in the right ventricle. In contrast, strenuous exercise with or without a preconditioning period produces a relative decrease in capillary luminal volume, surface, and numerical density. In the former case the diffusion distance for oxygen is decreased and in the latter it is increased. These data suggest that moderate exercise affects the microvasculature in ways that improve the efficiency of tissue oxygenation in the myocardium, whereas strenuous exercise has the opposite effect.

Adaptation, Physiological↗

Quantitative structural analysis of the myocardium during physiologic growth and induced cardiac hypertrophy: a review.

The quantitative structural properties of the ventricular myocardium during postnatal physiologic growth are compared with those accompanying an increased load in the adult rat heart to determine whether induced cardiac hypertrophy is a pathologic condition or simply a form of well compensated accelerated growth. The expansion of the ventricular myocardium during maturation shows a remarkable degree of well balanced compensatory response, because the capillary microvasculature, parenchymal cells and subcellular components of myocytes all grow in proportion to the increase in cardiac mass. In contrast, the increases in myocyte diameter and length caused by pressure hypertrophy, volume hypertrophy and infarction-induced hypertrophy are consistent with concentric, eccentric and a combination of concentric and eccentric hypertrophic growth of the whole ventricle, respectively. These cellular shape changes may represent a compensatory response of the myocardium at the cellular level of organization that tends to minimize the effects of an increased pressure or volume load, or both, on the heart. Cardiac hypertrophy, however, may also show alterations affecting capillary luminal volume and surface and the mitochondrial to myofibril volume ratio, which indicate an inadequate growth adaptation of the component structures responsible for tissue oxygenation and energy production. Thus, hypertrophy of the adult heart differs from that during physiologic growth, and the hypertrophied myocardium may exhibit structural abnormalities that can be expected to increase its vulnerability to ischemia.

Blood Pressure↗

Myocyte cell loss and myocyte hypertrophy in the aging rat heart.

To determine the effects of age on the myocardium, the functional and structural characteristics of the heart were studied in rats at 3, 10 to 12 and 19 to 21 months of age. Systemic arterial pressure, left ventricular pressure and its first derivative (dP/dt) and heart rate were comparable in the three animal groups. In the interval between 3 and 10 to 12 months, mean myocyte cell volume per nucleus increased 53 and 26% in the left and the right ventricle, respectively. The total number of myocyte nuclei remained constant in either ventricle. In the following period, between 10 to 12 and 19 to 21 months, a 39% further cellular hypertrophy on the left side of the heart was found in association with an 18% loss of cells in the ventricle. Cell loss was accompanied by discrete areas of interstitial and replacement fibrosis in the subendocardium. In contrast, no myocardial damage was observed in the right ventricle, and the measured 35% additional enlargement of myocytes occurred without a change in cell number. Thus, the aging left ventricle is composed of a smaller number of hypertrophied cells. Cellular hypertrophy may explain the unaltered cardiac function of the aged myocardium.

Aging↗

Lack of DNA fragmentation in rats treated with high oral doses of drugs acting on the central nervous system.

Five drugs acting on the central nervous system-chlorpromazine, triflupromazine, thioridazine, chlordiazepoxide, and ethosuximide--which provided conflicting results in previous genotoxicity assays have been tested for their DNA-damaging activity in vivo. The capability of these drugs of inducing DNA fragmentation was investigated by the use of two different techniques: rate of DNA strand separation in alkali as measured by hydroxylapatite chromatography, and changes of DNA viscometric behavior as detected by a new highly sensitive method. DNA damage, as checked by the first technique, was absent in both liver and gastric mucosa of rats given a single p.o. administration of 1/2 LD50 of the drugs. These negative results were confirmed by the subsequent viscometric analysis of liver DNA from rats treated with the same doses.

Animals↗

Response of the border zone to myocardial infarction in rats.

The response of the surviving myocardium 30 days after coronary artery occlusion was measured morphometrically in the regions bordering and remote from infarcts of different sizes. Mean cell volume per nucleus increased with infarct size in both zones, but the rate of change was greater in the border than in the remote portion of the unaffected myocardium. Capillary numerical density within the uninjured tissue progressively decreased with infarct size leading to an increased diffusion distance for oxygen. Although the magnitude of changes in capillary density was similar in the two regions of the ventricle, the analysis of the individual values in each heart showed that in infarcts comprising more than 11% of the ventricular wall capillary concentration and the path length for oxygen supply to the myocytes were affected more in the border zone than in the myocardium remote from the scar. In conclusion, the border zone participates in the hypertrophic recovery process after infarction, but the inadequate growth of the capillary microvasculature suggests that this region is more susceptible to additional ischemic episodes.

Animals↗

Primary intracranial lymphomas.

We reviewed the cases of 16 patients with primary intracranial lymphomas. The clinical and radiological data proved to be helpful in suggesting the diagnosis, but only tumoral biopsy provided unequivocal diagnosis. In our cases radiotherapy proved to be the most effective treatment.

Adult↗

Humoral inhibition of neutrophil chemotaxis in Crohn's disease.

In patients with Crohn's disease (CD) we investigated the C3 conversion of zymosan-activated serum (ZAS) and looked for the occurrence of chemotactic factor inactivation (CFI). We also studied the cell-directed inhibitory effect (CDI) of the CD patients' plasma and, in the same group, complement activation and complement-mediated deactivation. The mean value of ZAS C3 conversion in CD was no different from that of healthy controls, but in steroid-treated patients it was lower than in untreated CD. CFI occurred in 1 of the 23 CD sera tested, and CDI was observed in 6 out of the 22 patients tested. EDTA C3 conversion was present in 12 patients, and complement-mediated deactivation was associated with high values of EDTA C3 conversion. Our findings indicate that complement dysfunction and inhibitory factors of neutrophil chemotaxis are present in CD. These findings could explain the defective neutrophil migration into skin windows. Whether they are relevant to the pathogenesis of tissue injury or of infectious complications and are specific for CD, however, remains to be established.

Adult↗

Absence of DNA damage in mice and rats given high doses of five beta-adrenergic blocking agents.

Five beta-blockers (propranolol, metoprolol, oxprenolol, pindolol, and sotalol) were tested for their in vivo DNA-damaging activity by two different techniques: alkaline denaturation of DNA followed by hydroxylapatite chromatography, and a new viscometric method markedly more sensitive in detecting DNA fragmentation. DNA damage, as checked by the first technique, was absent either in liver and kidney of mice or in liver and gastric mucosa of rats given a single p.o. administration of 1/2 LD50 of the drugs. The subsequent viscometric analysis of liver DNA from rats treated with the same doses confirmed the above negative results.

Adrenergic beta-Antagonists↗

[Extension of necrosis and left ventricular function in recent myocardial infarct. Correlation between a QRS scoring system and various echocardiographic indexes].

The purpose of this study was to evaluate the extension of myocardial necrosis and the impairment of left ventricular function in patients with recent myocardial infarction by means of the standard 12-lead ECG. Then, we tried to correlate the QRS scoring system proposed by Wagner and coll. with some indexes obtained from a M-Mode and Two-Dimensional echocardiographic examination (echo-score, number of compromised areas, E-septum separation and left ventricular ejection fraction) in a group of 105 pts. (mean age 61.54 +/- 9.66 SD years). Patients were divided into three groups: 47 with anterior infarction, 45 with inferior infarction and 13 with anterior and inferior infarction. A statistically significant correlation was found between the QRS scoring system and (a) the infarct size (r between ECG-score and echo-score = 0.40, p less than 0.001; r between ECG-score and compromised areas = 0.47, p less than 0.001) and (b) left ventricular ejection fraction (r = -0.48, p less than 0.001), measured echocardiographically, particularly in pts. with anterior infarction. No correlation was found with the E-septum separation. In conclusion, the correlation between QRS scoring system and echo indexes appeared statistically significant, even if minimally applicable to single cases.

Arrhythmias, Cardiac↗

A boy with ring chromosome 15 derived from a t(15q;15q) Robertsonian translocation in the mother: cytogenetic and biochemical findings.

We describe a boy with a ring chromosome 15, showing the manifestations characteristic of this condition, ie, growth deficiency and unusual facial appearance with minor anomalies. The ring was derived from a t(15q;15q) chromosome of the mother, who had also had four spontaneous abortions. The respective karyotypes were 45,XX, -15,-15,+t(15q;15q) (mother) and 46,XY,-15,+r(15q;15q)mat (15q13 leads to cen leads to 15q26)(son). The ring chromosome lacked the short arms of the two translocated chromosomes 15 and was duplicated for a portion of the long arms near the centromere, probably cen leads to q13. Data from enzyme assays suggest that this duplicated region carries the alpha-mannosidase gene.

Adult↗

Malaria in the emergency department.

Eleven patients with malaria seen over five years in one emergency department demonstrate a trend toward more efficient diagnosis and outpatient treatment. Ten patients were diagnosed using a routine Wright's stained peripheral blood smear (three fortuitously). Because treatment of hospitalized patients consists of no more than oral chloroquine, the current regimen allows for outpatient management. Determination of species and extent of drug resistance, as well as eradication of Plasmodium vivax and P ovale, are referred to a consultant after 2 days of oral chloroquine therapy.

Adolescent↗

Genotoxic effects in rodents given high oral doses of ranitidine and sodium nitrite.

The possible intragastric nitrosation of ranitidine to genotoxic derivatives has been investigated in rats and mice given, by gavage, high single doses of this histamine H2 receptor antagonist along with NaNO2. Liver DNA fragmentation, as revealed in rats by both DNA alkaline elution and DNA alkaline denaturation followed by hydroxylapatite chromatography, was found to be dependent either on the molar ratio drug/nitrite or on the gastric pH. It occurred only with doses of 175 mg/kg ranitidine HCl + 80 mg/kg NaNO2 (molar ratio 1:2.32) or 350 mg/kg ranitidine HCl + 80 mg/kg NaNO2 (molar ratio 1:1.16) and concurrent reduction of gastric pH from 5.5 to 2-3 (produced by prolonged fasting). A further reduction of pH elicited by histamine injection increased the amount of DNA damage. DNA fragmentation in gastric mucosa showed a similar dependence on both pH and ranitidine/NaNO2 ratio, but was more marked than in liver. Simultaneous administration of ascorbic acid reduced the damage of gastric DNA. Oral administration of 175 mg/kg ranitidine HCl + 80 mg/kg NaNO2 in fasted and histamine-injected mice induced a modest but statistically significant increase in the frequency of sister chromatid exchanges in bone marrow cells.

Animals↗

[Rhabdomyoma of the interventricular septum in a one-day-old newborn infant. Echocardiographic diagnosis].

A case of interventricular septal rhabdomyoma in a one day-old newborn is presented. The newborn was moderately cyanosed. A 3/6 systolic murmur in basal area was present. An electrocardiogram showed the features of Wolff-Parkinson-White syndrome. A chest x-ray showed distinct cardiomegaly. M-Mode (MME) and Two-dimensional echocardiography (2DE) identified an interventricular septal mass within left ventricle and suggested the presence of left ventricular outflow obstruction. We emphasize the usefulness of MME and 2DE in accurately diagnosing intramural ventricular tumors in newborns.

Echocardiography↗