[Physiopathological and clinical aspects of renal insufficiency].
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Biomedical subjects
Publications and source records attributed to A Borghetti.
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Although analysis of the radio frequency signal is the most accurate approach to myocardial tissue characterization, clinical diffusion has been limited because of the complex technology required. Much easier to perform, videodensitometric analysis could represent a valuable alternative. Previous works carried out on radio frequency data have shown that the absolute value of ultrasonic back scatter increases while its diastole-to-systole variation decreases in the hypertrophied myocardium. This study was aimed at clarifying whether alterations in characterization indexes of ultrasonic tissue can be detected by means of a videodensitometric approach, whether a specific type of left ventricular (LV) hypertrophy can be identified with this method, and finally what possible relationships exist between parameters of contractile function and tissue characterization indexes. Myocardial echo intensity (MEI), its cyclic variation (CV), and the dynamic relationship between myocardial signal and wall thickness variations during the cardiac cycle were assessed in 20 healthy subjects, 11 patients with essential hypertension and LV hypertrophy, 15 patients with hypertrophic cardiomyopathy, and 4 patients with primary amyloidosis. The CV was lower in the interventricular septum of patients with cardiac hypertrophy as a group, compared with that of control subjects (13.0% +/- 5.6% versus 18.8% +/- 5.5%, p < 0.001), but it was similar among patients with different types of hypertrophy. In control subjects, a significant inverse correlation was found between the progressive decrease of the myocardial signal and the parallel increase in wall thickness during systole; this correlation was lost in 60% of patients with hypertrophic cardiomyopathy and 50% of those with amyloidosis, but only in 9% of patients with essential hypertension (chi square analysis 12.68, p < 0.01). The CV was associated with systolic wall thickening (r = 0.53, p = 0.0001) and fractional shortening (r = 0.44, p = 0.0014). MEI and its CV per se cannot distinguish among different types of LV hypertrophy; however, the loss of an inverse relationship between the myocardial signal and wall thickness may suggest abnormal myocardial conditions in individual patients with the same disease or comparable wall thickness.
Ouabain-resistant Na and Li effluxes in erythrocytes from 18 normal subjects and 19 hypertensive subjects were studied in fresh cells that contained about 9 mmol Li and 2.5 or 6.5 mmol Na per liter of erythrocytes after intact cells had been incubated for 5 hours in 110 mM Li, 40 mM Na medium, with or without ouabain 10(-4) M. Outward Na cotransport was estimated at both internal Na concentrations as the furosemide-sensitive unidirectional 22Na efflux from erythrocytes into a Na free-medium containing 75 mM MgCl2. The changes in furosemide-sensitive outward Na transport between the two levels of internal Na were considered as a measure of the response of Na cotransport to the changes in internal Na within its physiological range. At both levels of internal Na, outward Na cotransport was reduced in the majority but not in all of the patients with essential hypertension (p less than 0.05 at 2.5 mmol; p less than 0.001 at 6.5 mmol). The ratio of the changes in Na cotransport to those in internal Na was lower in the hypertensive patients than in the control subjects (17.2 mumol/liter red blood cells/hr/1 mmol in internal Na increase vs 42.2, p less than 0.001). The Li-Na countertransport was increased in a few patients with essential hypertension, with no relationship to cotransport. We conclude that, in essential hypertension, the outward Na + K cotransport is impaired in fresh erythrocytes not treated with PCMBS (2,5 p-chloromercuribenzene sulfonate) or nystatin, even when internal Na is around its physiological range.
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The control of vasomotion is a central issue in blood pressure regulation and is a primary goal of antihypertensive therapy. Calcium is the final messenger in the contractile mechanism of vascular smooth and cardiac muscle. Vasoconstrictor agents enhance the entry of Ca++ into vascular myocytes; vasodilators usually depress it. The most recent findings, based on direct measures of intracellular Ca++, have also highlighted the importance of calcium-sensitization mechanisms: vasoconstrictors sensitize the contractile apparatus to Ca++; vasodilators have an opposite effect. Cell calcium control alterations have been reported in different forms of hypertension. An increase in vascular myoplasmic Ca++ and a higher rate of calcium influx through specific, dihydropiridine-sensitive calcium channels have been found in genetic or secondary animal models. In hypertensive patients, an elevation of cytoplasmic Ca++ was noted in the platelets. Since Ca++ is a ubiquitous intracellular messenger, these changes may have profound implications for the pathophysiology of hypertension.
Effects of two protein restricted diets on dietary compliance, nutritional and metabolic state, and progression of chronic renal failure (CRF) were investigated. Twenty-one patients with CRF were randomly assigned to either a conventional low protein diet (0.6 g of protein/kg b.w./day) or to a very low protein diet, providing 0.4 g of protein/kg b.w./day, supplemented with a mixture of essential amino acids which contained HIS, TYR and a high proportion of branched chain amino acids. Nutrition, assessed by body weight, anthropometry, serum protein levels and nitrogen balance studies, was maintained in all patients. Some metabolic abnormalities of CRF (i.e., secondary hyperparathyroidism, glucose intolerance) improved in both groups. The supplemented diet provided better adherence to protein prescription, corrected the depletion of VAL and LEU in muscle and was more effective than conventional diet in slowing the rate of progression of CFR.