Biomedical subjects

L Nascimento

Publications and source records attributed to L Nascimento.

At least 19 recordsLinked to original sources

PubMed1990

[Doppler echocardiographic evaluation of right heart pressure in children with ventricular septal defect].

Thirty seven children with ventricular septal defects (VSD) alone or associated with other malformations were examined by Doppler echocardiography to evaluate systolic right ventricular pressure (SRVP) non-invasively. All patients underwent cardiac catheterisation within 48 hours of the Doppler estimation. The maximum interventricular pressure gradient could be assessed in 32 patients (86%) from the recording of the maximum velocity of the VSD jet using the simplified Bernoulli formula. The SRVP was calculated by subtracting the maximum interventricular pressure gradient from the systolic blood pressure measured by sphygmomanometry. The SRVP estimated by continuous wave Doppler ranged from 24 to 108 mmHg (mean: 60 mmHg) compared with 20 to 109 mmHg (mean: 64 mmHg) at catheterisation. Two types of correlation were sought: 1) between the maximum interventricular pressure gradient measured by Doppler echo and the peak-to-peak LV-RV pressure gradient (r = 0.95; SD = 6 mmHg; Y = 1.03 x X + 1.3); 2) and between the SRVP measured by Doppler and by catheterisation (r = 0.94; SD = 6 mmHg; Y = 1.06 x X + 7.7). These results show that the maximum velocity of the interventricular jet and thereby the SRVP may be accurately measured by Doppler echocardiography in the majority of patients with VSD.

Adolescent↗

PubMed1989

Effect of acute renal failure on free thyroid hormone levels in a thyrotoxic patient.

Acute renal failure in a previously undiagnosed case of thyrotoxicosis was accompanied by a rapid and spontaneous decline in thyroid hormone levels. Over a 2-week period, free triiodothyronine and thyroxine fell to the low levels seen in euthyroid patients with end-stage renal disease. Thyrotropin levels remained undetectable throughout, suggesting impairment of the pituitary-thyroid axis at the level of the thyroid gland. This may represent an important beneficial adaptation to severe illness and could explain the virtual absence of hyperthyroidism in renal failure patients.

Acute Kidney Injury↗

PubMed1988

Pituitary-thyroid function in chronic renal failure assessed by a highly sensitive thyrotropin assay.

Pituitary-thyroid function was assessed in 40 patients with chronic renal failure undergoing regular maintenance hemodialysis and in 35 normal subjects. Serum thyroid hormone levels were significantly lower in the dialysis patients than in the normal subjects (P less than 0.001) and were in the hypothyroid range in a high proportion of dialysis patients (total T3, 25%; free T3, 45%; total T4, 55%; free T4, 45%; and free T4 index, 38%). The reduced free thyroid hormone levels could not be explained by currently recognized assay artefacts. Serum TSH levels were higher than in the normal subjects (P less than 0.01), but still within the normal range for most (35 of 40) dialysis patients and did not correlate significantly with total or free thyroid hormone concentrations in either group. These results suggest some impairment in the thyroidal response to TSH and impaired pituitary response to low serum thyroid hormone levels, the latter implying resetting of the normal feedback mechanism such that diminished thyroid hormone production evokes a smaller than normal increase in TSH secretion. This diminished thyrotroph sensitivity to reduced serum thyroid hormone levels may be beneficial in severe nonthyroidal illness.

Adolescent↗

PubMed1986

Intact ability to lower urine pH in nonacidotic adrenalectomized rats.

Distal acidification was assessed in adrenalectomized (ADX) rats in which the development of acidosis was prevented by oral supplementation with NaHCO3, with or without glucocorticoid replacement. Totally corticosteroid-deficient nonacidotic rats were capable of lowering their urine pH in response to Na2SO4 infusion from a baseline of 7.47 +/- 0.22 to 4.83 +/- 0.1 (p less than 0.001). A similarly intact ability to lower the urine pH was also demonstrated in glucocorticoid-replaced mineralocorticoid-deficient rats. Absolute ammonium excretion was lower in ADX animals compared to controls (0.79 +/- 0.08 vs. 0.46 +/- 0.06 microEq/min, p less than 0.01) but when corrected for the difference in GFR, ammonium excretion was the same in ADX and adrenal-intact rats. During bicarbonate loading and at similar blood and urine pH, and bicarbonate concentrations, the U-B pCO2 gradient was similar in mineralocorticoid-deficient and adrenal intact rats (44 +/- 5.1 vs. 36 +/- 2.6 mm Hg, respectively). Amiloride administration to mineralocorticoid-deficient rats led to a reduction in the U-B pCO2 gradient from 30 +/- 4.5 to 10 +/- 3.0 mm Hg (p less than 0.002). These results indicate that the ability to lower the urine pH and raise the urine pCO2 is intact in the nonacidotic ADX rat; ammonium excretion in this model is reduced in proportion to the observed reduction in GFR, and amiloride administration inhibits acidification in ADX rats. The data strongly suggest the presence of a major site of aldosterone-independent, sodium-dependent acidification mechanism likely located at the level of the cortical collecting tubule.

Acidosis↗

PubMed1986

Effect of a radiographic contrast agent on renal function in the rat. Comparison with equiosmolar mannitol.

The renal effects of the radiographic contrast agent meglumine iothalamate (Conray; C) were evaluated in rats. C produced a 42% fall in glomerular filtration rate (p less than 0.05) and a 44% fall in effective renal plasma flow (p less than 0.05). The effects of C were blunted by both acute and chronic volume expansion. Equiosmolar mannitol produced similar hemodynamic responses as C. The fractional excretions of sodium and potassium were similar in rats given C or mannitol. The renal effects of C appear to be due to its hypertonicity. These effects may be modified by volume expansion.

Animals↗

PubMed1985

Hyperkalemic renal tubular acidosis: effect of furosemide in humans and in rats.

Furosemide increases urinary acidification in control subjects and in certain patients with normokalemic or hypokalemic distal renal tubular acidosis (RTA). We studied the effect of furosemide in 14 patients with hyperkalemic distal RTA. In a group of patients with pure selective aldosterone deficiency, furosemide increased net acid and K excretion in a fashion indistinguishable from controls. This effect of furosemide was observed both in the presence and in the absence of acute mineralocorticoid administration. In another group of patients with hyperkalemic distal RTA, furosemide failed to decrease urine pH and to increase net acid excretion despite acute mineralocorticoid administration. Plasma aldosterone was variable in this group in that some patients had appropriate levels of aldosterone for the degree of hyperkalemia, whereas in the other patients the levels were low. The failure of these patients to respond to furosemide, despite pharmacologic doses of mineralocorticoid, suggests that these patients had a defect in H+ secretion other than that attributable to aldosterone deficiency alone. To gain insight into the mechanism whereby furosemide increases urinary acidification, we studied control and amiloride-treated rats pretreated with mineralocorticoid. In response to furosemide, control rats had a significantly lower urine pH and higher net acid and K excretion than that observed in amiloride-treated rats. These data suggest that furosemide increases H+ and K excretion, at least in part, by creating a favorable electric gradient for secretion of these ions since these effects were blunted in presence of inhibition of distal Na transport by amiloride.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗

PubMed1984

Renal handling of sodium and calcium in hypercalciuria.

The renal handling of Ca in response to Na intake was evaluated in 12 patients with hypercalciuria and active kidney stone disease. There was no depression of urinary Ca excretion in response to the hypocalciuric effect of metolazone. Patients were hospitalized and their Ca and Na excretions measured while on a 190-mEq Na, 800-mg Ca, 1200-mg PO4- diet. These measurements were then repeated after Na intake decreased to 35 mEq/day while other variables, including diuretic dose and Ca intake, were unchanged. Two distinct responses were elicited by patients after Na restriction. In group I or the "responders" (n = 4), Ca excretion was reduced from 255 +/- 31 to 62 +/- 6 mg/24 hr. In the control group (n = 4), Ca excretion decreased from 95 +/- 8 to 57 +/- 11 mg/24 hr at similar levels of Na excretion. In group II or the "nonresponders" (n = 8), Ca excretion fell from 317 +/- 31 to 154 +/- 17 mg/24 hr when Na excretion was less than 50 mEq/24 hr. Metolazone with Na restriction normalized urine Ca excretion to the same order as in control subjects in group I. This is indicative of a mild Ca leak or a salt-sensitive leak. Despite diuretic and Na restriction most of the patients with hypercalciuria (group II) did not reabsorb Ca in a normal manner. This is indicative of a severe reabsorptive defect for Ca despite normal Na handling.

Body Weight↗

PubMed1982

Metolazone therapy of active calcium nephrolithiasis.

Metolazone, a nonthiazide diuretic with the hypocalciuric effect of the thiazides, was evaluated in patients with idiopathic calcium nephrolithiasis. During the mean 3-yr treatment period, there was a 77% decrease in stone incidence in 38 male patients (from 2.10 to 0.49 stones/patient/year). Urine calcium decreased 51% (from 231 +/- 19 to 114 +/- 7 mg/24 hr after 13 mo therapy). The treatment response was the same when these patients were divided into normocalciuric (n = 23), borderline hypercalciuric (n = 10), and hypercalciuric groups (n = 5). In six other patients with high sodium intake there was no decrease in urine calcium on stone formers regardless of the initial level of urine calcium excretion. High sodium intake may blunt and low intake potentiate the hypocalciuric effect of metolazone.

Calcium↗

PubMed1982

Methyldopa: single daily dose versus multiple daily dose.

A single-blind, prospective, crossover study of 27 ambulatory hypertensive outpatients was conducted to compare the antihypertensive effects of single daily dose versus multiple daily dose methyldopa regimens. Patients were randomly assigned to the two treatment modalities for a four-week study period. After four weeks patients were crossed over to the other study regimen. Each patient's blood pressure was determined three times daily, once each week. At the end of the study both treatment modalities were equally effective in controlling blood pressure levels. No serious adverse reactions were detected. This study has shown that patients currently on divided daily doses of methyldopa can be effectively treated on a single total dose of the medication.

Adult↗

PubMed1981

Renin response to volume contraction and indomethacin in spontaneously hypertensive rats.

1. The effects of volume contraction and indomethacin on renin response were examined in spontaneously hypertensive rats and Wistar-Kyoto normotensive rats. Volume contraction was induced by frusemide or by salt-restricted diet combined with frusemide administration. 2. Plasma renin levels were not altered by either procedure in spontaneously hypertensive rats (5.2 +/- 0.8 versus 5.6 +/- 0.9 ng h-1 ml-1). Normotensive rats responded to volume contraction with a sharp increase in plasma renin activity (13.1 +/- 1.2 to 23.3 +/- 1.1 ng h-1 ml-1). 3. Intraperitoneal injection of indomethacin for 1 week did not alter basal renin levels in either group. In contrast, indomethacin pretreatment caused renin to rise in response to frusemide in spontaneously hypertensive rats (4.7 +/- 0.8 to 27.1 +/- 1.8 ng h-1 ml-1). 4. These findings suggest that a prostaglandin normally inhibits the renin response of spontaneously hypertensive rats to frusemide-induced volume contraction. Inhibition of prostaglandin synthesis allows volume contraction to stimulate renin release.

Animals↗

PubMed1981