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Biomedical subjects

A P Quintanilla

Publications and source records attributed to A P Quintanilla.

At least 19 recordsLinked to original sources
PubMed1994

Unilateral renal papillectomy via laser or incisional techniques: chronic functional effects in the dog.

OBJECTIVE: To determine if selective renal papillectomy would impair urinary concentrating ability, thereby decreasing urinary calcium concentration. METHODS: Left papillectomy was performed in dogs using either incisional (n = 6) or Neodymium:yttrium-aluminum-garnet (Nd:YAG) laser (n = 5) techniques. Split renal function studies were then performed four months postoperatively to determine the effect on multiple parameters including inulin and para-aminohippurate (PAH) clearance, free water reabsorption, and calcium concentrations. Partially infarcted kidneys (n = 6) were evaluated in a similar fashion to determine the role of impaired glomerular filtration rate (GFR) in the observed concentrating defect occurring after papillectomy. RESULTS: Papillectomized kidneys demonstrated impaired free water reabsorption, resulting in a decreased urinary osmolality and an increased fractional excretion of water. Osmolar clearance [Na+] and Na+ excretion were unaffected by papillectomy, whereas [Ca++] was significantly reduced. While a slight defect in free water reabsorption existed following partial infarction, urinary osmolality was only minimally decreased, fractional excretion of water was unchanged, and Na+ excretion was decreased. CONCLUSIONS: The concentrating defect induced by papillectomy via either sharp excision or laser ablation is due to loss of medullary tissue and is greater than the defect resulting from impaired GFR, which is presumably due to decreased medullary solute delivery and increased flow of water in remaining nephrons. Since the physiologic consequences of papillectomy (formation of less concentrated urine with decreased [Ca++]) have potential clinical applicability, further study of this concept is warranted.

Animals↗
PubMed1990

Diuretics and cation transport in hypertensive blacks.

Thiazide diuretics are particularly efficacious in the treatment of hypertension in blacks. A number of observations suggest that many hypertensive blacks have features consistent with a status of "corrected" volume expansion. Our studies, as well as those of other investigators, show that the Na,K pump is inhibited in leucocytes and erythrocytes of blacks with essential hypertension. This observation is also consistent with the concept of volume expansion in hypertensive blacks, since the Na,K pump is inhibited in many forms of experimental volume expansion, including the administration of salt in normal humans. We postulate that the efficacy of thiazide diuretics may be related to their ability to stimulate the Na,K pump. We present data obtained in 13 black hypertensive men in whom Na efflux, and Na,K-ATPase in the erythrocyte rose significantly after 7 days of treatment with hydrochlorothiazide, 50 mg/day. Diuretic therapy may indirectly result in reduced intracellular calcium in the vascular smooth muscle.

Benzothiadiazines↗
PubMed1989

Stimulation of erythrocyte and renal Na+,K+-adenosine triphosphatase activity by antidigoxin antibody in normal rats.

1. A circulating ouabain-like factor which inhibits the Na+,K(+)-pump has been implicated in volume-expanded states. To assess the role of this putative factor in normovolaemic rats, we measured erythrocyte and renal Na+,K(+)-adenosine triphosphatase activity after the infusion of a mixture of high-affinity digoxin-binding Fab fragments (Digibind) capable of removing digoxin from pump sites. 2. Compared with either saline (vehicle) or sheep immunoglobin G, infusion of the antidigoxin antibody caused a moderate increase of Na+,K(+)-adenosine triphosphatase activity in the erythrocyte (saline 348 +/- 12; immunoglobulin G 339 +/- 16; antidigoxin antibody 432 +/- 22 nmol h-1 mg-1; P less than 0.005 by analysis of variance) and a larger increase in the renal cortex (saline 9.7 +/- 0.9; immunoglobulin G 9 +/- 1.4; antidigoxin antibody 24.3 +/- 1.8 mumol h-1 mg-1; P less than 0.0005 by analysis of variance) without a change in blood pressure. 3. These results are consistent with the presence of a digoxin-like inhibitor of the Na+,K+-pump in normal rats.

Animals↗
PubMed1988

Effect of high salt intake on sodium, potassium-dependent adenosine triphosphatase activity in the erythrocytes of normotensive men.

1. We measured ouabain-insensitive adenosine triphosphatase (ATPase), sodium, potassium-dependent adenosine triphosphatase (Na+,K+-ATPase) and intracellular Na+ and K+ in the erythrocytes of 19 healthy volunteers, before and after supplementation of their normal diet was 6.0-8.9 g of salt (102-137 mmol of NaCl) per day, for 5 days. 2. The subjects had a small but significant gain in weight. Mean plasma renin activity decreased from 1.57 to 0.73 pmol of angiotensin 1 h-1 ml-1 and plasma aldosterone from 0.46 to 0.24 nmol/l. 3. Total ATPase activity fell from 197.9 nmol of inorganic phosphate h-1 mg-1 during the control period to 173.5 during the high-salt period (P less than 0.0125). Na+, K+-ATPase activity fell from 162.2 to 141.4 nmol of inorganic phosphate h-1 mg-1 (P less than 0.05). Intracellular Na+ and intracellular K+ did not change. 4. These results are consistent with the hypothesis that salt-induced volume expansion causes the release of a factor inhibitory to the Na+ pump.

Adult↗
PubMed1987

Effect of treatment with hydrochlorothiazide on the red cell Na,K-adenosine triphosphatase in men with hypertension.

We studied the effect of hydrochlorothiazide, 50 mg daily, on Na,K-adenosine triphosphatase (ATPase) activity in the red cells of 10 black men with hypertension. We also examined net sodium and potassium movement in sodium-loaded, potassium-depleted, red cells. Treatment with hydrochlorothiazide resulted in a significant increase in mean ouabain-sensitive ATPase activity (+/- SEM) from 118.4 +/- 14.6 to 158.1 +/- 15.3 nmol phosphate released per milligram of protein (P = 0.0004). Ouabain-resistant ATPase did not change. Net sodium extrusion rose significantly, from 1.62 +/- 0.27 to 2.32 +/- 0.33 mmol/L/hr (P = 0.0275). We postulate that the enhanced activity of the Na,K pump results from the volume contraction induced by the diuretic. This interpretation is consistent with the concept that the Na,K pump is inhibited in volume expansion and volume-expanded hypertension. The finding of enhanced pump activity in subjects given treatment with hydrochlorothiazide suggests a possible mechanism of the antihypertensive action of diuretic therapy.

Adult↗
PubMed1986

Na-K-adenosine triphosphatase and cation content in the erythrocyte in essential hypertension.

We measured ouabain-sensitive and ouabain-resistant Na-K-adenosine triphosphatase (ATPase) activity in the red cells of 25 normotensive (average mean blood pressure [BP] 90.2 +/- 1.27 mm Hg) and 29 hypertensive subjects (average mean BP 115.3 +/- 2.45 mm Hg). Intracellular Na and K content were measured in 13 of the normotensive and 19 of the hypertensive subjects. All subjects were male, black, of comparable weight, and had not received antihypertensive medications for at least 30 days. Ouabain-sensitive ATPase activity was found significantly lower in the hypertensive than in the control group (140.2 +/- 11 and 97.6 +/- 7.6 nmol/mg/hr, respectively, P = 0.0008), whereas no significant difference in ouabain-insensitive ATPase was observed. Intracellular Na concentration was higher (9.47 vs. 7.24 mmol/L, P = 0.0144), and intracellular K concentration lower (82.8 vs. 88.8 mmol/L, P = 0.0425) in the hypertensive subjects. These results are consistent with diminished activity of the Na-K pump in black males with essential hypertension who have received no treatment.

Blood Pressure↗
PubMed1984

Effect of acute changes in serum digoxin concentration on renal digoxin clearance.

The effect of acute alterations of serum digoxin concentration (S DIG) on the renal clearance of digoxin (C DIG) was studied in six normal subjects undergoing water diuresis. Digoxin in a 5% dextrose and water solution was infused at a rate of 0.01 microgram/kg/min (low dose). One hour after the infusion began, three 20-min urine samples for clearance determination were taken. The digoxin infusion rate was then increased to 0.05 microgram/kg/min (high dose) and three additional urine samples were taken an hour later. With low doses of digoxin, the S DIG was (means +/- SD) 0.63 +/- 0.08 ng/ml, C DIG was 252.3 +/- 65.1 ml/min, inulin clearance (C IN) was 96.8 +/- 15.7 ml/min, the ratio C DIG/C IN was 2.59 +/- 0.38, and renal blood flow (C PAH) was 516 +/- 90 ml/min. With the high-dose infusion, S DIG rose to 3.23 +/- 0.44 ng/ml; C IN, C DIG, C DIG/C IN, and C PAH remained stable. C DIG correlated strongly with both C IN and C PAH. We conclude that in normal subjects undergoing water diuresis, C DIG/C IN is not altered by acutely increasing S DIG, digoxin is extensively secreted by the nephron, and C DIG is linearly related to renal plasma flow.

Adult↗
PubMed1984

Uremic myopathy.

Explore the source record for details and available documents.

Atrophy↗
PubMed1983

Cardiac and renal responses to cross-clamping of the descending thoracic aorta.

The present study was performed to document the relative efficacy of commonly applied techniques used adjunctively during 1 hour of descending thoracic aortic cross-clamping. Renal and cardiac responses were determined by standard laboratory methods. There were four experimental groups: (1) heparin-bonded shunt; (2) partial femoral-femoral bypass; (3) sodium nitroprusside; (4) control. Each of the experimental groups showed abnormal hemodynamic responses during cross-clamping. Elevations in left ventricular end-diastolic pressure (LVEDP) and systolic blood pressure were common events during clamping, and cardiac output often decreased. Nevertheless, left ventricular performance curves after cross-clamping showed similar increases in left ventricular stroke work (LVSW) with increasing preload. In addition, left ventricular biopsy specimens showed preservation of myocardial high-energy phosphate stores and essentially normal ultrastructural integrity. Radioactive microspheres generally showed increased myocardial blood flow during and after cross-clamping, but no evidence of preferential subendocardial ischemia. Examination of renal function showed a marked decrease in urine output, glomerular filtration rate, and renal plasma flow during cross-clamping. Following the release of the cross-clamp, renal function returned to 50% to 85% of baseline status. Since we could find no major advantage of any of the techniques employed under the present experimental conditions, we suggest that all of the techniques should be part of the surgical armamentarium and the particular preoperative and/or intraoperative findings in a specific case should determine which technique is most appropriate for a given patient.

Adenosine Triphosphate↗
PubMed1983

Muscle in chronic uremia--a histochemical and morphometric study of human quadriceps muscle biopsies.

This report describes qualitative and quantitative studies performed on ten muscle biopsies from chronic uremic patients on renal dialysis at light and electron microscopic (EM) levels. The muscle biopsies showed myopathic changes (variation in fiber size, central nuclei, and fiber splitting). Histochemical studies showed type II fiber atrophy and lipid deposits. The ultrastructural study showed disruption of myofibrillary architecture and subsarcolemmal deposits of glycogen, mitochondria, and lipids. Quantitative estimations of the subcellular organelles revealed a statistically significant increase in lipid and glycogen contents of the muscle. The myopathic changes, type II atrophy, and lipid and glycogen deposits in chronic uremic patients raise the question of the effects of uremia and/or chronic dialysis on muscle metabolism.

Adult↗
PubMed1982

Effect of quinidine on the renal clearance of digoxin in the presence of low and high serum digoxin concentrations.

The effect of an infusion of quinidine, 180 micrograms/kg/Min (base) on the fractional clearance of digoxin (CDIG/Cin) was studied in saline volume-expanded dogs given a constant infusion of digoxin of either 0.0067 micrograms/kg/min (low dose) or 0.120 micrograms/kg/min (high dose). CDIG/CIN decreased 28% from 1.42 +/- 0.36 during control periods to 1.01 +/- 0.03 (P less than .05) with quinidine in dogs given the low dose. In dogs given the high dose of digoxin, CDIG/CIN decreased 22% from 0.76 +/- 0.17 to 0.59 +/- 0.05 (p less than .05) with quinidine. It is concluded that quinidine reduces CDIG/CIN. High doses of digoxin also reduce CDIG/CIN. Inasmuch as quinidine reduces CDIG/CIN to the same extent in the presence of low or high dose digoxin, the effect of quinidine would appear to be mediated through a mechanism different from that of digoxin.

Animals↗
PubMed1981

Effect of volume expansion and furosemide diuresis on the renal clearance of digoxin.

The effect of volume expansion with normal saline and 10% mannitol and increasing urine flow rate with furosemide on the fractional renal clearance of digoxin (CDIG/CIN) was studied in dogs given a constant infusion of digoxin of 0.010 micrograms/kg/min. With saline and mannitol volume expansion CDIG/CIN increased from 0.58 +/- 0.33 (S.D) and 0.54 +/- 0.14, respectively, to 1.28 +/- 0.14 and 1.13 +/- 0.22, respectively (P less than .005), as urine flow increased from 0.5 to 24 ml/min. With furosemide urine flow increased from 0.5 to 22 ml/min but CDIG/CIN remained constant at 0.63 +/- 0.18. We concluded that volume expansion but not urine flow rate substantially increases CDIG/CIN. We speculate that digoxin is at least partially, it not entirely, reabsorbed passively in the proximal tubule.

Animals↗
PubMed1980

Renal tubular acidosis: mechanisms and management.

Renal tubular acidosis is not one entity but several. Even though all its forms are characterized by the kidney's inability to excrete an appropriately acid urine, the mechanism of the defect, its laboratory and clinical manifestations, and its management vary considerably. One type can cause disabling complications in various organ systems, while another is generally asymptomatic. Differential diagnosis is straightforward, and treatment effective.

Acidosis, Renal Tubular↗
PubMed1980

The renal clearance of digoxin is dependent upon the serum digoxin concentration.

The effect of alterations of serum digoxin concentrations on the renal clearance of digoxin (CDIG) was studied in seven dogs. Digoxin, 0.016 microgram/kg/min (low dose) in normal saline was infused at the rate of 1 ml/min. After 60 min of equilibration, five 15-min urine collections were made. The digoxin infusion was then increased to 0.112 microgram/kg/min (high dose) and five additional collections were made after equilibration. Digoxin was measured by 125I radioimmunoassay whose specificity was confirmed by high-pressure liquid chromatography. With low dose digoxin, the serum digoxin concentration was 0.5 +/- 0.2 (S.D.) ng/ml, CDIG 58 +/- 26 ml/min, inulin clearance (CIN) 48 +/- 8 ml/min and CDIG/CIN 1.2 +/- 0.5. With high dose infusion, the serum digoxin concentration rose to 5.2 +/- 1.4 ng/ml, CDIG decreased 43% to 33 +/- 13 ml/min and CDIG/CIN decreased 48% to 0.6 +/- 0.2 (P < .05 for both compared to control, while CIN remained constant. We conclude that CDIG is not as dependent upon glomerular filtration as previously thought. Increases in serum digoxin concentrations can significantly reduce CDIG without altering glomerular filtration rate.

Animals↗