Bicarbonate reabsorption in chronic renal failure studies in man and the rat.
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Absorption↗
Biomedical subjects
L Nascimento
Publications and source records attributed to L Nascimento.
Metolazone and spironolactone in cirrhosis and the nephrotic syndrome.
Eighteen patients with hepatic cirrhosis or nephrotic syndrome and having edema and/or ascites were treated during successive periods with metolazone 5 to 40 mg/day, spironolactone 100 mg/day, and with both diuretics concurrently. Metolazone alone produced a marked diuresis, natriuresis, and weight loss in 8 patients. Spironolactone alone had little effect, but the addition of metolazone renewed diuresis and natriuresis and resulted in additional substantial weight losses in all patients responsive to metolazone alone. Concurrent spironolactone and metolazone also induced moderate diuretic effects in some patients who failed to respond to either drug alone. The drugs were well tolerated; the administration of spironolactone with metolazone prevented decreases in serum potassium, which had occurred during treatment with metolazone alone.
Adult↗
Factors influencing the formation of urinary carbon dioxide tension.
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Aldosterone↗
Effect of parathyroid hormone on urinary acidification.
The effect of parathyroid hormone (PTH) administration on urinary acidification was studied in intact and thyroparathyroidectomized dogs. PTH administration resulted in a significant increase in urine pH and HCO3 excretion. In dogs with maximally acid urine caused by Na2SO4 infusion PTH administration also led to a significant increase in urine pH and to a decrease in ammonium excretion. To examine the effect of PTH on H+ secretion in the distal nephron we measured the urine-blood (U-B) PCO2 gradient in dogs with maximally alkaline urine (urine pH greater than 7.8) before and after PTH administration. After infusion of the hormone, HCO3 excretion increased significantly but the U-B PCO2 gradient remained unchanged. The effects of PTH infusion on urinary acidification in animals with distal renal tubular acidosis caused by LiCl administration were also studied. PTH administration to these dogs increased HCO3 excretion to the same level seen in normal dogs. These data suggest that PTH does not inhibit distal H+ secretion but increases HCO3 excretion by depressing proximal HCO3 reabsorption.
Acid-Base Equilibrium↗
The critical importance of urinary concentrating ability in the generation of urinary carbon dioxide tension.
Measurement of urine to blood (U-B) carbon dioxide tension (P(CO2)) gradient during alkalinization of the urine has been suggested to assess distal H(+) secretion. A fact that has not been considered in previous studies dealing with urinary P(CO2) is that dissolution of HCO(3) in water results in elevation of P(CO2) which is directly proportional to the HCO(3) concentration. To investigate the interrelationship of urinary HCO(3) and urinary acidification, we measured U-B P(CO2) in (a) the presence of enhanced H(+) secretion and decreased concentrating ability i.e., chronic renal failure (CRF), (b) animals with normal H(+) secretion and decreased concentrating ability, Brattleboro (BB) rats, and (c) the presence of both impaired H(+) secretion and concentrating ability (LiCl treatment and after release of unilateral ureteral obstruction). At moderately elevated plasma HCO(3) levels (30-40 meq/liter), normal rats achieved a highly alkaline urine (urine pH > 7.8) and raised urine HCO(3) concentration and U-B P(CO2). At similar plasma HCO(3) levels, BB rats had a much higher fractional water excretion and failed to raise urine pH, urine HCO(3) concentration, and U-B P(CO2) normally. At a very high plasma HCO(3) (>50 meq/liter), BB rats raised urine pH, urine HCO(3) concentration, and U-B P(CO2) to the same levels seen in normals. CRF rats failed to raise urine pH, urine HCO(3), and U-B P(CO2) normally at moderately elevated plasma HCO(3) levels; at very high plasma HCO(3) levels, CRF rats achieved a highly alkaline urine but failed to raise U-B P(CO2). Dogs and patients with CRF were also unable to raise urine pH, urine HCO(3) concentration, and U-B P(CO2) normally at moderately elevated plasma HCO(3) levels. In rats, dogs, and man, U-B P(CO2) was directly related to urine HCO(3) concentration and inversely related to fractional water excretion. At moderately elevated plasma HCO(3) levels, animals with a distal acidification defect failed to raise U-B P(CO2); increasing the plasma HCO(3) to very high levels resulted in a significant increase in urine HCO(3) concentration and U-B P(CO2). The observed urinary P(CO2) was very close to the P(CO2) which would be expected by simple dissolution of a comparable amount of HCO(3) in water. These data demonstrate that, in highly alkaline urine, urinary P(CO2) is largely determined by concentration of urinary HCO(3) and cannot be used as solely indicating distal H(+) secretion.
Acid-Base Equilibrium↗
On the mechanism of lithium-induced renal tubular acidosis.
The effect of lithium chloride administration on urinary acidification was studied in dogs. Lithium-treated dogs developed hyperchloremic metabolic acidosis with alkaline urine. Bicarbonate loading resulted in a normal increase in urinary Pco2 in normal dogs but failed to produce the same response in lithium-treated dogs. The bicarbonate titration curve of lithium-treated dogs revealed a small leak of bicarbonate at low plasma levels of bicarbonate; at high plasma levels bicarbonate reabsorption was significantly higher in lithium-treated dogs. This pattern of bicarbonate reabsorption is identical to that described in classic distal renal tubular acidosis. Sodium sulfate administration resulted in a normal urinary acidification ilithium-treated dogs. It is possible that lithium administration induces distal renal tubular acidosis by allowing excessive back-diffusion of acid. This excessive back-diffusion of acid would result in a low urinary Pco2 during bicarbonate loading. Sodium sulfate administration, by increasing the negative intratubular potential, would restrict back-diffusion of hydrogen ion and thereby result in a normal acidification in lithium-treated dogs. We previously demonstrated that postureteral obstruction of the kidney fails to increase urinary Pco2 during bicarbonate loading and to lower urinary pH with sodium sulfate. It is possible that a low urinary Pco2 during HCO3 loading can occur as a consequence of either diminished hydrogen ion secretion (postobstructed kidney) or excessive back-diffusion of acid (lithium administration). Further studies are indicated to determine whether both mechanisms may be found in patients with distal renal tubular acidosis.
Absorption↗
Effect of acetazolamide and parathyroid hormone on HCO3 and PO4 excretion.
It has been recently demonstrated that parathyroid hormone (PTH) inhibits renal cortical carbonic anhydrase. Based on this in vitro study, it was suggested that PTH depresses proximal reabsorption of phosphate and bicarbonate reabsorption in vivo by inhibiting carbonic anhydrase. To test this hypothesis, we measured bicarbonate and phosphate excretion in four groups of dogs. Group I received PTH for 2 hours; group II received acetazolamide for 2 hours; group III received PTH for 2 hours and acetazolamide in the 2nd hour; and in group IV, acetazolamide was given for 2 hours with PTH ADDED IN THE 2ND HOUR. Acetazolamide administration resulted in maximal bicarbonate excretion in the 1st hour and maximal phosphate excretion in the 2nd hour. Addition of acetazolamide to animals receiving PTH or addition of PTH to animals receiving acetazolamide resulted in additional increases in bicarbonate and phosphate excretion. These data demonstrate that PTH induces bicarbonate and phosphate excretion regardless of whether carbonic anhydrase is intact or nearly 100% inhibited by acetazolamide. These data do not support the hypothesis that PTH inhibits bicarbonate and phosphate reabsorption by inhibiting carbonic anhydrase.
Acetazolamide↗
The response of the human Fallopian tube to ergonovine and methyl-ergonovine in vivo.
Ergonovine maleate (EM) is a powerful stimulant of human tubal motility. It has been therefore thought that EM could interfere with normal ovum transport and serve as a contraceptive. The tube activating effects of EM and methyl EM were evaluated in 14 women and results confirmed that both are powerful stimulants of the human Fallopian tube. EM immediately post coitus significantly reduces the conception rate.
Ergonovine↗
Distribution of renal blood flow in dogs with congestive heart failure.
Studies were performed to determine whether the intrarenal distribution of cortical blood flow is altered in congestive heart failure. Utilizing the radioactive microsphere method, we studied eight dogs that developed congestive heart failure secondary to the construction of an aortocaval fistula. They had marked reduction in total renal blood flow not accompanied by intracortical redistribution of blood flow. All dogs had developed edema and/or ascites, and gained a mean of 3.4 kg; glomerular filtration rate, hematocrit, and urinary sodium excretion fell significantly. Renal vascular resistance increased; mean blood pressure and filtration fraction were unchanged. Furosemide was administered to a second group of nine fistula dogs. The drug produced a marked natriuresis associated with a decrease in outer cortical blood flow (zone 1) and an increase in midcortical zones 2 and 3; no change was observed in zone 4. We conclude: 1) chronic salt retention occurs in high-output heart failure in the absence of redistribution of renal cortical blood flow, and 2) the effect of furosemide on intrarenal hemodynamics of dogs with heart failure is similar to that seen in normal animals.
Animals↗
Lithium administration and phosphate excretion.
The phosphaturic effect of parathyroid hormone (PTH), cyclic adenosine monophosphate (cAMP), acetazolamide (Az), and HCO3 loading was studied in normal, thyroparathyroidectomized (TPTX), and Li-treated dogs. PTH administration to normal animals markedly increased fractional excretion (F) of PO4 but had a blunted effect on FPO4 in the Li-treated animals. Cyclic AMP likewise markedly increased FPO4 in the normal animals but had a markedly blunted effect in the Li-treated animals. Az led to a significant increase in FNa, FHCO3, and FPO4 in the normal animals. In the Li-treated dogs, Az induced a significant natriuresis and bicarbonaturia but failed to increase phosphaturia. HCO3 loading in normal dogs caused a significant phosphaturia while having little effect on FPO4 in Li-treated dogs. HCO3 loading to TPTX dogs was associated with a lower FPO4 as compared to normal HCO3-loaded animals. These data suggest that Li administration not only blocks the adenyl cyclase-cAMP system in the renal cortex, but it may also interfere with a step distal to the formation of cAMP, since the phosphaturic effect of both PTH and cAMP was markedly diminished in Li-treated animals.
Acetazolamide↗
[Late-presenting congenital diaphragmatic hernia: a possible cause of sudden respiratory distress in children]
OBJECTIVE: To emphasize that congenital defects of the diaphragm should be considered in the differential diagnosis of sudden onset of respiratory distress in children. MATHOD: Two illustrative cases of children (aged 2 years) with late presenting congenital diaphragmatic hernia who developed sudden respiratory distress and were managed at the University Hospital of Santa Maria are reported. The medical literature was reviewed to identify cases reports and other articles related to late presenting congenital diaphragmatic hernia. A computerized search was performed using the MEDLINE data base to identify papers published within the last 25 years. RESULTS: In both cases the initial clinical examination and plain chest X-rays were misinterpreted as another pleuropulmonary disease like pneumothorax/pneumatoceles. One of the children underwent to emergency chest tube placement without clinical improvement. The absence of respiratory symptoms that could justify this kind of pathology motivated a more careful investigation, involving fiberoptical endoscopy and intestinal seriography. This subsequent investigation revealed that the cause was late-presenting congenital diaphragmatic hernia. CONCLUSION: Although many congenital diaphragmatic hernias that present late have a history of chronic respiratory symptoms, some of them present with acute symptoms. A higher degree of attention is required to avoid confusion with other intrathoracic conditions, such as pneumatoceles and pneumothorax, if an incorrect diagnosis is to be avoided. Misinterpretation of the radiographs is likely if the possibility of a congenital diaphragmatic hernia is not considered, and may result in increased morbidity. Gastric atony may occur in the early postoperative period.
Journal Article↗
[Heart failure at an internal medicine department: a retrospective study].
The files of 222 patients (112 men) admitted to a Medical Department (Medicina 1) of the Hospital de Santa Maria (Lisbon) between 1/1/87 and 21/6/88 with the diagnosis of congestive heart failure (CHF) were studied retrospectively. The next parameters were considered: sex, age, cause of cardiac disease, duration of CHF, presence of diabetes, predispondent factors of CHF episodes, cardiac rhythm and blood pressure on admission, presence of rales, ascitis and edema, echocardiographic findings and evolution. Ischemic heart disease (IHD) (50%) and hypertensive heart disease (HHD) (31%) were the most frequent causes of CHF in this study. The mean age was 70 years, being higher in women (74 versus 66 years). Men were predominant in the younger groups. The rheumatic heart disease (RHD) group had the lowest mean age (54) while the cardiac diseases of unknown origin had the highest mean age (79). Patients with RHD were those with longer CHF (16 years) while patients with IHD, idiopathic cardiomyopathy and cor pulmonale had a shorter duration of CHF (less than 5 years). The respiratory infection was the most frequent predisponent factor (40%). In a high number of cases (31%) it was not possible to find the presumable cause of the CHF episode. Atrial fibrillation was the predominant disarrhythmia (44%) on admission, specially in patients with RHD. Patients with HHD isolated or associated to other causes were those with higher initial blood pressure. Echocardiographic studies were suggestive that HHD can be associated with CHF without a significant increase in left atrium and ventricle dimensions nor impairment of left ventricle systolic function. Echocardiographic analysis of larger numbers of patients and the study of left ventricular diastolic function and Doppler flow patterns will eventually contribute to a better understanding of CHF physiopathology.
Adult↗