PubMed Health⌕ Search

Biomedical subjects

H J Adrogué

Publications and source records attributed to H J Adrogué.

At least 19 recordsLinked to original sources
PubMed2001

Acid-base physiology.

Acid-base homeostasis involves chemical and physiologic processes responsible for the maintenance of the acidity of body fluids at levels that allow optimal function of the whole individual. The chemical processes represent the first line of defense to an acid or alkali load and include the extracellular and intracellular buffers, whereas the physiologic processes modulate acid-base composition by changes in cellular metabolism and by adaptive responses in the excretion of volatile acids by the lungs and fixed acids by the kidneys. The need for the existence of multiple mechanisms involved in acid-base regulation stems from the critical importance of the hydrogen ion (H+) concentration on the operation of many cellular enzymes and function of vital organs, most prominently the brain and the heart. The task imposed on the mechanisms that maintain acid-base homeostasis is large, since metabolic pathways are continuously consuming or producing H+, and the daily load of waste products for excretion in the form of volatile and fixed acids is substantial. We review the determinants of the acidity of body fluids, the mechanisms that maintain normal acid-base composition, and the overall defense to disruption in acid-base equilibrium. Specific topics include an examination of the scales of acidity, buffer systems, intracellular acid-base regulation, excretion of acids, alkali and acid loading, and normal acid-base composition. The limitations of arterial blood sampling in the assessment of acid-base status are also evaluated.

Acid-Base Equilibrium↗
PubMed2000

Hyponatremia.

Explore the source record for details and available documents.

Female↗
PubMed2000

Hypernatremia.

Explore the source record for details and available documents.

Female↗
PubMed1998

Low dialysate [K+] decreases efficiency of hemodialysis and increases urea rebound.

In a previous study, it was reported that hemodialysis with dialysate [K+] (KD) of 1.0 or 2.0 mmol/L caused an increase in BP shortly after completion of treatment due to arteriolar constriction. With this background, it was hypothesized that a low KD might decrease dialysis efficiency by a similar mechanism. To evaluate this hypothesis, paired observations of two consecutive 3-h treatments, with KD of 1.0 or 3.0 mmol/L, were performed in 14 stable end-stage renal disease patients. A KD of 1.0 mmol/L resulted in lower values for both urea reduction ratio and Kt/V evaluated at completion of dialysis and 1 h thereafter. Values at equilibrium were urea reduction ratio 42+/-1% versus 47+/-2% (P < 0.02), Kt/V 0.65+/-0.03 versus 0.73+/-0.03 (P < 0.02) for KD 1.0 or 3.0 mmol/L, respectively. The mechanisms responsible for the observed differences in dialysis efficiency were examined using a urea kinetics model that predicts urea sequestration caused by impaired blood flow to urea-rich tissues. For this purpose, urea rebound and its effect on Kt/V (by means of deltaKt/V, calculated as equilibrated minus single pool value) with KD 1.0 and 3.0 mmol/L were assessed. Greater urea rebound, 12.8+/-1.6% versus 8.6+/-1.4% (P < 0.001), and larger deltaKt/V, 0.12+/-0.01 versus 0.10+/-0.02 (P < 0.02), were observed with KD 1.0 mmol/L compared with 3.0 mmol/L. The theoretical model accurately predicted the deltaKt/V observed with KD 1.0 mmol/L. It is concluded that a low KD decreases dialysis efficiency. This effect is likely caused by reduced blood perfusion to nonvisceral organs, largely skeletal muscle. Conversely, hemodialysis with KD 3.0 mmol/L facilitates tissue perfusion, minimizes urea trapping in poorly perfused areas, and improves the efficiency of this treatment modality.

Blood Urea Nitrogen↗
PubMed1997

Aiding fluid prescription for the dysnatremias.

OBJECTIVE: The goal of the present study was to develop a novel approach that facilitates the prescription of fluid therapy in patients with abnormal serum sodium concentration. METHODOLOGY AND RESULTS: The novel approach is based on a simple equation, derived from established principles on the distribution of sodium in body fluids, that estimates the impact of a unit dose, i.e., 1 l of any infusate on the patient's serum sodium concentration. In accordance with the equation, the expected change in the patient's serum sodium concentration in response to 1 l of any infusate (delta[Na+]s) is obtained by subtracting the sodium concentration of the patient's serum from the sodium concentration of the infusate, each expressed in mEq/l, and dividing the result by the patient's estimated total body water expressed in liters (adding 1 l to account for the volume of the infusate). The amount of the particular infusate to be administered over the course of any given time period can be easily computed by dividing the desired delta[Na+]s at the end of the period by the calculated delta[Na+]s effected by 1 l of the infusate. The utility and limitations of the proposed approach are presented. CONCLUSIONS: The novel equation is not a means for formulating therapy. Rather, it provides, simply and expeditiously, quantitative projections that can assist the physician in implementing the selected treatment plan for patients with dysnatremias.

Algorithms↗
PubMed1996

Inappropriately high plasma renin activity accompanies chronic loss of renal function.

Stimulation of both the systemic and local renin-angiotensin systems participates in the pathogenesis of tissue injury observed in experimental renal disease. However, substantial information demonstrating excessive activation of the renin-angiotensin system in patients with chronic renal disease is not available in spite of the well-established role of this system in the progression of renal damage. This investigation examined the plasma renin activity (PRA) and the ratio of this parameter to the simultaneously measured glomerular filtration rate (PRA/GFR) in normal volunteers (mean values 3.2 ng/ml/h and 3.0 ng/ml/h/100 ml GFR, respectively) and in patients with chronic renal disease (1.6 ng/ml/h and 28.5 ng/ml/h/100 ml GFR, respectively). A mean tenfold increase in the PRA/GFR ratio was observed in patients with chronic renal disease as compared to normal volunteers. The observed augmentation in PRA was not caused by physiologic mechanisms aimed at conserving urinary sodium since a positive correlation was found between PRA/GFR and the fractional excretion of sodium (y = 2.75 + 2.23x; r = 0.781, p < 0.01), as opposed to that of normal controls (y = 5.3 - 1.46x; r = -0.640, p < 0.01). Consequently, our results support the existence of inappropriate activation of the renin-angiotensin system in humans with chronic renal disease. Such stimulation might play a critical role in the pathophysiology of advanced renal injury.

Adult↗
PubMed1996

Role of dietary factors in the hypertension of African Americans.

Epidemiological and experimental data suggest that dietary constituents are among the causative factors that contribute to the higher prevalence and severity of hypertension in African Americans as compared with European Americans. Given the difficulty of cleanly separating a change in one dietary nutrient from concomitant changes in others, it has been difficult to reliably attribute an observed effect on blood pressure level and hypertension prevalence to the specific dietary constituent under study. Nevertheless, because hypertension is virtually nonexistent in societies whose dietary sodium chloride intake is very low, it appears that a sodium chloride intake in excess of that required to maintain adequate extracellular fluid volume is necessary but not sufficient for hypertension to be manifest. Additional factors are clearly necessary in the development of hypertension because most individuals, including African Americans, can ingest a high sodium chloride diet without developing hypertension. Evidence for the potential importance of other dietary constituents is also discussed, as are dietary strategies that effectively reduce blood pressure in hypertensive individuals. The data presented support the need for continued research into dietary constituents as potential factors contributing to the etiology of hypertension, as well as effective adjuncts to the management of this very common health problem.

Black or African American↗
PubMed1995

Acute decreases in serum potassium augment blood pressure.

Potassium depletion is a risk factor for cardiovascular diseases, including hypertension, and frequently is encountered in patients with end-stage renal disease. Since the treatment of end-stage renal disease might result in K+ depletion and postdialysis hypokalemia, we investigated the relationship between acute K+ removal by hemodialysis and changes in blood pressure at the completion of treatment compared with predialysis and 1-hour postdialysis blood pressure. The effects of three different dialysate potassium concentrations ([K+]d; 1.0, 2.0, and 3.0 mmol/L) were investigated in 11 patients. Hemodialysis-induced K+ removal, serum [K+], total body K+, and blood pressure were measured. The use of 1.0, 2.0, or 3.0 mmol/L [K+]d resulted in the removal of 77.0 +/- 6.5, 54.5 +/- 7.9, and 42.5 +/- 9.9 mmol of K+ per treatment, respectively (P < 0.05, [K+]d 1.0 v [K+]d 3.0). Predialysis and postdialysis serum [K+] were 4.9 +/- 0.2 and 3.6 +/- 0.1 mEq/L for 1.0 mmol/L [K+]d, 5.1 +/- 0.3 and 3.9 +/- 0.1 mEq/L for 2.0 mmol/L [K+]d, and 5.3 +/- 0.3 and 4.2 +/- 0.2 mEq/L for 3.0 mmol/L [K+]d, respectively (P < 0.001 for each [K+]d). The baseline total body K+ corrected for gender, age, and race was 92% of predicted normal level and did not change significantly with the use of different [K+]d. Blood pressure decreased during hemodialysis as excess fluid was removed, regardless of [K+]d. Significant increases in blood pressure did occur 1 hour postdialysis compared with levels measured at the completion of treatment ("rebound hypertension") when hemodialysis was performed with 1.0 and 2.0 mmol/L, but not with 3.0 mmol/L [K+]d.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1995

Vascular relaxation probably mediates the antihypertensive effect of a high-potassium diet: a role for enhanced vascular Na,K-ATPase activity.

OBJECTIVE: to evaluate the effect of dietary potassium on blood pressure and vascular contractility in adult rats of two strains, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats. DESIGN: 'Potassium-induced relaxation' was evaluated in aortic rings as a functional measure of Na,K-ATPase activity in the vascular wall. The rats were fed one of three diets: regular (American Institute of Nutrition-76 rat chow); high-sodium (7% sodium chloride) or high-sodium plus potassium (7% sodium chloride and 13.4% potassium citrate) for 12 +/- 1 weeks. RESULTS: SHR fed the high-sodium diet had a mean blood pressure of 157 +/- 8 mmHg, as compared with 130 +/- 9 mmHg for those on a regular diet (P < 0.01). SHR fed the potassium-supplemented diet had a blood pressure of 122 +/- 9 mmHg (P < 0.01 versus the high-sodium diet group). The mean blood pressure of WKY rats was 78 +/- 3 mmHg and did not differ among the dietary groups. The 'potassium-induced relaxation' response of aortic rings from SHR and WKY rats fed a potassium-supplemented diet was significantly higher (P < 0.05) than that in animals in the corresponding high-sodium dietary group. This observation in potassium-supplemented rats is interpreted as indicative of increased Na,K-ATPase activity in the vascular wall. CONCLUSIONS: A potassium-rich diet in SHR receiving a high sodium intake was associated with lower blood pressure and higher vascular Na,K-ATPase activity. A similar effect of this diet on vascular Na,K-ATPase was observed in WKY. We propose that the antihypertensive effect of a potassium-rich diet is mediated, at least in part, by stimulation of vascular Na,K-ATPase activity.

Animals↗
PubMed1994

Identification of GTP-binding proteins in turtle urinary bladder epithelial cells.

Water and electrolyte transport in turtle urinary bladder closely resembles that present in the mammalian collecting tubule. Although cAMP is known to participate in the control of mucosal transport processes, the GTP-binding inhibitory Gi and stimulatory Gs proteins which link receptors on the cell surface to the adenylate cyclase system remain to be identified in this urinary epithelium. To this end, individual cells harvested from the mucosal surface of the turtle bladder were isolated using a discontinuous density Ficoll gradient. Examination by electron microscopy of the material from the different layers of the Ficoll gradient confirmed that bands II and III contained carbonic anhydrase-rich cells and granular cells, respectively. Identification of Gi and Gs in carbonic anhydrase-rich and granular cells was accomplished using pertussis (PT) and cholera toxins to promote [32P] ADP ribosylation of the proteins. Separation of Gi and Gs from other cell proteins was accomplished using polyacrylamide gel electrophoresis and autoradiography. Pretreatment of cells with 0.2% triton X-100 substantially magnified the ADP-ribosylation of Gi by PT. A doublet form of Gi was present in the 40-kD region and indicated heterogeneity of the PT substrate in granular and carbonic anhydrase-rich cells. Gs was observed as a single polypeptide at the 42-kD region in both cell types. A distinct 45-kD peptide not present in mammalian collecting tubule was identified by both toxins in granular cells and by cholera toxin in carbonic anhydrase-rich cells. In summary, this investigation identified and characterized Gi and Gs proteins in carbonic anhydrase-rich and granular cells from the mucosa of turtle urinary bladder.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylate Cyclase Toxin↗
PubMed1993

Demonstration of an apical chloride conductive pathway in granular cells of toad urinary bladder.

Chloride electrodiffusion across the apical membrane of granular cells from toad urinary bladder, an analogue of mammalian principal cells, was examined using the patch clamp technique. A chloride conductance was demonstrated in cell-attached membrane patches exposed to barium chloride pipette solutions. A change in the pipette chloride concentration from 30 to 100 mM caused a shift in the current voltage curve which demonstrated chloride selectivity. The chloride conductance was also examined in excised, inside out membrane patches using choline chloride solutions (chloride:choline selectivity ratio was 18:1). A closed and two open chloride conductive states were found (states A and B, 10.1 +/- 1.0 and 17.2 +/- 5.5 pS, respectively, p < 0.01). Incubation of the preparation with arginine vasopressin, dibutyryl-cAMP, or 8-bromo-cAMP approximately doubled chloride conductance to 16.6 +/- 1.7 pS (p < 0.01). The enhanced electrodiffusion was accounted for by a shift in the channel kinetics from the closed state C to the high conductance state B (p < 0.05, n = 9). 4,4'-Diisothio-cyanatostilbene- 2,2'-disulfonic acid (DIDS) and 9-anthracene-carboxylic acid (9-AC) failed to block the chloride currents. In conclusion, the regulated apical chloride conductance described would balance the sodium and potassium electrodiffusive pathways and maintain a stable membrane potential, facilitating overall conductive transport by these cells.

Animals↗
PubMed1990

Influence of acute and chronic respiratory alkalosis on preexisting chronic metabolic alkalosis.

The severity of the alkalemia produced by a reduction in arterial carbon dioxide tension (PaCO2) in normal humans and animals is ameliorated by buffer and renal responses that diminish the levels of plasma bicarbonate concentration ([HCO3-]p). These adjustments have even greater potential importance in preventing extreme degrees of alkalemia when hypocapnia occurs in the presence of an initially elevated [HCO3-]p (mixed respiratory and metabolic alkalosis). The aim of the present study was to characterize the acute (approximately 3 h) and chronic (5 days) acid-base effects of respiratory alkalosis when superimposed on chronic metabolic alkalosis. Ten dogs were made alkalotic by the repeated administration of ethacrynic acid and the provision of a chloride-restricted diet. Hypocapnia (delta PaCO2 = 10 mmHg) was then superimposed by exposing the animals to 11% O2 in an environmental chamber. A large fall in [HCO3-]p occurred in the acute hypocapnic phase that was further augmented in the chronic phase; the corresponding delta [HCO3-]p/delta PaCO2 slopes were 0.43 and 0.71 meq.l-1.mmHg-1, respectively, values substantially larger than those previously reported for hypocapnia in normals as well as in animals with preexisting HCl acidosis. Hyperlactatemia was responsible, on average, for 43% of the decrement in [HCO3-]p during acute hypocapnia but for only 20% of the delta [HCO3-]p during the chronic phase of the study. The striking decrement in [HCO3-]p observed in response to the chronic reduction in PaCO2 was sufficient not only to prevent the development of extreme alkalemia but also to offset entirely the effect of hypocapnia on plasma [H+].

Acute Disease↗
PubMed1989

Salutary effects of modest fluid replacement in the treatment of adults with diabetic ketoacidosis. Use in patients without extreme volume deficit.

The optimal rate of fluid administration to correct the volume deficit associated with diabetic ketoacidosis remains undefined. Thus, this study evaluates prospectively in adult patients without extreme volume deficit two regimens of therapy that differed exclusively in the rate of fluid infusion. In protocol 1 (12 patients), normal saline was infused at 1000 mL/h (approximately 14 mL/kg per hour) in the initial 4 hours and 500 mL/h (approximately 7 mL/kg per hour) during the subsequent 4 hours. In protocol 2 (11 patients), normal saline was infused at half the rates of protocol 1. For plasma bicarbonate level, the increment from admission levels at 2, 4, 8, 16, and 24 hours after admission was greater with protocol 2 at all times, attaining a statistically significant difference at 4 hours (3.7 vs 0.7 mmol/L) and at 24 hours (13.2 vs 8.4 mmol/L). These data support cautious restraint in the volume of fluid replacement used in the therapy of diabetic ketoacidosis, since prompt recovery, lack of any harmful effects, and a significant reduction in the overall cost of medical therapy are achieved with lower rates of saline infusion.

Adult↗
PubMed1989

Assessing acid-base status in circulatory failure. Differences between arterial and central venous blood.

To assess arteriovenous differences in acid-base status, we measured the pH and partial pressure of carbon dioxide (PCO2) in blood drawn simultaneously from the arterial and central venous circulations in 26 patients with normal cardiac output, 36 patients with moderate and 5 patients with severe circulatory failure, and 38 patients with cardiac or cardiorespiratory arrest. The patients with normal cardiac output had the expected arteriovenous differences: venous pH was lower by 0.03 unit, and venous PCO2 was higher by 0.8 kPa (5.7 mm Hg). These differences widened only slightly in those with moderate cardiac failure. Additional simultaneous determinations in mixed venous blood from pulmonary arterial catheters were nearly identical to those in central venous blood. In the five hypotensive patients with severe circulatory failure there were substantial differences between the mean arterial and central venous pH (7.31 vs. 7.21) and PCO2 (5.8 vs. 9.0 kPa [44 vs. 68 mm Hg]). Large arteriovenous differences were present during cardiac arrest in patients whose ventilation was mechanically sustained, whether sodium bicarbonate had been administered (pH, 7.27 vs. 7.07; PCO2, 5.8 vs. 8.6 kPa [44 vs. 65 mm Hg]) or not (pH, 7.36 vs. 7.01; PCO2, 3.7 vs. 10.2 kPa [28 vs. 76 mm Hg]). By contrast, in patients with cardiorespiratory arrest, large arteriovenous differences were noted only when sodium bicarbonate had been given (pH, 7.24 vs. 7.01; PCO2, 9.5 vs. 16.9 kPa [71 vs. 127 mm Hg]). We conclude that both arterial and central venous blood samples are needed to assess acid-base status in patients with critical hemodynamic compromise. Although information about arterial blood gases is needed to assess pulmonary gas exchange, in the presence of severe hypoperfusion, the hypercapnia and acidemia at the level of the tissues are detected better in central venous blood.

Acid-Base Equilibrium↗