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Biomedical subjects

A I Arieff

Publications and source records attributed to A I Arieff.

At least 37 records · Page 2Linked to original sources
PubMed1996

Abnormalities of water metabolism in the elderly.

Hypernatremia is a frequent problem at the extremes of age, but particularly so in elderly individuals. Changes in the physiological responses to water deprivation with increasing age may be of particular interest in understanding the pathogenesis of hypernatremia in the elderly. When comparing healthy elderly men to younger controls, there are differences in the response to water deprivation. In older men, there are deficits in both the intensity and threshold of the thirst response. The ability to concentrate the urine also declines with age. There is both a decline in glomerular filtration rate and an increased incidence of renal disease with advancing age, which may contribute to impaired ability to conserve water. Because of a decrease in the percent total body water with age, equal volumes of fluid loss in young and old individuals may represent more severe dehydration in the elderly. Hyponatremia is seen in all age groups, but there are important differences in the elderly. When compared with postmenopausal women, menstruant (of childbearing age) women are over 25 times more likely to suffer permanent brain damage as a complication of hyponatremic encephalopathy. Furthermore, menstruant women suffer seizures or respiratory arrest at far higher levels of plasma sodium (110 to 130 mmol/L) than occurs in postmenopausal women (95 to 123 mmol/L).

Aged↗
PubMed1995

Age, gender, and vasopressin affect survival and brain adaptation in rats with metabolic encephalopathy.

Children and menstruant women are far more likely than men to develop metabolic brain damage from hyponatremia. We evaluated brain adaptation and mortality from hyponatremia in male and female rats of three different age groups. With acute hyponatremia, the mortality was 84% in prepubertal rats vs. 15% in adults and 0% in elderly rats. With chronic hyponatremia, mortality was 13% in adult males vs. 62% in females. Testosterone pretreatment significantly decreased mortality (from 62 to 9% in adult females, and from 100% to zero in prepubertal rats), but estrogen significantly increased mortality (from 13 to 44% in adult males). With acute hyponatremia in adult rats, brain sodium was significantly decreased (-17%), but in prepubertal rats it was actually increased (+ 37%). Cerebral perfusion during chronic hyponatremia was significantly impaired in adult females vs. males or controls (P < 0.01). Neither vasopressin administration nor chronic hyponatremia induced with desmopressin resulted in any mortality or decrement of cerebral perfusion. Thus age, gender, and the cerebral effects of vasopressin are major determinants of mortality in experimental metabolic encephalopathy.

Adaptation, Physiological↗
PubMed1995

Hormonal dependence of the effects of metabolic encephalopathy on cerebral perfusion and oxygen utilization in the rat.

Previous studies have demonstrated that in adult rats with chronic hyponatremia, both symptoms of encephalopathy and mortality largely depend upon the gender of the animal and the presence of elevated plasma levels of vasopressin (AVP). Since effects of AVP on blood vessels may be gender dependent, the present study was designed to compare the effects of chronic (4 days) hyponatremia on cerebral blood flow (CBF), cerebral oxygen consumption (CMRO2), and cerebral perfusion index (CPI) in adult male and female rats. CBF (intra-arterial 133Xe injection method) and CMRO2 (arteriovenous difference of cerebral oxygen contentxCBF) were measured in normonatremic and hyponatremic (hyponatremia induced with 140 mmol/L glucose and either AVP or desmopressin [dDAVP], plasma sodium = 100 to 110 mmol/L) adult rats of both genders. The CPI was assessed from magnetic resonance imaging of the transit of magnetic susceptibility contrast agent through the brain. Female rats with AVP-induced chronic hyponatremia had a 36% decrease in CBF and a 60% decrease in CMRO2. In male animals, both parameters were not different from control values. AVP-induced hyponatremia resulted in a 45% decrease in CPI in female rats, but hyponatremia induced with dDAVP did not affect CPI in either male or female rats. Chronic (4 days) administration of AVP did not affect CPI in either male or female normonatremic rats. When rats with AVP-induced chronic hyponatremia were pretreated with estrogen, the CPI in males was not different from that in females. Our results demonstrate that during AVP-induced chronic hyponatremia in female rats, there is significant depression of both oxygen utilization and blood flow in the brain.

Animals↗
PubMed1995

Pulmonary complications of hyponatremic encephalopathy. Noncardiogenic pulmonary edema and hypercapnic respiratory failure.

OBJECTIVE: To determine the causes of hypoxia in patients with hyponatremic encephalopathy. DESIGN: Retrospective cohort study. SETTING: Consultation and referral service of two university medical centers and community hospitals. PATIENTS: Forty adults with postoperative hyponatremic encephalopathy and hypoxia of whom 30 had noncardiogenic pulmonary edema and 10 had hypercapnic respiratory failure. MAIN MEASUREMENTS: We evaluated the chest radiographs and measured plasma electrolytes, arterial blood gas values, pulmonary artery pressure, pulmonary capillary wedge pressure (PCWP), cardiac output, and net fluid retention. RESULTS: Forty patients with hyponatremic encephalopathy had hypoxia (arterial PO2 below 70 mm Hg), of whom 30 had pulmonary edema and 10 had hypercapnia (PCO2 above 50 mm Hg). Among the 30 patients with pulmonary edema, the serum sodium (+/- SD) was 114 +/- 7 mmol/L, arterial pH was 7.24 +/- 0.16, PCO2 was 45 +/- 15 mm Hg, and PO2 was 42 +/- 16 mm Hg. The cardiac index was 3.6 +/- 0.4 L/min/M2, pulmonary artery pressure was 26/16 mm Hg, and PCWP was 12 +/- 6 mm Hg. There was pulmonary edema, with normal heart size. The hypoxic patients who did not have pulmonary edema had significant hypercapnia (PCO2 = 91 +/- 29 mm Hg, p < 0.001). CONCLUSIONS: Patients with postoperative hyponatremic encephalopathy can develop hypoxia by at least two different mechanisms: noncardiogenic pulmonary edema or hypercapnic respiratory failure.

Adult↗
PubMed1994

Mechanisms of brain injury associated with partial and complete occlusion of the MCA in cat.

High-speed MR diffusion/perfusion imaging was performed to assess variable degree stenosis of the MCA and the formation of cytotoxic edema in a cat model of acute ischemia. Sodium transport was estimated in synaptosomes isolated from moderately perfused or non-perfused brain tissue. Complete MCA occlusion for 50-75 min produced a major disruption of brain sodium transport, whereas continued preservation of ion homeostasis and the activation of adaptive cell volume regulatory systems was associated with longer duration of moderate severity of ischemia. Preservation of neuronal ion homeostasis might be one of the main mechanisms contributing to the relative tolerance of the brain to moderate reductions in cerebral blood flow.

Animals↗
PubMed1994

Severe brain edema associated with cumulative effects of hyponatremic encephalopathy and ischemic hypoxia.

Hyponatremia in cats produced brain edema, detectable by both magnetic resonance imaging (MRI) and increased brain water, with a compensatory decrease of brain sodium. Sodium transport was measured in synaptosomes from hyponatremic cat cerebral cortex. The sodium efflux via Na(+)-K(+)-ATPase was significantly higher (144%) than control, while sodium influx via the Na+/H+ antiporter was significantly decreased (74%). Both responses tend to decrease brain intracellular sodium and thus, brain cell osmolality. Ischemia following unilateral middle cerebral artery occlusion also resulted in brain edema. However, the efflux of sodium via both Na(+)-K(+)-ATPase and sodium channels actually decreased, both maladaptive responses. Furthermore, when ischemia was superimposed upon hyponatremia, all of the cerebral adaptive changes which had been induced by hyponatremia alone were rendered ineffective. This resulted in further elevations of brain water and sodium. Hyponatremia superimposed upon ischemia thus worsens the brain edema associated with ischemia alone. Thus, ischemia impairs the ability of the brain to adapt to hyponatremia, probably by eliminating the compensatory mechanisms of brain sodium transport initiated by hyponatremia.

Animals↗
PubMed1994

Vasopressin inhibits calcium-coupled sodium efflux system in rat brain.

Centrally released vasopressin plays an important role in the regulation of brain water and electrolyte composition and can affect brain intracellular pH and ATP synthesis in vivo. In this study, we evaluated the effects of [Arg8]vasopressin (AVP) on the Na(+)-Ca2+ exchanger, an important pathway in the regulation of cell Ca2+ concentration. It was found that AVP inhibited the Na(+)-Ca2+ exchanger in rat brain synaptosomes. This effect was completely blocked by the vasopressin V1-receptor antagonist d(CH2)5[(O-Me) Tyr2, Arg8]vasopressin. In addition, the vasopressin V2-receptor agonist 1-desamino-8-D-arginine vasopressin had no effect on the Na(+)-Ca2+ exchanger in rat brain synaptosomes. Depletion of intracellular Ca2+ by caffeine also had no effect on the effect of AVP on the Na(+)-Ca2+ exchanger. Na+ uptake by other pathways was also evaluated. It was found that AVP had no effect on Na+ uptake by pathways other than the Na(+)-Ca2+ exchanger. It is concluded that AVP inhibits the Na(+)-Ca2+ exchanger in neuronal membranes through vasopressin V1 receptors. Since this pathway is important in the regulation of cell volume and cytosolic Ca2+ in excitable tissue, AVP may impair neuronal cell repolarization in the central nervous system.

Animals↗
PubMed1994

Hypoxic and ischemic hypoxia exacerbate brain injury associated with metabolic encephalopathy in laboratory animals.

Hypoxemia is a major comorbid factor for permanent brain damage in several metabolic encephalopathies. To determine whether hypoxia impairs brain adaptation to hyponatremia, worsening brain edema, we performed in vitro and in vivo studies in cats and rats with hyponatremia plus either ischemic or hypoxic hypoxia. Mortality with hypoxic hypoxia was 0%; with hyponatremia, 22%; and with hyponatremia+hypoxia, 100%. Hyponatremia in cats produced brain edema, with a compensatory decrease of brain sodium. Ischemic hypoxia also resulted in brain edema, but with elevation of brain sodium. However, when ischemic hypoxia was superimposed upon hyponatremia, there was elevation of brain sodium with further elevation of water. Outward sodium transport in cat cerebral cortex synaptosomes was measured via three major pathways through which brain osmolality can be decreased. After hyponatremia, sodium transport was significantly altered such that brain cell osmolality would decrease: 44% increase in Na(+)-K(+)-ATPase transport activity (ouabain inhibitable); 26% decrease in amiloride-sensitive sodium uptake. The change in veratridine-stimulated sodium uptake was not significant (P > 0.05). When ischemic hypoxia was superimposed upon hyponatremia, all of the cerebral adaptive changes induced by hyponatremia alone were eliminated. Thus, hypoxia combined with hyponatremia produces a major increase in brain edema and mortality, probably by eliminating the compensatory mechanisms of sodium transport initiated by hyponatremia that tend to minimize brain swelling.

Amiloride↗
PubMed1994

Metabolic encephalopathy as a complication of renal failure: mechanisms and mediators.

Among patients with end-stage renal disease, nervous system dysfunction remains a major cause of disability. Patients with chronic renal failure who have not yet received dialysis may develop symptoms ranging from mild sensorial clouding to delirium and coma. Dialysis itself is associated with at least three distinct disorders of the CNS: dialysis disequilibrium syndrome; dialysis dementia; and progressive intellectual dysfunction. Peripheral neuropathy is also a major cause of disability in uremic subjects. It is believed that aluminum contributes to the pathogenesis of dialysis dementia. Biochemically, brain calcium is elevated in patients with renal failure, probably because of actions of parathyroid hormone on the brain. The diagnosis of dialysis disequilibrium syndrome, intellectual dysfunction, dialysis dementia, and uremic neuropathy can be made by the characteristic clinical pictures of these syndromes and the exclusion of other causes of nervous system dysfunction.

Animals↗
PubMed1994

Safety and efficacy of intravenous Carbicarb in patients undergoing surgery: comparison with sodium bicarbonate in the treatment of mild metabolic acidosis. SPI Research Group. Study of Perioperative Ischemia.

OBJECTIVES: To compare the safety and efficacy of intravenous Carbicarb with intravenous sodium bicarbonate in well-oxygenated patients who developed metabolic acidosis while undergoing major surgery. Carbicarb is an equimolar solution of sodium bicarbonate and sodium carbonate (Na2CO3). It does not undergo significant breakdown to CO2 and H2O, nor does it increase CO2 concentrations to the same extent as does pure sodium bicarbonate. Because of these characteristics, Carbicarb may be a more suitable agent than bicarbonate in the treatment of metabolic acidosis. DESIGN: Prospective, double-blind, randomized, multicenter trial. SETTING: Veterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco), and the University of Massachusetts Medical Center, Worcester, MA. PATIENTS: We prospectively studied 36 patients who underwent either cardiac surgery or major noncardiac surgery and developed intraoperative metabolic acidosis (pH < 7.35 and whose serum bicarbonate concentration decreased by > 3 mmol). INTERVENTIONS: Patients were randomly assigned to receive either sodium bicarbonate (1 mEq sodium/mL, n = 18) or 1 mol Carbicarb (1 mEq sodium/mL, n = 18) administered by intravenous bolus over a 30-sec period. MEASUREMENTS AND MAIN RESULTS: For Carbicarb-treated patients, the mean arterial pH increased from 7.31 +/- 0.008 (baseline) to 7.36 +/- 0.009 10 mins after treatment; for the sodium bicarbonate-treated patients, the mean pH increased from 7.31 +/- 0.006 to 7.37 +/- 0.01. The increases in pH were statistically significant for both groups (p = .0001). There was no statistically significant difference between treatment groups in the number of repetitions of initial dose that was required to correct acidosis. Hemodynamic variables remained unchanged in both treatment groups during the study period, with the exception of the mean cardiac output which increased from 6.1 +/- 0.4 (baseline) to 6.9 +/- 1.4 L/min (60 mins after treatment) in a subset of Carbicarb-treated patients and decreased from 6.7 +/- 1.3 to 6.0 +/- 1.2 L/min in a subset of sodium bicarbonate-treated patients, p = .048 (between groups); and the mean pulmonary artery occlusion pressure decreased from 19 +/- 2 mm Hg (baseline) to 8 +/- 3 mm Hg (45 mins after treatment) in the Carbicarb-treated patients, and decreased from 18 +/- 2 to 13 +/- 4 mm Hg in the sodium bicarbonate-treated patients, p = .012 (between groups). Systemic utilization of lactate increased from 0.3 +/- 1.0 mmol/min (baseline) to 5.6 +/- 4.3 mmol/min (45 mins after treatment) in Carbicarb-treated patients, and increased from 1.0 +/- 0.6 mmol/min (baseline) to 1.5 +/- 1.3 mmol/min in the sodium bicarbonate-treated patients, p = .033 (between groups). The administration of Carbicarb was safe. No patients were discontinued from the study because of adverse events. CONCLUSIONS: Carbicarb corrects metabolic acidosis as well as sodium bicarbonate. However, the potential therapeutic advantage of Carbicarb remains to be determined, especially in patients with more severe metabolic acidosis.

Acidosis↗
PubMed1993

Endometrial ablation complicated by fatal hyponatremic encephalopathy.

OBJECTIVES: To investigate the occurrence of hyponatremic encephalopathy and the effects of therapy for symptomatic hyponatremia on outcome in women undergoing endometrial ablation. DESIGN AND SETTING: Consultations from university-affiliated and community hospitals from June 1991 to June 1992. PATIENTS: Four generally healthy women who underwent elective endometrial ablation for dysfunctional bleeding and developed hyponatremic encephalopathy. INTERVENTIONS: Three patients were promptly treated with hypertonic (514 mmol/L) sodium chloride such that the serum sodium level increased from 102 to 123 mmol/L within 24 hours. The fourth patient was not treated until after suffering grand mal seizures followed by respiratory arrest. MAIN OUTCOME MEASURES: Of the four patients who developed hyponatremic encephalopathy, the diagnosis was established before respiratory arrest occurred in three. The operative procedure was terminated and all three were aggressively treated with intravenous hypertonic sodium chloride, which raised the serum sodium level to modestly hyponatremic levels (120 to 130 mmol/L). All three completely recovered without sequelae. The fourth patient suffered respiratory arrest before therapy could be initiated. The patient remained comatose, and central diabetes mellitus and insipidus developed. She never regained consciousness and died after several days. Autopsy revealed cerebral edema and tonsillar herniation. RESULTS: The mean (+/- SD) preoperative serum sodium level was 138 +/- 1 mmol/L; at the time of diagnosis of hyponatremia, it was 107 +/- 13 mmol/L. In two patients, hyponatremic encephalopathy was diagnosed intraoperatively because of tremulousness and either hypothermia or hypoxemia. In the other two patients, the diagnosis was made postoperatively because of headache, nausea, emesis, and in one of these patients, respiratory arrest. CONCLUSIONS: Women undergoing elective endometrial ablation can develop severe symptomatic hyponatremia, which can be fatal. The presence of symptoms suggesting hypo-osmolality should lead to immediate measurement of plasma sodium level. If hyponatremia with hypo-osmolality is present, early and appropriate therapy for the hyponatremia should be instituted before respiratory insufficiency occurs.

Adult↗