Skeletal Muscle Metabolism in Uremic Rats: A &lt;sup&gt;31&lt;/sup&gt;P-Magnetic Resonance Study

Thompson, Campbell; Kemp, Graham J.; Green, Yvonne S.; Rix, Louise K.; Radda, George K.; Ledingham, J. G. G.

doi:10.1159/000187218

Cited by 7 publications

(4 citation statements)

References 19 publications

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“…How ever, it is reduced when measured in the presence of Hepes solution; this has to be intepreted as a consequence of depressed Na+/H + exchanger activity which is more directly demonstrated by a lesser decrease in the patient than in controls of pHj after exposure of lymphocytes to the specific Na+/H + exchanger inhibitor EIPA, and by a lower recovery rate from an induced intracellular acido sis. Normal pHj as indicated by HCO3/CO2 studies is in agreement with 31P-NMR studies in uremic rats [12] and men [9,10] showing that muscle cells maintain pH; within normal ranges despite extracellular metabolic acidosis. Using the same 31P-NMR technique, Monti et al [3] found a lower pHj in uremic HD patients; however, this study was performed in erythrocytes, in which pH; may be less tightly regulated, and more influenced by extracellu lar pH than in other nucleated body cells [25].…”

Section: Discussionsupporting

confidence: 85%

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Lymphocytic Intracellular pH and Na+/H+ Exchanger Activity in Hemodialysis Patients

Rombolà

Colussi²,

Guastoni³

et al. 1995

Am J Nephrol

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We have evaluated intracellular pH (pH_i) and Na⁺/H⁺ exchanger activity in peripheral lymphocytes from 16 patients on regular acetate hemodialysis. All the patients were taking oral NaHCO₃ supplementation (30 mmol/day), to maintain predialysis arterial blood acid-base status within normal range (pH 7.36 ± 0.02, P_HCO3- 23.3 ± 1.2 mM, pC0₂ 40.9 ± 1.4 mm Hg). pH_i was measured, using the fluorescent probe BCECF (2’,7’-bis-carboxyethyl-5,6-carboxyfluorescein), both in nominal absence of bicarbonate (Hepes solution, pH 7.4; n = 10) and in the presence of HCO₃^-/CO₂ buffer system (pH 7.4, [HCO₃^-] 25 mM, PCO₂ 40 mm Hg; n = 6). Predialysis pH_i did not differ from controls when measured in the presence of HCO₃^-/CO₂ (7.28 ± 0.04 vs. 7.29 ± 0.04, p = NS), but was lower in dialysis patients than in normal subjects (7.11 ± 0.04 and 7.20 ± 0.02, respectively; p < 0.05) when measured in Hepes solution. This suggested that bicarbonate-independent pH_i regulation was abnormal in dialysis patients. To further characterize this abnormality of pH_i regulation, lymphocytes were exposed to ethylisopropylamiloride, a specific Na⁺/H⁺ antiporter inhibitor, in Hepes solution; this maneuver induced a significantly lower decrement in pH_i (0.04 ± 0.04 vs. 0.15 ± 0.03, p < 0.05) in dialysis patients than in controls, indicating reduced Na⁺/H⁺ exchanger activity in the patients. The rate of pHi recovery during the first 30 s after induction of various degrees of cell acidification (pH_i range 6.2-7.0), which in the absence of HCO₃^-/CO₂ is dependent on Na⁺/H⁺exchanger activity, was also reduced in the patients as compared to controls (p < 0.001). These findings demonstrate depressed Na⁺/H⁺ exchanger activity in lymphocytes from patients on chronic maintenance hemodialysis; accounting for the lower pHi in Hepes solution. However, this abnormality does not prevent pH_i to be mainteined in the normal range in the presence of the physiological buffer HCO₃^-/CO₂ and possibly in vivo.

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Section: Discussionsupporting

confidence: 85%

“…However, other investigations in man [6][7][8][9][10] and in animals [1 1 , 1 2 ] have found normal pH; in uremia.…”

Section: Introductionmentioning

confidence: 99%

Lymphocytic Intracellular pH and Na+/H+ Exchanger Activity in Hemodialysis Patients

Rombolà

Colussi²,

Guastoni³

et al. 1995

Am J Nephrol

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“…Also, the end-of-exercise PCr consumption, when scaled to the total work output, was significantly higher in patients. Similarly to data previously reported in both humans and rats, the rates of both PCr degradation and glycogenolysis declined with time throughout exercise whereas oxidative contribution to ATP production increased so that ATP turnover became virtually all oxidative by five minutes of exercise (13,27).…”

Section: Discussionsupporting

confidence: 81%

Investigation of Muscle Bioenergetics in the Marfan Syndrome Indicates Reduced Metabolic Efficiency

Crilley¹,

Bendahan²,

Boehm³

et al. 2007

J. of Cardiovascular Magnetic Resonance

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“…Acute and chronic anemia are associated with increased arterial lactate concentrations for a given metabolic rate (18);and more specifically, graded reduction in [Hb] is associated with increased skeletal muscle lactate output during exercise (17). However, there are no differences in resting or exercise skeletal muscle pl-l, as a function of anemia in rat (19) or human (20). Finally, no relationship was found between [Hb] and either resting pl-l, or its threshold in the current study.…”

Section: Discussionmentioning

confidence: 99%

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

Evans

Al-Himyary²,

Hrovat³

et al. 1997

Am J Respir Crit Care Med

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Although lung transplantation improves exercise capacity by removal of a ventilatory limitation, recipients' postoperative maximum oxygen uptake (VO2max) remains markedly abnormal. To determine if abnormal skeletal muscle oxidative capacity contributes to this impaired aerobic capacity, nine lung transplant recipients and eight healthy volunteers performed incremental quadriceps exercise to exhaustion with simultaneous measurements of pulmonary gas exchange, minute ventilation, blood lactate, and quadriceps muscle pH and phosphorylation potential by 31P-magnetic resonance spectroscopy (31P-MRS). Five to 38 mo after lung transplantation, peak VO2 was decreased compared with that of normal control subjects (6.7 +/- 0.4 versus 12.3 +/- 1.0 ml/min/kg, p < 0.001), even after accounting for differences in age and lean body weight. Neither ventilation, arterial O2 saturation nor mild anemia could account for the decrease in aerobic capacity. Quadriceps muscle intracellular pH (pH(i)) was more acidic at rest (7.07 +/- 0.01 versus 7.12 +/- 0.01 units, p < 0.05) and fell during exercise from baseline values at a lower metabolic rate (282 +/- 21 versus 577 +/- 52 ml/min, p < 0.001). Regressions for pH(i) versus VO2, phosphocreatine/inorganic phosphate ratio (PCr/Pi) versus VO2, and blood lactate versus pH(i) were not different. Among transplant recipients, the metabolic rate at which pH(i) fell correlated closely with VO2max (r = 0.87, p < 0.01). The persistent decrease in VO2max after lung transplantation may be related to abnormalities of skeletal muscle oxidative capacity.

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Skeletal Muscle Metabolism in Uremic Rats: A <sup>31</sup>P-Magnetic Resonance Study

Cited by 7 publications

References 19 publications

Lymphocytic Intracellular pH and Na<sup>+</sup>/H<sup>+</sup> Exchanger Activity in Hemodialysis Patients

Lymphocytic Intracellular pH and Na<sup>+</sup>/H<sup>+</sup> Exchanger Activity in Hemodialysis Patients

Investigation of Muscle Bioenergetics in the Marfan Syndrome Indicates Reduced Metabolic Efficiency

Abnormal skeletal muscle oxidative capacity after lung transplantation by 31P-MRS.

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