Emerging roles of chloride channels in human diseases

Puljak, Livia; Kilic, Gordan

doi:10.1016/j.bbadis.2005.12.008

Cited by 59 publications

(68 citation statements)

References 122 publications

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“…In the rat brain at 4.7 Tesla T 1 and T 2 values of T 1 ¼ (40 AE 5) ms and T 2 ¼ (34 AE 2) ms are reported (31). For 35 Cl monoexponential signal decays and transversal relaxation times of T 2 ¼ 12.5-100 ms for Cl À in solutions with arginine, histidine, lysine and alanine are reported (17). Furthermore, monoexponential signal decays and T 2 times in the range of 22-30 ms are obtained for Cl À ions bound to proteins (cytochrome c) (19).…”

Section: Introductionmentioning

confidence: 97%

“…The performance of the rf coil setup and the MRI pulse sequence is demonstrated on a phantom, a healthy rat and on a rat displaying a focal cerebral infarction. To the best of our knowledge here we present the first in vivo 35 Cl images acquired with MRI and exemplary measurement of the T 1 and T 2 relaxation time in vivo.…”

Section: Introductionmentioning

confidence: 98%

“…In order to investigate the feasibility of combined in vivo 1 H, 23 Na and 35 Cl MRI we developed a rf coil setup to measure 1 H, 23 Na and 35 Cl signals in one scanning session without moving the subject or changing the setup. The performance of the rf coil setup and the MRI pulse sequence is demonstrated on a phantom, a healthy rat and on a rat displaying a focal cerebral infarction.…”

Section: Introductionmentioning

confidence: 99%

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In vivo chlorine‐35, sodium‐23 and proton magnetic resonance imaging of the rat brain

et al. 2010

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In this study we demonstrate the feasibility of combined chlorine-35, sodium-23 and proton magnetic resonance imaging (MRI) at 9.4 Tesla, and present the first in vivo chlorine-35 images obtained by means of MRI. With the experimental setup used in this study all measurements could be done in one session without changing the setup or moving the subject. The multinuclear measurement requires a total measurement time of 2 h and provides morphological (protons) and physiological (sodium-23, chlorine-35) information in one scanning session. Chlorine-35, sodium-23 and high resolution proton images were acquired from a phantom, a healthy rat and from a rat displaying a focal cerebral infarction. Compared to the healthy tissue a signal enhancement of a factor of 2.2 +/- 0.2 in the chlorine-35 and a factor of 2.9 +/- 0.6 in the sodium-23 images is observed in the areas of infarction. Exemplary unlocalized measurement of the in vivo longitudinal and transversal relaxation time of chlorine-35 in a healthy rat showed multi-exponential behaviour. A biexponential fit revealed a fast and a slow relaxing component with T(1,a) = (1.7 +/- 0.4) ms, T(1,b) = (25.1 +/- 1.4) ms, amplitudes of A = 0.26 +/- 0.02, (1-A) = 0.74 +/- 0.02 and T(2,a) = (1.3 +/- 0.1) ms, T(2,b) = (11.8 +/- 1.1) ms, A = 0.64 +/- 0.02, (1-A) = 0.36 +/- 0.02. Combined proton, sodium-23 and chlorine-35 MRI may provide a new approach for non-invasive studies of ionic regulatory processes under physiological and pathological conditions in vivo.

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Section: Introductionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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In vivo chlorine‐35, sodium‐23 and proton magnetic resonance imaging of the rat brain

et al. 2010

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“…Cellular Cl alterations due to dysfunctions in Cl channels result in a broad spectrum of diseases (Puljak and Kilic, 2006;Veizis and Cotton, 2007;Tang et al, 2010). Thus, conceptually, hyperchloremia caused by saline infusion cannot be viewed as normal.…”

Section: Hyperchloremia and Hyperchloremic Acidosis Are Abnormalmentioning

confidence: 99%

0.9% saline is neither normal nor physiological

Sun

Yap

et al. 2016

J. Zhejiang Univ. Sci. B

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Abstract:The purpose of this review is to objectively evaluate the biochemical and pathophysiological properties of 0.9% saline (henceforth: saline) and to discuss the impact of saline infusion, specifically on systemic acid-base balance and renal hemodynamics. Studies have shown that electrolyte balance, including effects of saline infusion on serum electrolytes, is often poorly understood among practicing physicians and inappropriate saline prescribing can cause increased morbidity and mortality. Large-volume (>2 L) saline infusion in healthy adults induces hyperchloremia which is associated with metabolic acidosis, hyperkalemia, and negative protein balance. Saline overload (80 ml/kg) in rodents can cause intestinal edema and contractile dysfunction associated with activation of sodium-proton exchanger (NHE) and decrease in myosin light chain phosphorylation. Saline infusion can also adversely affect renal hemodynamics. Microperfusion experiments and real-time imaging studies have demonstrated a reduction in renal perfusion and an expansion in kidney volume, compromising O 2 delivery to the renal parenchyma following saline infusion. Clinically, saline infusion for patients post abdominal and cardiovascular surgery is associated with a greater number of adverse effects including more frequent blood product transfusion and bicarbonate therapy, reduced gastric blood flow, delayed recovery of gut function, impaired cardiac contractility in response to inotropes, prolonged hospital stay, and possibly increased mortality. In critically ill patients, saline infusion, compared to balanced fluid infusions, increases the occurrence of acute kidney injury. In summary, saline is a highly acidic fluid. With the exception of saline infusion for patients with hypochloremic metabolic alkalosis and volume depletion due to vomiting or upper gastrointestinal suction, indiscriminate use, especially for acutely ill patients, may cause unnecessary complications and should be avoided. More education regarding saline-related effects and adequate electrolyte management is needed.

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“…17,18 Chloride has an important role in salt sensing and NT-proBNP, pg/mL 3000 (3000 to 5177) 3000 (2971 to 3000) 3000 (3000 to 4952) 3000 (3000 to 3622) 0.003 In-hospital thiazide diuretic use 29. ter Maaten et al Chloride in Acute Heart Failure seems to be the main driver in the kidney's ability to sense volume overload, because chloride-containing solutions, but not non-chloride-containing sodium solutions, elicited a response from the kidney. 4,5 Chloride has also been shown to reduce renin release, in contrast to non-chloride-containing sodium salts, which do not affect renin levels.…”

Section: Chloride and Response To Therapymentioning

confidence: 99%

Hypochloremia, Diuretic Resistance, and Outcome in Patients With Acute Heart Failure

Maaten

Damman²,

Hanberg

et al. 2016

Circ: Heart Failure

110

120

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Recently, 3 studies demonstrated a strong, independent association between hypochloremia and an increased risk of mortality in both acute and chronic heart failure. [9][10][11] Both of these studies demonstrated that the prognostic value of chloride was greater than that of sodium. These studies are however limited because of several factors, such as the use of a chronic heart failure cohort from the 1990s and cohorts that are not

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Emerging roles of chloride channels in human diseases

Cited by 59 publications

References 122 publications

In vivo chlorine‐35, sodium‐23 and proton magnetic resonance imaging of the rat brain

In vivo chlorine‐35, sodium‐23 and proton magnetic resonance imaging of the rat brain

0.9% saline is neither normal nor physiological

Hypochloremia, Diuretic Resistance, and Outcome in Patients With Acute Heart Failure

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