Effects of acetazolamide on cerebrospinal fluid ions in metabolic alkalosis in dogs

1987 ◽  
Vol 62 (4) ◽  
pp. 1582-1588 ◽  
Author(s):  
S. Javaheri

We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cisternal CSF [Na+] remained relatively constant during metabolic alkalosis. In group I CSF [Cl-] decreased 3.6 and 8.2 meq/l, respectively, 2.5 and 5 h after induction of metabolic alkalosis. Respective increments in CSF [HCO3-] were 3.4 and 6.0 meq/l. In acetazolamide-treated dogs, during metabolic alkalosis, increments in CSF [HCO3-] (4.8 and 7.2 meq/l, respectively, at 2.5 and 5 h) and decrements in CSF [Cl-] (9.1 and 13.3 meq/l) were greater than those observed in group I. We conclude that, in dogs with metabolic alkalosis and bilateral ligation of renal pedicles, acetazolamide impairs CSF regulation of HCO3- and Cl- ions; acetazolamide not only failed to impede HCO3- rise but actually appeared to increase it. The mechanisms for these observations are discussed.

Author(s):  
H.O. Soloviova

The adaptation of late premature babies to the new life conditions is difficult and requires careful monitoring of all vital parameters in the postnatal period. The general immaturity of the newborns in combination with the metabolic and hypoxic disorders "leaves only a narrow corridor" to develop babies their compensatory possibilities. There is an urgent need to investigate posthypoxic myocardial ischemia in newborns due to the fact that in the neonatal period, early diagnosis and correct treatment can prevent long-term adverse consequences of existing disorders. The aim of this study was to develop an approach for early detection of cardiac rhythm disturbances and conduction disorders in late premature infants, who underwent perinatal hypoxia. A single-center study included 93 late premature babies who were born at the Perinatal Center, Poltava, in 2019 – 2020. Group I consisted of newborns (n ​​= 47) with hypoxic-ischemic damage of the central nervous system; group II included premature babies (n = 46) with hypoxic-hemorrhagic damage of the central nervous system. Long-term monitoring of the electrocardiogram was performed with further conversion of the altered QRST-QRST complexes into 2D format with a multi-coloured representation of all components of the ventricular electrical systole. Among heterotopic cardiac arrhythmias, supraventricular extrasystoles were most often recorded in 89.4 ± 4.8% of the children of group I and in 67.4 ± 6.1% of newborns in group II with daytime distribution in both groups. Ventricular extrasystoles were found as significantly more frequent in newborns of group I (21.3 ± 6.3%) compared with children in group II (10.9 ± 6.1%), with a significant increase in the area of ​​ectopic ventricular complexes (1492.2) that indicates a prolonged depolarization process. The study of the bioelectrical activity of the heart based on the findings obtained by monitoring the electrocardiogram with the qualitative and quantitative analysis of the convertible QRST-QRST complexes increases the efficiency of visual diagnosis of electrical instability of the myocardium in late premature infants with perinatal damage of the central nervous system.


1986 ◽  
Vol 61 (2) ◽  
pp. 633-639 ◽  
Author(s):  
S. Javaheri ◽  
J. Kennealy ◽  
C. D. Runck ◽  
R. G. Loudon ◽  
M. B. Pine ◽  
...  

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.


PEDIATRICS ◽  
1963 ◽  
Vol 31 (6) ◽  
pp. 1024-1027
Author(s):  
Audrey E. Evans

Fifty lumbar punctures were performed on each of three groups of leukemic children. The three categories studied were (1) those with central nervous system manifestations, (2) those free of symptoms following effective treatment, and (3) those not yet having developed central nervous system symptoms. The patients in Group I all had abnormal cerebrospinal fluid. Those examined before or between episodes referable to the central nervous system had normal findings, with rare exceptions. Positive results in the patients without symptoms almost always indicated the early recurrence of central nervous system symptoms.


1996 ◽  
Vol 40 (3) ◽  
pp. 825-826 ◽  
Author(s):  
S Jaruratanasirikul ◽  
R Hortiwakul ◽  
T Tantisarasart ◽  
N Phuenpathom ◽  
S Tussanasunthornwong

To measure the concentrations of azithromycin in the central nervous system, 20 patients with brain tumors (group I) received a single 500-mg oral dose of azithromycin either 24, 48, 72, or 96 h prior to the tumor removal operation and 10 patients with cataracts undergoing surgery (group II) and 7 patients scheduled to undergo lumbar puncture (group III) received the same dose of azithromycin 24 h prior to the operation or procedure. Serum from all patients, brain tissue from group I, aqueous humor from group II, and cerebrospinal fluid from group III were assayed for azithromycin concentration. The mean concentrations of azithromycin in brain tissue 24, 48, 72, and 96 h after administration were 2.63 +/- 2.58, 3.64 +/- 3.81, 0.74 +/- 0.37, and 0.41 micrograms/g, respectively. In contrast, the concentrations of azithromycin in cerebrospinal fluid and aqueous humor of the eye were very low or undetectable. Therefore, these data show that azithromycin appears to be widely distributed into brain tissue but not into cerebrospinal fluid or aqueous humor of the eye.


Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.


Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Petr Kelbich ◽  
Aleš Hejčl ◽  
Jan Krejsek ◽  
Tomáš Radovnický ◽  
Inka Matuchová ◽  
...  

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.


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