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  • Alternate Cl  (1)
  • Key words: Cerebral injury — Hypothermia — Cardiopulmonary bypass  (1)
  • 1
    ISSN: 1432-2013
    Keywords: Key words Brush-border ; Membrane vesicle ; Cystic fibrosis transmembrane regulator (cftr) ; Alternate Cl ; conductance
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstracts  Brush-border membrane vesicles (BBMV) were prepared from whole Balb/c mice kidneys by a Mg2+ precipitation technique. The presence of an intrinsic Cl–conductance co-expressed with Na+/glucose cotransport was inferred by the anion dependence of [14C]glucose uptake and overshoot with inward Na+-anion gradients. In Na+-equilibrated conditions, an inside-negative membrane potential difference (p.d.) produced by an inward Cl–gradient alone was capable of driving intravesicular [14C]glucose accumulation. The apparent anion conductance had a selectivity of Br– = I– = Cl– 〉  F–〉〉 gluconate, was inhibited by 0.5 mM 5-nitro-2- (3-phenylpropylamino)-benzoic acid (NPPB) but was unaffected by 0.5 mM 4,4′-diisothiocyanatostilbene 2,2′-disulphonate (DIDS). BBMV were isolated from mice in which the CFTR gene had been disrupted by a termination mutation (–/–) and compared with normal litter mates (+/+) and heterozygotes (–/+)[18]. [14C]Glucose uptake in NaCl media was significantly greater than glucose uptake in Na gluconate media for all three genotypes measured at 20 s: for homozygous –/– animals [14C]glucose uptake was increased by 2.80 ± 0.53 fold in Cl–media compared to gluconate media, n = 6; for wild-type +/+, by 2.16 ± 0.53 fold, n = 8; and for heterozygous +/– animals, by 2.17 ± 0.45 fold, n = 8. The observation of a Cl–-dependent component in BBMV isolated from homozygous –/– mutant animals shows that the chloride conductance in these vesicles cannot be due to cftr expression.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1971
    Keywords: Key words: Cerebral injury — Hypothermia — Cardiopulmonary bypass
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Choreoathetosis, seizures, and impaired mental development continue to occur in children undergoing cardiopulmonary bypass (CPB) and profound hypothermia with or without circulatory arrest. Although there is some evidence that the hypothermia itself may be causing these neurologic problems, skepticism remains because of lack of evidence from experimental studies simulating the clinical setting. In this experimental study, we examined the effect of profound and moderate hypothermia on the brain while maintaining normal flow rates during CPB. Ten adult mongrel dogs equally divided into two groups were anesthetized and subjected to CPB and varying levels of hypothermia (group 1, ≤15°C; group 2, ≤32°C). Both groups were kept at the desired temperature for 1 hour prior to rewarming and discontinuation of CPB. The dogs were euthanized 4–6 weeks later and neuropathologic studies were performed. The mean CPB flow rates during cooling and at the desired rectal temperature were comparable in both groups: group 1, 108 ± 10 ml/kg/min versus 106 ± 7 ml/kg/min in group 2 (p= NS) and 95 ± 12 ml/kg/min in group 1 versus 101 ± 5 ml/kg/min in group 2 (p= NS). Because of the difference in temperature between the two groups, the mean cooling time (onset of CPB to desired rectal temperature) was longer in group 1 (70 ± 14 minutes) than in group 2 (28 ± 11 minutes, p= 0.007). Hence, the total mean CPB time was also longer in group 1 (198 ± 25 minutes) than in group 2 (143 ± 13 minutes, p= 0.002). The lowest mean blood and rectal temperature achieved in group 1 were 11 ± .9°C and 12 ± 1°C versus 29 ± .4°C (p 〈 0.001) and 30 ± .6°C (p= 0.001), respectively, in group 2 (p= 0.001). Neuronal loss and degeneration was noted in all dogs in group 1 ranging from 2 to 8 cells per 1000 cells counted compared to none in group 2 (p= 0.05). These lesions occurred in both the basal ganglia and the cortex, although they were more marked in the caudate when compared to the cortex and cerebellum. Both in the cortex and in the caudate, neuronal loss was more marked around the capillaries. We conclude that the use of profound hypothermia of ≤15°C and maintenance of normal flow rates during cooling at this temperature for 1 hour produces neuronal loss and degeneration in the brain. These lesions being more marked around capillaries points to the vulnerability of the neurons, probably because of their high lipid content to injury from the cold perfusate.
    Type of Medium: Electronic Resource
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