The effect of long-term intake of 0.6% NaCl solution on survival of Brattleboro rats, both homozygous for diabetes insipidus (DI) and heterozygous (non-DI), was investigated. Studies included whether the survival of animals could be influenced a) by the age at which the high salt intake started (either from prepuberty, i.e. from the 4th week, or after sexual maturation, i.e. from the 12th week of age); b) by uninephrectomy (UNX) which elicited hypertension in DI rats drinking saline from youth. All non-DI and those DI rats that drank saline only from adulthood, survived for the whole duration of the experimental, i.e. 14 weeks. Only 43% of animals survived in the group of DI rats drinking saline from youth. This high mortality was reduced by UNX carried out either simultaneously or 8 weeks after the onset of saline drinking. DI rats consumed several times more saline than non-DI rats. Nevertheless, the consumption was greater in the low-mortality than in the high-mortality group. Salt intake was moderately lowered by UNX. Plasma Na+ concentration was higher in rats of the high-mortality group and it was not affected by UNX. In DI rats plasma volume was greater than in non-DI rats and its values in the low-mortality group exceeded those ones of the high-mortality group. It was decreased by UNX in the low-mortality group but this was not true for the high-mortality group. It is concluded that high mortality in DI rats consuming saline from prepuberty is abolished by the intervention producing hypertension. The role of hypertension in a protection against the toxic effects of salt is discussed.
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Cien Saude Colet
January 2025
Departamento de Epidemiologia e Métodos Quantitativos em Saúde, Escola Nacional de Saúde Pública Sergio Arouca, Fundação Oswaldo Cruz. Rio de Janeiro RJ Brasil.
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School of Food Science and Engineering, Chongqing Technology and Business University, Chongqing 400067, China.
Neuroinflammation plays an indispensable role in neural damages after ICH, responsible for the induced high mortality and poor prognosis. NLRP3 inflammasome, which is known mediated by ROS, has been widely documented to aggravate brain injuries. Therefore, suppressing neural injuries by ROS/NLRP3 pathway may be beneficial in treating ICH.
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