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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Cardiovascular and respiratory outcome of preconditioned rats submitted to chronic intermittent hypoxia

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Author(s):
Perim, Raphael R. [1] ; Bonagamba, Leni G. H. [1] ; Machado, Benedito H. [1]
Total Authors: 3
Affiliation:
[1] Univ Sao Paulo, Sch Med Ribeirao Preto, Dept Physiol, BR-14049900 Ribeirao Preto, SP - Brazil
Total Affiliations: 1
Document type: Journal article
Source: Experimental Physiology; v. 100, n. 9, p. 1008-1017, SEP 1 2015.
Web of Science Citations: 8
Abstract

New Findings What is the central question of this study? What are the effects of hypoxic preconditioning upon the cardiovascular and respiratory responses to subsequent episodes of chronic intermittent hypoxia? What is the main finding and its importance? The cardiovascular and respiratory responses to a chronic intermittent hypoxia protocol were not altered by previous exposure to intermittent or sustained hypoxia. These findings show that preconditioning to hypoxia produced neither facilitation nor protection from the cardiovascular and respiratory dysfunctions in response to subsequent episodes of chronic intermittent hypoxia in juvenile rats. Rats exposed to chronic intermittent hypoxia (CIH) develop hypertension, which is associated with changes in the coupling of sympathetic and respiratory activities. In this study, we hypothesized that previous preconditioning to intermittent or sustained hypoxia would affect cardiovascular and respiratory changes produced by subsequent protocols of CIH. To test this hypothesis, male Wistar rats were preconditioned to either 10days of CIH or 24h of sustained hypoxia (SH). After the initial exposure to hypoxia, rats were maintained in normoxic conditions for 15days before a new protocol of CIH during 10days. Cardiovascular and respiratory variables obtained from groups of preconditioned rats were compared with a group of rats exposed to CIH for the first time and also to a group of rats maintained in normoxic conditions throughout the period of time of the respective preconditioning protocol. The data show that CIH produced a similar increase in arterial pressure and heart rate in both CIH and SH preconditioning protocols. Respiratory parameters during basal conditions were also not affected by preconditioning to either CIH or SH. We conclude that previous exposure to CIH or SH preconditioning does not facilitate or prevent the cardiovascular changes produced by CIH. (AU)