Therapeutic hypothermia after cardiac arrest increases the plasma level of B-type natriuretic peptide
Adult
Aged, 80 and over
Heart Failure
Male
Hemodynamics
Myocardial Infarction
Blood Pressure
Stroke Volume
Middle Aged
Cardiovascular System
Article
Heart Arrest
3. Good health
03 medical and health sciences
0302 clinical medicine
Hypothermia, Induced
Natriuretic Peptide, Brain
Humans
Female
Biomarkers
Aged
DOI:
10.1038/s41598-020-72703-2
Publication Date:
2020-09-23T10:03:36Z
AUTHORS (13)
ABSTRACT
AbstractNatriuretic peptides (NPs) regulate blood pressure and fluid homeostasis and exert various effects on the cardiovascular system. Recently, the relationship between NPs and the energy metabolism has been reported, and using a cell culture experiment system, we previously showed that NP activated brown cells in a low temperature environment while also suppressing a decrease in the cell temperature. However, few reports have described the secretion of NPs in cold environments, and there have been almost no studies of B-type natriuretic peptide (BNP) in humans. We investigated how NPs respond to cold environments in 21 patients who underwent therapeutic hypothermia (TH) after cardiac arrest. The plasma BNP levels were significantly increased (more than fivefold) during TH (logarithmically from 1.98 ± 0.79 to 2.63 ± 0.59, P < 0.01). During TH, diastolic pulmonary artery pressure (PAP) significantly decreased, and there were no significant changes in the stroke volume index (SVI). This increase of BNP was not associated with any hemodynamic changes. In contrast to our findings for BNP, the change in A-type NP (ANP) was quite small. We detected a significant increase in the plasma BNP levels during TH, unrelated to hemodynamics. This elevation of BNP levels seems to be potential influenced by hypothermia.
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